Community Minded

Community Minded summaries are written by ASN Community Leaders and are published weekly in the ASN In The Loop newsletter. The summaries highlight a recent popular, controversial or other outstanding discussion in the ASN Communities. If you are interested in writing for Community Minded, please contact Mark Fitzgerald, mfitzgerald@asn-online.org

Is diabetes insipidus a contraindication to kidney donation?
A 21-year-old man with a history of congenital monogenic nephrogenic diabetes insipidus is brain dead after a car accident. His renal function (GFR) is entirely normal except for a concentration defect. Could or should these two young otherwise healthy kidneys be harvested for donation? Join this discussion.
Summary provided by Roger Rodby, MD, FASN. 

Antiphospholipid Syndrome in Pregnancy
A-29-year-old woman, who has triple positive antiphospholipid antibody (high titers of anticardiolipin, LAC and B2 glycoprotein 1) syndrome with a history of 2 DVTs, is maintained on warfarin. She is now pregnant. She is changed to Lovenox, but, because of her very high risk of thrombosis, the obstetricians want you to consider PLEX and IVIg. What are the data for this and is it robust enough to proceed? What do you think?
Summary provided by Roger Rodby, MD, FASN. 

Help with Hyponatremia?
A 77-year-old man presents with seizures and confusion and is found to have a PNa of 113 meq/l and a workup makes the diagnosis of SIADH. His PNa is increased slowly to 133 meq/l, but his confusion and seizures continue. Extensive imaging fails to show an etiology for his SIADH or his continued seizures. As an outpatient, his PNa drifts back to the mid-120s. Tolvaptan is not covered by his insurance. Urea is administered, but his PNa is still < 130 meq/l. What are your options? What could be the cause of his SIADH and persistent seizures? Ideas abound in this discussion.
Summary provided by Roger Rodby, MD, FASN. 

Polydipsia from a solute diuresis, diabetes insipidus or both?
A 22-year-old man has extreme polyuria (10.5 liters a day) following a hospitalization with mononucleosis. He denies any dietary changes. His PNa is “only” 139. His urine osmolality is 210 mosm/kg so his polyuria is partially driven by a high solute intake. But even if this is in complete diabetes insipidus, shouldn’t his PNa be higher? Is there any way to sort this out without a formal water deprivation test? What would you do next? Join the discussion.
Summary provided by Roger Rodby, MD, FASN. 

Smoldering myeloma or a monoclonal gammopathy of renal significance?
A 62-year-old man carries a diagnosis of smoldering IgA kappa multiple myeloma by hematology criteria. But he also has Fanconi syndrome and a rising creatinine in the setting of 20% plasma cells in his bone marrow. The nephrologist view is that this is clearly not a monoclonal gammopathy of unknown significance (MGUS), but one of renal significance (MGRS) and a renal biopsy is not necessary. However, the hematologist is not convinced and it may require a renal biopsy. Would you proceed with that or encourage a second (hematology) opinion? Join this discussion.
Summary provided by Roger Rodby, MD, FASN. 

Maintenance therapy for C1q nephropathy?
A patient with “C1q nephropathy” (Is this a real entity or just a variant of minimal change disease?) has steroid dependent nephrotic syndrome. Rituximab has helped but it just keeps relapsing after 12 months of no immunosupression. Other maintenance regimens have failed or were not tolerated. Is there a role for chronic rituximab in this condition, and, if so, what dose, how often, and is it safe to give for years? What do you think?
Summary provided by Roger Rodby, MD, FASN. 

Extreme electrolyte abnormalities associated with eating disorders
Usually associated with a distorted perception of one’s weight, bulimia, anorexia, diuretic and laxative abuse are not rare disorders. Despite having psychologic roots, they are extremely difficult to treat. The forced loss of electrolytes can lead to marked derangements in metabolic profiles. Prolonged hypokalemia can also lead to CKD, which is the case in these similar tragic and seemingly helpless cases. Read these three threads (one, two, three) to learn more and offer your thoughts.
Summary provided by Roger Rodby, MD, FASN. 

Hypercalcemia and HTN
A 36-year old man has mild hypercalcemia. The PTH is 105 and parathyroid sestamibi imaging is normal. Does this patient have primary hyperparathyroidism or familial hypocalciuric hypercalcemia? Will urinary calcium excretion make the diagnosis? How sensitive are these tests and how can you confidently distinguish between the two if you want to send the patient for parathyroid adenoma exploration? This thread attempts to answer these questions.
Summary provided by Roger Rodby, MD, FASN. 

IgA Vasculitis
A 51-year-old woman presents with proteinuria, hematuria and a lower extremity rash. The biopsy showed crescentic IgA nephropathy. Depending on the degree of crescents, KDIGO (2012) recommends cyclophosphamide and prednisone. But while rituximab just keeps winning us over for other GNs, is there a role for it in IgAN? The answer evolves quite a bit this thread progresses. Would you use it?
Summary provided by Roger Rodby, MD, FASN. 

Scleroderma Renal Crisis
A 52-year-old woman with a history of scleroderma presents with malignant hypertension and AKI. Does she need a renal biopsy? Her creatinine keeps climbing despite blood pressure control with an ACE inhibitor. Should a different agent be used? What is the prognosis for SRC? Is there anything else to do but wait? What do you think?
Summary provided by Roger Rodby, MD, FASN. 

Anuric AKI
A 51-year-old female presents with back pain is found to have a lumbar mass on MRI and undergoes spine surgery. Four days after a CT with contrast, and two days after an otherwise unremarkable postoperative course, she develops AKI with a creatinine of 2.5 mg/dl. She becomes anuric. Imaging shows mild hydronephrosis at best, but she is found to have retroperitoneal lymphadenopathy. Is this “post-op ATN,” delayed contrast associated AKI, or could this be a non-dilated obstruction? Is anuria a helpful clue? Your urologist refuses to intervene without obvious hydronephrosis. This case is very illustrative of the tried and true tenet, “never miss obstruction,” in AKI. How would you have handled this case?
Summary provided by Roger Rodby, MD, FASN. 

Polydipsia and polyuria
A 22-year-old man develops polyuria and polydipsia. He denies excessive water or solute intake, but has a measured urine volume of >10 liters a day with a random urine osmolality of 210 mosm/kg. He denies excessive water, protein or sodium intake, but things just don’t add up (literally). Is this a water diuresis, a solute diuresis, or both? How do we sort this out? This very interesting physiologic discussion is perfect for all nephrologists.
Summary provided by Roger Rodby, MD, FASN. 

Migraine headaches and hyponatremia
A 24-year-old woman acutely develops severe hyponatremia (<120) almost every time she gets a migraine headache. This resolves spontaneously when the migraine goes away but usually requires hospitalization for observation. What can be done to prevent this, assuming the migraines cannot be prevented? Should the patient receive “prophylactic” SIADH treatment at the first inkling of a migraine, and if so with what? This is a simple but informative physiological discussion that could significantly impact a patient’s QOL. Learn more.
Summary provided by Roger Rodby, MD, FASN. 

Embedded PD catheter complication
A 63-year-old woman has a PD catheter inserted with the tubing “embedded” in the subcutaneous tissue in anticipation of needing it later, at which time it would be externalized for normal use. The tissue over the embedded catheter becomes red and edematous. Is this an infection, an allergic reaction, or something else? How do we determine the etiology of this and does this mean that the catheter should be removed? Embedded peritoneal catheters is a very popular access procedure equivalent to “fistula first” in HD but how did this go wrong? Follow this thread to find out.
Summary provided by Roger Rodby, MD, FASN. 

Management of Hypercalcemia in Pregnant Transplant Recipient
A 30-year-old woman with a stable renal transplant since 2015 has hypercalcemia (mid 12 mg/dl range) from hyperparathyroidism. She is pregnant and can no longer take cinacalcet because of unknown safety during pregnancy. Should this simply be watched, or should she undergo parathyroid surgery and what are the risks? A decision was made, and it doesn’t necessarily turn out well although the nature of the less than optimal outcome may come as a surprise. Join this fascinating discussion.
Summary provided by Roger Rodby, MD, FASN. 

Elevated ANCA titers pre-renal transplant
A 30-year-old man with ESRD from MPA has a donor. The patient has been on dialysis for almost a year. His initial presentation was “renal limited” vasculitis and he presented with advanced renal disease requiring dialysis, so he only received a month of treatment. His clinical course on dialysis has been uneventful. In evaluating him for transplant he is found to have an MPO level that has gone from 1100 to 1350 over the last 5 months. What is the value of this biomarker pre-transplant? Does this predict vasculitis recurrence? Should this high ANCA level be targeted with immunosuppression before advancing to transplantation even though he is otherwise asymptomatic? What do you think? 
Summary provided by Roger Rodby, MD, FASN. 

A brown tumor?
A patient on peritoneal dialysis develops a swelling in his shoulder. CT and MRI identifies a multilobular cystic mass that clinically diagnoses as a brown tumor, but there is enough calcium in the mass that tumoral calcinosis has not been ruled out. Additionally, the patient’s PTH level is only 3-400. Does that relatively low-level rule out a hyperparathyroid lesion such as a brown tumor? Should B-2 microglobulin related amyloidosis in the differential diagnosis? How do we sort this out and how it is best treated? Follow this thread to find out. 
Summary provided by Roger Rodby, MD, FASN. 

Congo red positive glomeruli in a renal transplant
A 73-year-old man develops proteinuria in his kidney transplant. A biopsy shows strong congo red staining and randomly scattered fibrils on EM suggesting amyloidosis, but some of the fibrillary structures look larger and more organized than typical primary amyloidosis. A non-amyloid yet “congophilic” glomerulopathy that should be considered is Fibrillary GN. Is mass spec on the tissue always required as the next step in confirming and identifying the specific etiology of amyloid? Can the tissue be analyzed for DNAJB9? What other data do we need to make a diagnosis?
Summary provided by Roger Rodby, MD, FASN. 

An elderly man with a serum Na of 164 and yet no thirst
An 80-year-old man presents with a serum sodium of 164 meq/l and a urine osmolality of 960 mosm/kg. He has no thirst. Imaging of his hypothalamus in unremarkable. He is severely psychologically impaired, and the discussion focuses around the causes of adipsic hypernatremia and the practical solutions. How would you end up managing this individual? 
Summary provided by Roger Rodby, MD, FASN. 

When do you biopsy a diabetic?
A 48-year-old man with seven years of diabetes presents with 14 grams of proteinuria and a creatinine of 1 mg/dl. Is there a role for a serologic work-up? Is there a role for a renal biopsy? This thread starts with those questions and moves into “Occam’s razor” and “Hickam’s dictum.” Where these questions really answered in this thread of more than 50 responses? See for yourself.
Summary provided by Roger Rodby, MD, FASN. 

Raw Milk leads to Brucella and AKI
A 60-year-old woman from upper Egypt drank raw milk and developed Brucella bacteremia and AKI. She was initially hypotensive but responded to antibiotics, but her AKI continued to progress. She was found to have profound hypocomplementemia which brought up the possibility that this was an infectious related GN. What are the renal lesions associated with Brucellosis and what will happen? Follow this thread to find out.
Summary provided by Roger Rodby, MD, FASN. 

Lupus patient refusing biopsy – What are your options?
A 28-year-old woman with SLE is serologically and clinically active with proteinuria and hematuria. She adamantly refuses a renal biopsy. What treatment approach makes the most sense and should she get prophylactic osteoporosis treatment? As an aside, the very interesting question of any effect bariatric surgery may have on autoimmune diseases is also discussed.  
Summary provided by Roger Rodby, MD, FASN. 

Calciphylaxis in a Patient on Peritoneal Dialysis
This discussion started in January 2019 but is resurrected with a patient that did not tolerate sodium thiosulfate (STS). What are the many options for this devastating disease? Should PD patients get transferred to HD to facilitate STS administration? Is there a role for Vit K empirically and if so what route and how often? Should dialysis be intensified? Should you take a stepwise approach or go for the Kitchen Sink? Opinions abound despite almost no randomized trial data. 
Summary provided by Roger Rodby, MD, FASN. 

A former cop goes down with unexplained metabolic acidosis
A retired policeman presents with confusion after working with polyurethane lacquer in a closed garage. His blood gas shows a respiratory alkalosis with a [HCO3] of 15 and an anion gap of 14. His lips are red, but CO levels are minimal and methemoglobin levels were also normal. A suggestion is made of the possibility of toluene inhalation causing a non-anion gap metabolic acidosis (in addition to an independent respiratory alkalosis). A fun discussion ensues about this rare condition and how toluene may be an excellent or ridiculous diagnosis. 
Summary provided by Roger Rodby, MD, FASN. 

Scleroderma Renal Crisis and AKI – Can we influence the prognosis?
A 52 year old woman with a history of scleroderma develops severe hypertension. The blood pressure is controlled with ACE inhibition, but acute renal failure develops. This is assumed to be scleroderma renal crisis but is a renal biopsy necessary? What is the role of HTN versus its acute lowering in the development of acute renal failure? Is RAASi a double-edged sword? Should the ACEi dose be minimized if the blood pressure can be controlled with other agents? What would you recommend? 
Summary provided by Roger Rodby, MD, FASN. 

Monoclonal gammopathy of renal significance with no clonal cell line identified
A 60 year old woman presents with nephrotic syndrome and a kidney biopsy reveals a proliferative GN with monoclonal IgG3 read as monoclonal gammopathy of renal significance (MGRS). Evaluation of the serum and the urine fail to demonstrate a monoclonal gammopathy. A bone marrow biopsy is similarly unremarkable without any clonal population of cells identified. The hematologist therefore fails to acknowledge this as a clonal lymphocyte or plasma cell disorder. The treatment for this MGRS is clonal directed therapy, but what do you do if a clone cannot be identified? This is not an uncommon scenario that nephrologists need to recognize and educate some of our hematologist colleagues. A treatment algorithm is suggested in this most interesting case
Summary provided by Roger Rodby, MD, FASN. 

Timing of Preemptive Kidney Transplantation: Is the only way not to be too late to be too early? 
A 52-year-old man with autosomal dominant polycystic kidney disease, eGFR around 20, has a suitable living kidney donor. He wishes to proceed with a living donor kidney transplant. Should he postpone transplant until eGFR is declining to 10-15 or even lower or undergo transplant? What are the pros and cons? When is the best time for a preemptive kidney transplant and do patients with preemptive kidney transplants have better patient and graft survival and if so why? This thread attempts to answer these questions. The opinions are quite divided in this lively discussion
Summary provided by Mark Lerman, MD, FASN. 

Severe Nephrotic Syndrome in a Renal Transplant associated with CMV Viremia 
A 54 year-old Caucasian man s/p cadaver renal transplant from an AA donor presents with sudden onset of AKI and nephrotic syndrome (SCr 0.8 to 2.3 mg/dl with urine P/C ratio of 22 g/g). His CMV prophylaxis had been stopped 3 months prior and he became severely viremic with CMV. A biopsy revealed mild cellular rejection Banff 1A, TMA and a single collapsing FSGS lesion. EMs showed only diffuse FP effacement. He is treated with IV steroids and ganciclovir with resolution of CMV viremia. The AKI resolved and proteinuria improved to 4g/g. It is postulated that his acute CMV viremia triggered an interferon storm leading to upregulated APOL1 (donor was AA) mediated podocyte toxicity causing collapsing GN. What do you do now? Watch? Ganciclovir? Use an interferon inhibitor? Change immunosuppression? Join this fascinating discussion.
Summary provided by Vasil Peev, MD.

Relapsing Membranous Glomerulonephritis 
A 47 year old woman had membranous GN 8 years ago but went into spontaneous remission and had been fine until she developed 8 grams of proteinuria and a PLA2R antibody ELISA level of >500. PLA2R histologic staining and serum levels were not available when she first developed MGN 8 years ago. Does she need a repeat renal biopsy? Given that she had a spontaneous remission with her first episode, should she be watched for spontaneous remission again, or does this level of proteinuria and PLA2R antibody level mandate treatment now? What are your thoughts? 
Summary provided by Roger Rodby, MD, MS.

Steroid dependent MCD 
A patient has steroid dependent minimal change disease (MCD). He also has CKD. What are the treatment options? One thing is for certain, steroid dependent MCD can be put into long term remission if approached even moderately aggressively. But should CNIs be avoided in patients with CKD? Should rituximab be the first choice and if so, how hard is it to get approval for this agent? What are accepted rituximab protocols? Read the thread for an important discussion about this debilitating condition. 
Summary provided by Roger Rodby, MD, MS.

Hyponatremia: What is the best approach? 
A 74 year old woman with lung cancer presents with symptomatic hyponatremia with a PNa of 115 meq/l. After initial treatment gets her PNa up to 123, she is fluid restricted and her PNa does not budge. What is the role of urine Na and K and osmolality in this new steady state? What are the pros and cons of fluid restriction, increased osmotic intake with oral urea, and ADH antagonism with tolvaptan? If tolvaptan is used, what should the starting dose be? This is a practical discussion.
Summary provided by Roger Rodby, MD, MS.

Do steroids quickly change histology? 
Your patient needs a renal biopsy but it may take up to a week before you have results. You would like to immediately start steroids because delay may put the patient at risk, but you are concerned about the effect that will have on the histology. What do we know about this topic? Should your decision to wait or treat be based on the clinical presentation (nephrotic or nephritic syndrome?) This post explores this dilemma.  
Summary provided by Roger Rodby, MD, MS.

Recurrent FSGS and plasmapheresis after donor transplant 
A 30-year old man with ESRD received a cadaver donor transplant. His ESRD was from FSGS at age 13 suggesting primary FSGS. The transplant functioned initially but then developed AKI associated with high levels of proteinuria. Is this time frame too early for recurrent FSGS? While the proteinuria is suggestive of recurrent disease, the AKI suggests rejection. Should the patient get empiric plasmapheresis, or a renal biopsy, or both? Vastly different opinions are offered in this case. What would you do?
Summary provided by Roger Rodby, MD, MS.

Mannitol & CRRT for Elevated ICP 
Increased intracranial pressure (ICP) can quickly lead to brain herniation and death. Mannitol is often used to acutely lower ICP in patients with intact renal function. But what do you do when renal failure is present, and you cannot expect an osmotic diuresis? Do you use a form of renal replacement therapy? Is mannitol the best option or should hypertonic saline be used? There are many complicating factors when intracranial hypertension accompanies renal failure that are discussed in this interesting thread
Summary provided by Roger Rodby, MD, MS.

Treatment Failure for Lupus Nephritis - What Next? 
A 44-year old woman with DPGN lupus nephritis receives induction therapy with pulse dose steroids followed by MMF and oral steroids. She initially responds but then develops worsening renal failure associated with microangiopathic hemolytic anemia. Various options are discussed including plasmapheresis, rituximab, cyclophosphamide and even eculizumab! Which would you opt for?
Summary provided by Roger Rodby, MD, MS.

Detecting Citrate Toxicity 
Citrate is often used as an anticoagulant for continuous renal replacement therapy. Its use can be tricky and there are risks of many electrolyte abnormalities. What is citrate toxicity? How would it present, and can there be both too little and too much citrate? This thread discusses the physiology behind citrate use in CRRT.
Summary provided by Roger Rodby, MD, MS.

Stuck in the Tunnel: Catheter Removal 
Tunneled hemodialysis catheters are typically temporary and thus eventually need to be removed. The longer they are in the more they may adhere to the tunnel or even internally to the vein. What is the safest way of removing them and what are the possible risks if the method of removal is simply by pulling hard? As common as these catheters are, this thread demonstrates how different people do things very differently.
Summary provided by Roger Rodby, MD, MS.

Hypercalcemia and HTN - Benign or Not? 
A 36 year old man has mild hypercalcemia. The PTH is 105 and parathyroid sestamibi imaging is normal. Does this patient have primary hyperparathyroidism or familial hypocalciuric hypercalcemia (FHH)? Will urinary calcium excretion make the diagnosis? How sensitive are these tests and how can you confidently distinguish between the two if you want to send the patient for parathyroid adenoma exploration? This thread attempts to answer these questions.
Summary provided by Roger Rodby, MD, MS.

Year in Review
As we approach the close of 2019, thank you for your ongoing support of ASN Communities. This has been a great year of participation and engagement. A year ago, we began publishing weekly “Community Minded” summaries highlighting provocative or challenging discussions from ASN Communities. The most popular was “Tubulointerstitial Nephritis in a Young Patient,” followed by “When is the Right time for CRRT?” Over 1,500 conversations took place this year in Communities with participation from members representing 180 countries. Another highlight this year was the CJASN published article, Foamy Urine: Is this a Sign of Kidney Disease, that sprang from a Communities conversation. To learn more about the educational value of Communities, please read the Kidney News Online Communities Year in Review article. Thank you again for your participation!

IgA Vasculitis
A 51-year-old woman presents with proteinuria, hematuria and a lower extremity rash. The biopsy showed crescentic IgA nephropathy. Depending on the degree of crescents, KDIGO (2012) recommends cyclophosphamide and prednisone. But while rituximab just keeps winning us over for other GNs, is there a role for it in IgAN? The answer evolves quite a bit this thread progresses. Would you use it?
Summary provided by Roger Rodby, MD, MS.

Acute Kidney Injury with immune check point inhibitors, is it all acute interstitial nephritis (AIN)?
A patient with known lung cancer and CKD receives the immune check point inhibitor- pembrolizumab( PD-1 inhibitor) for a few months. AKI ensues few months post treatment. How closely tied is this rise in creatinine to the PD-1 inhibitor? Can this happen even months following the initiation of treatment? Is it AIN? or could this be acute tubular injury, vasculitis or a glomerular process? Is a kidney biopsy necessary? This is a very interesting discussion in the Onco-Nephrology forum on an emerging topic of AKI with PD-1 inhibitors in nephrology. What are your thoughts? How would you treat?
Summary provided by Kenar D. Jhaveri, MD

Citrate toxicity while on CRRT
A potential complication of CRRT is Citrate toxicity. When citrate enters the patient’s circulation, each mole of citrate is potentially metabolized in the Krebs cycle to bicarbonate mostly in the liver mitochondria. Metabolic acidosis can occur when citrate accumulates in patients who cannot metabolize citrate (weak acid), such as those with liver failure. The criteria that we use to detect citrate toxicity include worsening metabolic acidosis, ionized hypocalcemia from unmetabolized calcium-citrate complexes, rising total calcium levels which lead to a disproportional rise in total systemic calcium to ionized calcium ratio of greater than 2.5. Therapy involves reducing or discontinue citrate infusion, increasing convective or diffusive clearance of citrate and increasing calcium infusion to correct ionized hypocalcemia. Unsure if uncommon or under reported, share your experience in this thread.
Summary provided by Jorge Castaneda, MD

Membranous GN, what are the risks of recurrence?
Few things are more devastating that the loss of a transplanted kidney to the disease that caused the failure of the native kidneys in the first place! With the discovery of antiphospholipase 2 receptor antibodies, the understanding of the pathophysiology and management of idiopathic membranous glomerulonephritis (iMGN) has exploded. How can this information be used to determine the risk of iMGN recurrence in a renal transplant, and should we also use this to decide if and when a transplant should be done?
Summary provided by Roger Rodby, MD, MS.

What is the role of the newer potassium lowering agents?
Sodium polystyrene sulfonate (SPS) has been the “go-to” for hyperkalemia for years. It is not liked by patients (palatability) and it has been rarely associated with colonic necrosis. In the last several years two new medications have been approved by the FDA for hyperkalemia: Lokelma (sodium zirconium cyclosilicate) and Veltassa (patiromer). How, should, and will these drugs replace SPS? Should they be used for the acute reduction in potassium? This Communities thread suggest that they are here to stay and that SPS will likely become a thing of the past. Are you using them yet?
Summary provided by Roger Rodby, MD, MS

Treatment of acute hyponatremia?
Because osmotic demyelination syndrome (ODS) can have devastating consequences, few things are harder and scarier for a nephrologist than the acute treatment of hyponatremia. Like Goldilocks and the three bears, it needs to be “just right”, which is easier said than done even with a well-planned and diligent management strategy. ODS is a consequence of a too rapid increase in extracellular osmolality in chronic hyponatremia where cell volume is essentially normal. What about acute hyponatremia? Are the risks the same? How do we even know if it is acute vs chronic? These questions are discussed in this Communities thread.
Summary provided by Roger Rodby, MD, MS


MGUS or MGRS? When to and what to biopsy?
An 83-y/o man with diabetes is found to have an IgG kappa paraprotein with a markedly elevated free kappa serum level. His bone marrow evaluation while very abnormal does not meet the requirements for a diagnosis of multiple myeloma. Therefore, a renal biopsy seems to be required to make the diagnosis of a monoclonal gammopathy of renal significance so he can receive treatment. Are there increased risks in an 83-y/o patient? Is there a role of a fat pad biopsy first, and what are the sensitivities and specificities of that less invasive test? How would you treat in this very interesting case?
Summary provided by Roger Rodby, MD, MS

Should midodrine be used for dialysis associated hypotension?
Midodrine is commonly prescribed for patients that become hypotensive during dialysis, despite little data on its efficacy. It is generally considered benign, but its use has been associated with an increased mortality. Is this related to the drug or the increased morbidity and mortality of the patient population that needs it? The discussants fall into two very different camps: pro-midodrine and anti-midodrine. Which camp are you in?
Summary provided by Roger Rodby, MD, MS


Hypophosphatemia from IV iron?
One of the newer intravenous iron preparations ferric carboxymaltose has been associated with profound hypophosphatemia. There are no other proximal tubular defects associated with this medication. The drug appears to increase FGF23 levels with resultant hyperphosphaturia despite hypophosphatemia (PO4 wasting), similar to the hypophosphatemia seen in oncogenic osteomalacia. Is this an idiosyncratic reaction? Is there a genetic predisposition? Questions remain but this is a side effect worthy of notice as we use this drug in CKD.
Summary provided by Roger Rodby, MD, MS

“Essential hypernatremia” – A reset osmostat?
A patient is found to have a plasma sodium (PNa) of 159 meq/l and a urine osmolality of 1000 mosm/l yet denies thirst. He is given IV D5W and starts diluting his urine when his PNa is reduced to 152! It appears he has a reset osmostat, but just what is that? How closely tied are thirst and osmotic ADH release? Is a “reset osmostat” a single disease or could it have many pathologies, and does this patient need imaging of his hypothalmus? This is a very interesting discussion of a very uncommon disease state but reinforces our knowledge of normal thirst and water handling mechanisms.
Summary provided by Roger Rodby, MD, MS

Is there a role for low protein diets for CKD?
The Modification of Diet in Renal Disease (MDRD) results were published in 1994 as a “negative” trial but some questions still remain. Was the MDRD properly powered? Was the GFR slope outcome measure flawed? This thread reevaluates the role of protein restriction not only for slowing progression of renal disease, but also for delaying the need for dialysis through decreased uremic toxins, especially with a “plant based” diet. Did we “throw out the baby with the bath water”?


Home HD without a partner?
There are financial incentives for any home dialysis therapy. Peritoneal dialysis does not require a partner, but traditionally hemodialysis performed alone was simply considered way too risky. However, machine technology and patient monitoring have improved. What is the FDA’s stance on this? Are the conservative practices in the US the same as the rest of the world? This thread may open your eyes and open up options for your patients!

Nephrotic syndrome in a patient with one normal sized and one small kidney
A 60-y/o man presents with edema and is found to have 9 g/d of proteinuria and a creatinine of 1.7 mg/dl. His BP was 200/100. His kidney ultrasound shows asymmetric kidneys, 11.1 and 8.5 cm in length. Several questions arise. With the HTN do you work him up for renal artery stenosis? Should he be considered having a solitary kidney from a renal biopsy risk standpoint? The proteinuria improves with BP control and some opinions are to do a serologic workup alone and just watch the patient while others think that renal artery visualization and then possible a renal biopsy are indicated. What do you think?
Summary provided by Roger Rodby, MD, MS

A 55 year old woman with Unexplained Hypokalemia: A rare disease or something she is doing to herself?
A 55-y/o woman presents with potassium levels that run 2.5 meq/l despite taking 60 meq of K a day. Her blood pressure is normal. Her renin and aldo are both very low. This lively discussion focuses on the work-up of hypokalemia and just how difficult it can be if you cannot rely on a history. Urine chemistries can help but not if you cannot be sure what the patient may or may not be taking. This case has a solution but don’t just skip to the end, follow the thread and see what you think first.
Summary provided by Roger Rodby, MD, MS


A tough case of IgA nephropathy
A 48 y/o woman presents with HTN and a creatinine that increased from 0.9 to 2.6 mg/dl in only 7 months. A renal biopsy demonstrates IgA nephropathy with 40% of glomeruli sclerotic, 20% segmental sclerosis, 11% crescents and 6% segmental necrosis. KDIGO requires 50% crescents and rapid renal failure to consider cyclophosphamide. This patient’s IgAN has clearly been very destructive thus far. Do you follow KDIGO and give only steroids or treat more aggressively like a vasculitis? And is there a role for rituximab or plaquinil? What would you do?
Summary provided by Roger Rodby, MD, MS


Peritoneal Dialysis in a scuba diving instructor?

A patient with CKD is approaching ESRD and is considering PD. The patient is a scuba diving instructor and thus many questions arise. What are the risks of an exit site infection in salt water v fresh water? Should special care be taken to the exit site? Should he wear a wet or dry suit? Should he drain before diving? And finally, a very interesting concern that arose in the discussion is the risk of central volume overload from the movement of fluid from the interstitial space to the intravascular space because of the increased atmospheric pressure, risking potentially disastrous pulmonary edema while underwater!
Summary provided by Roger Rodby, MD, MS

A 63 year old Woman with Hyponatremia and Polyuria
A 63-y/o woman with schizophrenia presents with seizures and a PNa of 111 meq/l. She receives 3% saline but then develops polyuria and overcorrects requiring D5W and DDAVP. Subsequent history describes a patient with polydipsia. Her Uosm was 162 mosm/kg. The discussion focuses around the topic of psychogenic polydipsia and the exact role that the degree of urinary dilution and the amount solute intake plays in the ability to excrete excessive water intake. Using oral urea to increase solute load is discussed at length, with some nice calculations showing the expected effect it will have on the BUN. Can you follow the math in this discussion?
Summary provided by Roger Rodby, MD, MS

Do Buttonholes cause more or less infections?
Buttonhole associated infections have been a topic of growing concern over the past few years. With the utility of this technique to facilitate self-cannulation, particularly among home hemodialysis patients, discussing the pros and cons of buttonholes is especially relevant in the midst of efforts to promote home therapies. While infection due to technique deviation has been a concern, there are other concerns including bacterial colonization of buttonhole tracts and practicality of using buttonholes for in-center dialysis. Read this interesting thread to learn more.
Summary provided by Leslie Wong, MD, MBA, FASN

A patient with advanced CKD and a monoclonal gammopathy, do you biopsy?
A 46-y/o man presents with severe HTN, a serum creatinine of 11, a benign urine but with a urine protein/creatinine ratio of 5 g/g. Serologies unremarkable but he has a monoclonal IgG-lambda in his blood. He is also found to have new onset CHF. Is this all just malignant HTN or could he have a monoclonal gammopathy of renal significance or even amyloid? Kidney size is 7.4 and 8.6 cm. There are very different opinions on the need for a renal biopsy as well as the safety given the patient’s HTN and CKD. What would you do?
Summary provided by Roger Rodby, MD, MS

Is the time right for CRRT, and who should provide it?
A 42-y/o man is emergently cannulated for VV ECMO for ARDS and develops oliguria. His labs after several hours reveal a BUN of 32 mg/dL and creatinine of 0.9 mg/dL. On a flow of ~ 5 L/min and 100% oxygen his pH is 7.35 and lactate is 1.8. He has made only 20 ml/hr of urine output over 5 hours. There is minimal improvement with a diuretic challenge and the patient is already 3 liters positive in fluid balance. Is it time to start him on CRRT? Should it be started now by the intensivist or can it wait until tomorrow when the nephrologist arrives. What is the evidence for starting RRT early and should this be a procedure provided exclusively by nephrologists? Read the discussion and let us know what you would have done.

Summary provided by Rajit Basu, MD, MS


How do you treat AKI in resource-poor settings?
Medical resources are almost unlimited in developed countries. Certainly, something as “simple” as dialysis is easy to provide for patients with AKI. But what about countries where resources can be extremely limited? What options do you have? This discussion explores the options that may be available, with an attempt “to think outside the box” when it comes to these difficult clinical and socioeconomic scenarios.


Hyponatremia in a 76 y/o man on Vasopressin for Sepsis
A 76-year-old man required vasopressin for sepsis and developed severe hyponatremia over a 3 day period. The vasopressin was discontinued, and he had an immediate water diuresis. Vasopressin has both V1 (vascular pressor) and V2 (renal ADH) activity but ADH activity with hyponatremia (as was present in this case) is very rarely seen when it is used as a pressor in the ICU setting. Read this very interesting thread for some explanation of this interesting physiology.
Summary provided by Roger Rodby, MD, MS


Is moderately increased albuminuria in DM benign?
RASS inhibition providing renoprotection is a main component in the management of hypertensive proteinuric diabetic kidney disease. What do you do if you have a diabetic patient with low grade proteinuria but a normal BP since the seminal studies on this topic involved patients with an elevated blood pressure? How far can you extrapolate a study? Let us know your thoughts.
Summary provided by Roger Rodby, MD, MS


HTN in a 20 Year Old with a Positive Family History for HTN?
A 20-year-old has hypertension for 1 year. His father age was also found to have HTN at age 30.The patient has a normal [HCO3] and a normal [K]. Work-up thus far has shown normal renal artery Doppler studies, normal urinalysis, creatinine, renin, aldosterone and AM cortisol levels. Workup for pheochromocytoma is negative. Given the family history of HTN in his father at a such a young age as well, does the patient deserve genetic studies for an inheritable form of HTN? Not everyone agrees on the answer to that question in this Discussion!

Summary provided by Roger Rodby, MD, MS


D-RTA and NSAIDS
NSAIDs and distal renal tubular acidosis? How can that be? NSAIDs are over the counter, they are inexpensive, and their use is very very common. But if they caused an RTA, how could that not be common knowledge. Well apparently, there is a link to their (oddly only ibuprofen) use, but mostly in much higher than typically prescribed doses and usually in conjunction with codeine. Is this just some odd toxicology trivia, or is this something we really should be aware of? You decide after you read this thread.

Summary provided by Roger Rodby, MD, MS

Does Internal Jugular Vein Thrombosis Need Anticoagulation?
A 62-year-old ESRD patient receives HD through a R internal jugular vein non-tunneled catheter. A bacteremia mandates the catheter removal. She receives antibiotics and the infection clears. Her AV fistula is not mature, and she needs a tunneled HD catheter. Upon placing the catheter under ultrasound, a clot is incidentally found in the IJ vein. The primary medical service wants to start heparin and warfarin. What is the role of anticoagulation for catheter related clots in the neck and arms? Do you have to anticoagulate, remove the catheter? The ASN Communities gets the experts’ opinions on this one.
Summary provided by Roger Rodby, MD, MS

IgA vasculitis
An 80-year-old develops a skin rash, abdominal pain with rectal bleeding, hematuria and AKI. A skin biopsy showed leukocytoclastic vasculitis, but immunofluorescent staining was not performed. ANCA testing is negative. He is treated with steroids alone and the rash, abdominal pain and renal function all improve. He refuses a renal biopsy. How do we go forward in treating this apparent case of HSP? The majority of the data on treating HSP comes from the pediatric literature, but HSP in adults has a worse prognosis than HSP in children. Should this change our diagnostic and therapeutic approach to adults with this presentation? What do you do when guidelines are vague? Read this discussion for some opinions on this matter.

Summary provided by Roger Rodby, MD, MS

Membranous Glomerulonephritis
The ability to test for antibodies to PLA2R in blood and on the kidney has been one of the major advancements in the diagnosis and treatment of Glomerular Diseases of the last decade if not longer. Should “primary MGN” be defined by these antibodies and if so, what does it mean if the serum tests negative but the tissue positive. And what is the role of antibodies to thrombospondin (THSD7A)? How do the results of these antibody tests influence treatment decisions? These issues and more are tackled.
Summary provided by Roger Rodby, MD, MS

Alpha-ketoanalogues to Slow Progression of CKD 4-5?
It has been almost 25 years since the Modification of Diet in Renal Disease (MDRD) results were published in the NEJM. While the MDRD was a negative trial, protein restriction may still be of value in slowing the progression of kidney disease. This is the basis for this Communities thread. The background behind the MDRD is discussed, as well as what went “wrong”. Was it truly a negative trial or did it succumb to some bad luck based on outcome measures and recruitment population? This study will never be repeated, so we need to make the best of what we have. The practicalities of protein restriction and ketoanalogue supplementation are discussed as well.
Summary provided by Roger Rodby, MD, MS

Lithium, Bipolar Disorder & Hypercalcemia
A patient on long-term lithium (Li) for bipolar disorder develops hypercalcemia (11 mg/dl). The PTH is mildly elevated and this is most likely related to Li use. While other drugs have been used to replace Li in patients with psychiatric disorders in which one of the many renal complications of Li occurs, this patient is very resistant to trying an alternative. What is the mechanism of Li induced hypercalcemia? What work-up is required and just how concerning is this Ca level in the context of its etiology? Does it even need “treatment”? ASN Communities offers expert opinions in this interesting thread. How would you approach this patient?
Summary provided by Roger Rodby, MD, MS


Contraception in CKD
What is the role of contraception discussions for women with CKD? What are the risks of pregnancy in CKD, and are some of these risks disease dependent that may dictate just what form of contraception may be preferred? How much does CKD affect fertility and should they be aware of that so that they do not delay trying to get pregnant as their CKD may progress and affect fertility even further. These topics are often an overlooked. What is your practice?
Summary provided by Roger Rodby, MD, MS

Sodium Bicarbonate in Respiratory Acidosis
What should you do with a patient with a moderately severe mixed metabolic and respiratory acidosis that needs dialysis? What are the acid base concerns related to the treatment? What is the physiology behind these concerns? This discussion gets to the basics of buffer function as well as CO2 production and excretion. It is never a bad time to review basic physiological principles. If they were easy everyone could be a nephrologist!
Summary provided by Roger Rodby, MD, MS

AA Amyloidosis with Crescents in Rheumatoid Arthritis Patient
Adding insult to injury, AA amyloidosis is a devastating complication that may appear after years of a similarly devasting chronic inflammatory illness. Add crescentic GN to this mix and you really have yourself a real diagnostic and therapeutic quandary. Are these two independent glomerular processes? Either way, what are the options for treating AA amyloid in RA whether the crescents are related or not? The pros opine in this illuminating discussion. How do you treat your patients with these conditions?
Summary provided by Roger Rodby, MD, MS


RRT for Patient with Cerebral Aneurysm
A 63-year-old female presents with an intracranial hemorrhage (with subdural and intraventricular extension and a saccular aneurysm) is found to have renal failure from previously undiagnosed polycystic kidney disease and requires renal replacement therapy (RRT). Concerns about RRT induced acute blood pressure changes or disequilibrium syndrome bring up the discussion of what is the safest method of RRT to minimize the risk of cerebral hypoperfusion or cerebral edema: CRRT, gentle hemodialysis, or even peritoneal dialysis. The pros and cons of each of these options are discussed in this interesting thread.
Summary provided by Roger Rodby, MD, MS

Organ Donor Pool
With the expanding list of patients requiring kidney transplants, there is acknowledgement by the medical community that we have yet to identify the most optimal way of allocating/utilizing many of our donor organs. The discard rate is unacceptably high. In 2013, OPTN/UNOS revised existing policies for Public Health Service’s increased risk (PHS-IR) donors and nucleic acid testing (NAT) helped identify which PHS-IR donors were at highest risk for transmission of hepatitis B, C and HIV. Underutilization of these organs continues. Use of high KDPI kidney­­s and better distribution of available kidneys remain two areas in need of improvement. Identifying ways to more effectively utilize and distribute these resources remains a goal of the transplant community. Read the thread to learn more and comment about these ideas.
Summary provided by Mark Lerman, MD


Post Parathyroidectomy Hospital Stay
A simple question is posed: “Do patients get discharged on the same day or stay for several days after the surgery? What is your protocol? How long do patients usually stay as an inpatient?” This is an important question because many patients develop “Hungry Bone Syndrome (HBS) following parathyroidectomy for severe secondary or tertiary hyperparathyroidism. It is important to appreciate that HBS can be a dangerous but accepted immediate or delayed outcome of parathyroidectomy. Risk factors, natural history, and treatment options for HBS, and proposes strategies that may even be used to prevent this disorder are discussed in length. Opinions span the globe from West Virginia to Singapore.
Summary provided by Roger Rodby, MD, MS

Dialysis Decisions in Pregnancy Pre-ESRD
We recently had two dialysis-in-pregnancy posts: “Pregnant Transplant Patient with Poor Renal Function” and “Pregnant Patient With CKD 4”. Clear guidelines exist on managing the rare ESRD pregnant patient, but there is less known about how to manage pre-ESRD CKD and pregnancy. In the former, renal replacement therapy (RRT) is increased to target a weekly KT/V as high as 6-8 and a BUN as low as <20 mg/dl. But when do you start RRT on a non-ESRD CKD pregnant patient, and given that for any level of BUN and creatinine, that patient should healthier than an anuric patient on dialysis, should the BUN target be different? These important questions are pondered in these posts.
Summary provided by Roger Rodby, MD, MS

Natural History of AKI
Acute kidney injury – how good are nephrologists in predicting AKI recovery, and how long is it going to take until the recovery process is complete? Does it continue to improve in some cases over a year or more? Is delayed recovery from AKI now being increasingly recognized? Many outpatient dialysis facilities are now excepting patients with acute kidney injury that are dialysis dependent. Is delayed recovery in these patients being missed? What is the impact of different drug regimens? Do you know the baseline kidney function prior to AKI? What additional research is needed? Join the conversation to learn how your peers answered these questions and to tell us how you would answer them.
Summary provided by Mark Lerman, MD, FASN

Hypertensive Donors
An otherwise healthy 34-year-old man wants to donate a kidney. He has HTN for 2 years only, and is controlled (127/87 as measured using ABPM) with only perindopril 4 mg/day. His BMI is 23 kg/m2, he has no proteinuria and his creatinine is 0.95. He has no target organ damage. Should he be considered for donation? What are the risks of mild HTN on a solitary kidney going forward knowing he should have many years of life ahead of him. Can “do no harm” go too far? The experts do not agree with each other on this ethical and medical dilemma. What is your opinion?
Summary provided by Roger Rodby, MD, MS

ARBs and Lung Cancer
RAAS inhibitor use (ACEi and ARBs) is fairly ubiquitous in cardiology, nephrology and general medicine. Over the last year we have seen FDA warnings on three different generic ARBs finding trace amounts of various carcinogens in them. We hear about one, and change our patient to a different ARB, only to find that it later is also reported to contain a carcinogen! And around the same time a report comes out linking ACEi use to lung cancer. What do we make of these issues? Is this prudent information we should act on or “Chicken Little”? You will need to form your own opinion and approach as the Discussants struggle with this dilemma. What approach(es) have you taken?
Summary provided by Roger Rodby, MD, MS

What Degree of Hemodynamic Instability Will Preclude Even CRRT
The question posed “What degree of hemodynamic instability will preclude even CRRT”? Realizing that CRRT was developed precisely for patients too unstable for intermittent hemodialysis, some patients still seem too hemodynamically tenuous to tolerate any form of RRT. What are the considerations that give us concern about isovolemic CRRT in these most unstable patients? Are these concerns warranted? Is there a point of futility? What is the role of PD in AKI and what are the special considerations that may make it less or more desirable means of RRT in this setting? Hopefully this discussion will illuminate your management or at least stimulate thought about this ICU AKI unstable patient population.
Summary provided by Roger Rodby, MD, MS

Advising Junior Faculty on How to Publish
Junior faculty who are not involved in research are often challenged to get their work published. It’s not just that they are unknown but they don’t know how to approach the process. To which journal should they submit their case reports, reviews, or quality improvement projects? How should they start and on what topic? How can they learn from rejection letters? What skills must be mastered to become an effective scientific writer? The discussion participants, all from different stages in their careers and all of whom have published, have offered some terrific feedback that anybody looking to publish should read. It’s not too late to join the conversation in the Career Advancement Community and add your recommendations and feedback.
Summary provided by Kambiz Kalantari, MD, MS

Foamy Urine
We are all taught that “foamy urine” is classic for nephrotic syndrome. But just how specific is foamy urine for predicting proteinuria? Is proteinuria alone enough or do you need accompanying lipiduria? And how does proteinuria cause foamy urine in the first place? Is foamy urine different than urine with bubbles? This Discussion delves into this interesting and perhaps whimsical topic. Read it if for no other reason than to learn some trivia on what makes beer foam.
Summary provided by Roger Rodby MD, FACP, FASN

Supporting the Mission
Studies have indicated that how we deliver nephrology education may improve interest in nephrology as a future career for trainees. Kidney educators are reviewing and evaluating new and unique methods for teaching and sharing of information. Do different tools lend themselves to different specialties or disease conditions like Acid Base and Electrolyte issues? What is the role of social media in training? Do Concept Maps work? Are small group learning sessions effective? Should educators consider the development of a nephrology toolbox that would contain unique tips and techniques? Are Flipped Classrooms the answer? Read the thread to learn more about these and other ideas. What innovative ideas have you implemented, or would you recommend?

Summary provided by Anna Burgner, MD

Puzzling Hyponatremia
A 72 year old man with a history of a pituitary tumor presents with seizures and a serum Na of 125 meq/l. He appeared hypovolemic and his UNa was <20 meq/l. He was given normal saline, and his PNa increased to 130 meq/l, but his UNa remained <20 and he developed edema. He was subsequently found to have hypopituitary hypocortisolism. He was given hydrocortisone alone and his PNa eventually normalized. The discussion focused on how hypocortisolism can cause hyponatremia and it being a SIADH like syndrome, realizing the difficulties in this diagnosis when the patient initially developed edema as he was clearly in a Na and Water retaining state, something that would rule out SIADH. The discussants expressed their own ideas on whether or not the hyponatremia seen in hypoadrenalism qualifies as a form of SIADH, or has its own pathophysiology. Is this just a matter of semantics? Read the thread and form your own opinion.
Summary provided by Roger Rodby MD, FACP, FASN

Uncontrolled Blood Pressure in HD Patient
A 45 year old male on hemodialysis has uncontrolled blood pressure despite seven blood pressure medications to the point that he requires frequent admissions to the intensive care unit. Medication compliance is not the issue since he takes these medications when admitted but usually ends up requiring an IV nicardipine drip to control his blood pressure. What is the cause of “resistant” hypertension in this patient and the many just like him? Is there a role for bilateral nephectomy or vascular radio frequency ablation? Is this simply a volume issue and if so what is the best approach to get him to a lower dry weight? Is there a role for online hematocrit monitors, IVC diameter measurements, fluid status by bioempedance measurements, BNP levels and low sodium dialysates. This discussion is strengthened by being full of opinions and experiences from nephrologists that have been practicing for many decades.
Summary provided by Roger Rodby MD, FACP, FASN

Calciphylaxis in PD Patient
A 68 year old female with ESRD on peritoneal dialysis (PD) develops calciphylaxis (calcemic uremic arteriopathy CUA). She is poorly compliant with any attempts at medical treatment for her CUA. The treating doctors want to give her sodium thiosulfate (STS). But while STS is typically given intravenously after hemodialysis (HD) to patients before they leave the HD unit, STS administration is a patient receiving PD is logistically very different. Should the patient be temporarily converted to HD specifically for STS treatment? Can STS be given intra-peritoneally and if so how often and at what dose? Can it be given orally? Very different opinions and experiences are expressed in this international discussion.
Summary provided by Roger Rodby MD, FACP, FASN

Proteinuria/Nephrotic Syndrome in Pregnancy
A 30 year old woman develops progressive proteinuria in the third trimester of an otherwise uncomplicated pregnancy. Her blood pressure and renal function are normal and she has no edema. Many questions arise. Should a biopsy be done? Should she be delivered early? What blood tests should be done? Are diuretics safe? Is an empiric trial of steroids indicated? Should she be anticoagulated? Could this be preeclampsia? How should we define hypertension in pregnancy since so much weighs on this finding. Will we someday be measuring sFlt and PIGF ratios to help us with that diagnosis and will we have targeted therapies to make that ratio more favorable for a successful term pregnancy? Many questions are proposed and many differing opinions abound in this lively discussion.
Summary provided by Roger Rodby MD, FACP, FASN

Tubulointerstitial Nephritis in a Young Patient

A 19 year old woman presents with hypertension and CKD. Her urinalysis is entirely normal and her kidneys are slightly echogenic. A renal biopsy has only 3 glomeruli, 2 of which are globally sclerosed, and there is extensive acute and chronic interstitial inflammation. What has caused this severe renal disease in such a young woman? Can hypertension alone explain these findings? What other work-up should be considered? Should genetic testing be done for autosomal dominant interstitial nephritis or nephronophthisis? Should she receive an empiric trial of steroids? Is there a role for another biopsy? Read the thread to see what the discussants decide.
Summary provided by Roger Rodby MD, FACP, FASN


Community Minded summaries are written by ASN Community Leaders and are published weekly in the ASN In The Loop newsletter. The summaries highlight a recent popular, controversial or other outstanding discussion in the ASN Communities. If you are interested in writing for Community Minded, please contact Susan Willner, swillner@asn-online.org. 

Hypercalcemia and HTN
A 36 year old man has mild hypercalcemia. The PTH is 105 and parathyroid sestamibi imaging is normal. Does this patient have primary hyperparathyroidism or familial hypocalciuric hypercalcemia (FHH)? Will urinary calcium excretion make the diagnosis? How sensitive are these tests and how can you confidently distinguish between the two if you want to send the patient for parathyroid adenoma exploration? This thread attempts to answer these questions.
Summary provided by Roger Rodby, MD, MS.

Year in Review
As we approach the close of 2019, thank you for your ongoing support of ASN Communities. This has been a great year of participation and engagement. A year ago, we began publishing weekly “Community Minded” summaries highlighting provocative or challenging discussions from ASN Communities. The most popular was “Tubulointerstitial Nephritis in a Young Patient,” followed by “When is the Right time for CRRT?” Over 1,500 conversations took place this year in Communities with participation from members representing 180 countries. Another highlight this year was the CJASN published article, Foamy Urine: Is this a Sign of Kidney Disease, that sprang from a Communities conversation. To learn more about the educational value of Communities, please read the Kidney News Online Communities Year in Review article. Thank you again for your participation!

IgA Vasculitis
A 51-year-old woman presents with proteinuria, hematuria and a lower extremity rash. The biopsy showed crescentic IgA nephropathy. Depending on the degree of crescents, KDIGO (2012) recommends cyclophosphamide and prednisone. But while rituximab just keeps winning us over for other GNs, is there a role for it in IgAN? The answer evolves quite a bit this thread progresses. Would you use it?
Summary provided by Roger Rodby, MD, MS.

Acute Kidney Injury with immune check point inhibitors, is it all acute interstitial nephritis (AIN)?
A patient with known lung cancer and CKD receives the immune check point inhibitor- pembrolizumab( PD-1 inhibitor) for a few months. AKI ensues few months post treatment. How closely tied is this rise in creatinine to the PD-1 inhibitor? Can this happen even months following the initiation of treatment? Is it AIN? or could this be acute tubular injury, vasculitis or a glomerular process? Is a kidney biopsy necessary? This is a very interesting discussion in the Onco-Nephrology forum on an emerging topic of AKI with PD-1 inhibitors in nephrology. What are your thoughts? How would you treat?
Summary provided by Kenar D. Jhaveri, MD

Citrate toxicity while on CRRT
A potential complication of CRRT is Citrate toxicity. When citrate enters the patient’s circulation, each mole of citrate is potentially metabolized in the Krebs cycle to bicarbonate mostly in the liver mitochondria. Metabolic acidosis can occur when citrate accumulates in patients who cannot metabolize citrate (weak acid), such as those with liver failure. The criteria that we use to detect citrate toxicity include worsening metabolic acidosis, ionized hypocalcemia from unmetabolized calcium-citrate complexes, rising total calcium levels which lead to a disproportional rise in total systemic calcium to ionized calcium ratio of greater than 2.5. Therapy involves reducing or discontinue citrate infusion, increasing convective or diffusive clearance of citrate and increasing calcium infusion to correct ionized hypocalcemia. Unsure if uncommon or under reported, share your experience in this thread.
Summary provided by Jorge Castaneda, MD

Membranous GN, what are the risks of recurrence?
Few things are more devastating that the loss of a transplanted kidney to the disease that caused the failure of the native kidneys in the first place! With the discovery of antiphospholipase 2 receptor antibodies, the understanding of the pathophysiology and management of idiopathic membranous glomerulonephritis (iMGN) has exploded. How can this information be used to determine the risk of iMGN recurrence in a renal transplant, and should we also use this to decide if and when a transplant should be done?
Summary provided by Roger Rodby, MD, MS.

What is the role of the newer potassium lowering agents?
Sodium polystyrene sulfonate (SPS) has been the “go-to” for hyperkalemia for years. It is not liked by patients (palatability) and it has been rarely associated with colonic necrosis. In the last several years two new medications have been approved by the FDA for hyperkalemia: Lokelma (sodium zirconium cyclosilicate) and Veltassa (patiromer). How, should, and will these drugs replace SPS? Should they be used for the acute reduction in potassium? This Communities thread suggest that they are here to stay and that SPS will likely become a thing of the past. Are you using them yet?
Summary provided by Roger Rodby, MD, MS

Treatment of acute hyponatremia?
Because osmotic demyelination syndrome (ODS) can have devastating consequences, few things are harder and scarier for a nephrologist than the acute treatment of hyponatremia. Like Goldilocks and the three bears, it needs to be “just right”, which is easier said than done even with a well-planned and diligent management strategy. ODS is a consequence of a too rapid increase in extracellular osmolality in chronic hyponatremia where cell volume is essentially normal. What about acute hyponatremia? Are the risks the same? How do we even know if it is acute vs chronic? These questions are discussed in this Communities thread.
Summary provided by Roger Rodby, MD, MS


MGUS or MGRS? When to and what to biopsy?
An 83-y/o man with diabetes is found to have an IgG kappa paraprotein with a markedly elevated free kappa serum level. His bone marrow evaluation while very abnormal does not meet the requirements for a diagnosis of multiple myeloma. Therefore, a renal biopsy seems to be required to make the diagnosis of a monoclonal gammopathy of renal significance so he can receive treatment. Are there increased risks in an 83-y/o patient? Is there a role of a fat pad biopsy first, and what are the sensitivities and specificities of that less invasive test? How would you treat in this very interesting case?
Summary provided by Roger Rodby, MD, MS

Should midodrine be used for dialysis associated hypotension?
Midodrine is commonly prescribed for patients that become hypotensive during dialysis, despite little data on its efficacy. It is generally considered benign, but its use has been associated with an increased mortality. Is this related to the drug or the increased morbidity and mortality of the patient population that needs it? The discussants fall into two very different camps: pro-midodrine and anti-midodrine. Which camp are you in?
Summary provided by Roger Rodby, MD, MS


Hypophosphatemia from IV iron?
One of the newer intravenous iron preparations ferric carboxymaltose has been associated with profound hypophosphatemia. There are no other proximal tubular defects associated with this medication. The drug appears to increase FGF23 levels with resultant hyperphosphaturia despite hypophosphatemia (PO4 wasting), similar to the hypophosphatemia seen in oncogenic osteomalacia. Is this an idiosyncratic reaction? Is there a genetic predisposition? Questions remain but this is a side effect worthy of notice as we use this drug in CKD.
Summary provided by Roger Rodby, MD, MS

“Essential hypernatremia” – A reset osmostat?
A patient is found to have a plasma sodium (PNa) of 159 meq/l and a urine osmolality of 1000 mosm/l yet denies thirst. He is given IV D5W and starts diluting his urine when his PNa is reduced to 152! It appears he has a reset osmostat, but just what is that? How closely tied are thirst and osmotic ADH release? Is a “reset osmostat” a single disease or could it have many pathologies, and does this patient need imaging of his hypothalmus? This is a very interesting discussion of a very uncommon disease state but reinforces our knowledge of normal thirst and water handling mechanisms.
Summary provided by Roger Rodby, MD, MS

Is there a role for low protein diets for CKD?
The Modification of Diet in Renal Disease (MDRD) results were published in 1994 as a “negative” trial but some questions still remain. Was the MDRD properly powered? Was the GFR slope outcome measure flawed? This thread reevaluates the role of protein restriction not only for slowing progression of renal disease, but also for delaying the need for dialysis through decreased uremic toxins, especially with a “plant based” diet. Did we “throw out the baby with the bath water”?


Home HD without a partner?
There are financial incentives for any home dialysis therapy. Peritoneal dialysis does not require a partner, but traditionally hemodialysis performed alone was simply considered way too risky. However, machine technology and patient monitoring have improved. What is the FDA’s stance on this? Are the conservative practices in the US the same as the rest of the world? This thread may open your eyes and open up options for your patients!

Nephrotic syndrome in a patient with one normal sized and one small kidney
A 60-y/o man presents with edema and is found to have 9 g/d of proteinuria and a creatinine of 1.7 mg/dl. His BP was 200/100. His kidney ultrasound shows asymmetric kidneys, 11.1 and 8.5 cm in length. Several questions arise. With the HTN do you work him up for renal artery stenosis? Should he be considered having a solitary kidney from a renal biopsy risk standpoint? The proteinuria improves with BP control and some opinions are to do a serologic workup alone and just watch the patient while others think that renal artery visualization and then possible a renal biopsy are indicated. What do you think?
Summary provided by Roger Rodby, MD, MS

A 55 year old woman with Unexplained Hypokalemia: A rare disease or something she is doing to herself?
A 55-y/o woman presents with potassium levels that run 2.5 meq/l despite taking 60 meq of K a day. Her blood pressure is normal. Her renin and aldo are both very low. This lively discussion focuses on the work-up of hypokalemia and just how difficult it can be if you cannot rely on a history. Urine chemistries can help but not if you cannot be sure what the patient may or may not be taking. This case has a solution but don’t just skip to the end, follow the thread and see what you think first.
Summary provided by Roger Rodby, MD, MS


A tough case of IgA nephropathy
A 48 y/o woman presents with HTN and a creatinine that increased from 0.9 to 2.6 mg/dl in only 7 months. A renal biopsy demonstrates IgA nephropathy with 40% of glomeruli sclerotic, 20% segmental sclerosis, 11% crescents and 6% segmental necrosis. KDIGO requires 50% crescents and rapid renal failure to consider cyclophosphamide. This patient’s IgAN has clearly been very destructive thus far. Do you follow KDIGO and give only steroids or treat more aggressively like a vasculitis? And is there a role for rituximab or plaquinil? What would you do?
Summary provided by Roger Rodby, MD, MS


Peritoneal Dialysis in a scuba diving instructor?

A patient with CKD is approaching ESRD and is considering PD. The patient is a scuba diving instructor and thus many questions arise. What are the risks of an exit site infection in salt water v fresh water? Should special care be taken to the exit site? Should he wear a wet or dry suit? Should he drain before diving? And finally, a very interesting concern that arose in the discussion is the risk of central volume overload from the movement of fluid from the interstitial space to the intravascular space because of the increased atmospheric pressure, risking potentially disastrous pulmonary edema while underwater!
Summary provided by Roger Rodby, MD, MS

A 63 year old Woman with Hyponatremia and Polyuria
A 63-y/o woman with schizophrenia presents with seizures and a PNa of 111 meq/l. She receives 3% saline but then develops polyuria and overcorrects requiring D5W and DDAVP. Subsequent history describes a patient with polydipsia. Her Uosm was 162 mosm/kg. The discussion focuses around the topic of psychogenic polydipsia and the exact role that the degree of urinary dilution and the amount solute intake plays in the ability to excrete excessive water intake. Using oral urea to increase solute load is discussed at length, with some nice calculations showing the expected effect it will have on the BUN. Can you follow the math in this discussion?
Summary provided by Roger Rodby, MD, MS

Do Buttonholes cause more or less infections?
Buttonhole associated infections have been a topic of growing concern over the past few years. With the utility of this technique to facilitate self-cannulation, particularly among home hemodialysis patients, discussing the pros and cons of buttonholes is especially relevant in the midst of efforts to promote home therapies. While infection due to technique deviation has been a concern, there are other concerns including bacterial colonization of buttonhole tracts and practicality of using buttonholes for in-center dialysis. Read this interesting thread to learn more.
Summary provided by Leslie Wong, MD, MBA, FASN

A patient with advanced CKD and a monoclonal gammopathy, do you biopsy?
A 46-y/o man presents with severe HTN, a serum creatinine of 11, a benign urine but with a urine protein/creatinine ratio of 5 g/g. Serologies unremarkable but he has a monoclonal IgG-lambda in his blood. He is also found to have new onset CHF. Is this all just malignant HTN or could he have a monoclonal gammopathy of renal significance or even amyloid? Kidney size is 7.4 and 8.6 cm. There are very different opinions on the need for a renal biopsy as well as the safety given the patient’s HTN and CKD. What would you do?
Summary provided by Roger Rodby, MD, MS

Is the time right for CRRT, and who should provide it?
A 42-y/o man is emergently cannulated for VV ECMO for ARDS and develops oliguria. His labs after several hours reveal a BUN of 32 mg/dL and creatinine of 0.9 mg/dL. On a flow of ~ 5 L/min and 100% oxygen his pH is 7.35 and lactate is 1.8. He has made only 20 ml/hr of urine output over 5 hours. There is minimal improvement with a diuretic challenge and the patient is already 3 liters positive in fluid balance. Is it time to start him on CRRT? Should it be started now by the intensivist or can it wait until tomorrow when the nephrologist arrives. What is the evidence for starting RRT early and should this be a procedure provided exclusively by nephrologists? Read the discussion and let us know what you would have done.

Summary provided by Rajit Basu, MD, MS


How do you treat AKI in resource-poor settings?
Medical resources are almost unlimited in developed countries. Certainly, something as “simple” as dialysis is easy to provide for patients with AKI. But what about countries where resources can be extremely limited? What options do you have? This discussion explores the options that may be available, with an attempt “to think outside the box” when it comes to these difficult clinical and socioeconomic scenarios.


Hyponatremia in a 76 y/o man on Vasopressin for Sepsis
A 76-year-old man required vasopressin for sepsis and developed severe hyponatremia over a 3 day period. The vasopressin was discontinued, and he had an immediate water diuresis. Vasopressin has both V1 (vascular pressor) and V2 (renal ADH) activity but ADH activity with hyponatremia (as was present in this case) is very rarely seen when it is used as a pressor in the ICU setting. Read this very interesting thread for some explanation of this interesting physiology.
Summary provided by Roger Rodby, MD, MS


Is moderately increased albuminuria in DM benign?
RASS inhibition providing renoprotection is a main component in the management of hypertensive proteinuric diabetic kidney disease. What do you do if you have a diabetic patient with low grade proteinuria but a normal BP since the seminal studies on this topic involved patients with an elevated blood pressure? How far can you extrapolate a study? Let us know your thoughts.
Summary provided by Roger Rodby, MD, MS


HTN in a 20 Year Old with a Positive Family History for HTN?
A 20-year-old has hypertension for 1 year. His father age was also found to have HTN at age 30.The patient has a normal [HCO3] and a normal [K]. Work-up thus far has shown normal renal artery Doppler studies, normal urinalysis, creatinine, renin, aldosterone and AM cortisol levels. Workup for pheochromocytoma is negative. Given the family history of HTN in his father at a such a young age as well, does the patient deserve genetic studies for an inheritable form of HTN? Not everyone agrees on the answer to that question in this Discussion!

Summary provided by Roger Rodby, MD, MS


D-RTA and NSAIDS
NSAIDs and distal renal tubular acidosis? How can that be? NSAIDs are over the counter, they are inexpensive, and their use is very very common. But if they caused an RTA, how could that not be common knowledge. Well apparently, there is a link to their (oddly only ibuprofen) use, but mostly in much higher than typically prescribed doses and usually in conjunction with codeine. Is this just some odd toxicology trivia, or is this something we really should be aware of? You decide after you read this thread.

Summary provided by Roger Rodby, MD, MS

Does Internal Jugular Vein Thrombosis Need Anticoagulation?
A 62-year-old ESRD patient receives HD through a R internal jugular vein non-tunneled catheter. A bacteremia mandates the catheter removal. She receives antibiotics and the infection clears. Her AV fistula is not mature, and she needs a tunneled HD catheter. Upon placing the catheter under ultrasound, a clot is incidentally found in the IJ vein. The primary medical service wants to start heparin and warfarin. What is the role of anticoagulation for catheter related clots in the neck and arms? Do you have to anticoagulate, remove the catheter? The ASN Communities gets the experts’ opinions on this one.
Summary provided by Roger Rodby, MD, MS

IgA vasculitis
An 80-year-old develops a skin rash, abdominal pain with rectal bleeding, hematuria and AKI. A skin biopsy showed leukocytoclastic vasculitis, but immunofluorescent staining was not performed. ANCA testing is negative. He is treated with steroids alone and the rash, abdominal pain and renal function all improve. He refuses a renal biopsy. How do we go forward in treating this apparent case of HSP? The majority of the data on treating HSP comes from the pediatric literature, but HSP in adults has a worse prognosis than HSP in children. Should this change our diagnostic and therapeutic approach to adults with this presentation? What do you do when guidelines are vague? Read this discussion for some opinions on this matter.

Summary provided by Roger Rodby, MD, MS

Membranous Glomerulonephritis
The ability to test for antibodies to PLA2R in blood and on the kidney has been one of the major advancements in the diagnosis and treatment of Glomerular Diseases of the last decade if not longer. Should “primary MGN” be defined by these antibodies and if so, what does it mean if the serum tests negative but the tissue positive. And what is the role of antibodies to thrombospondin (THSD7A)? How do the results of these antibody tests influence treatment decisions? These issues and more are tackled.
Summary provided by Roger Rodby, MD, MS

Alpha-ketoanalogues to Slow Progression of CKD 4-5?
It has been almost 25 years since the Modification of Diet in Renal Disease (MDRD) results were published in the NEJM. While the MDRD was a negative trial, protein restriction may still be of value in slowing the progression of kidney disease. This is the basis for this Communities thread. The background behind the MDRD is discussed, as well as what went “wrong”. Was it truly a negative trial or did it succumb to some bad luck based on outcome measures and recruitment population? This study will never be repeated, so we need to make the best of what we have. The practicalities of protein restriction and ketoanalogue supplementation are discussed as well.
Summary provided by Roger Rodby, MD, MS

Lithium, Bipolar Disorder & Hypercalcemia
A patient on long-term lithium (Li) for bipolar disorder develops hypercalcemia (11 mg/dl). The PTH is mildly elevated and this is most likely related to Li use. While other drugs have been used to replace Li in patients with psychiatric disorders in which one of the many renal complications of Li occurs, this patient is very resistant to trying an alternative. What is the mechanism of Li induced hypercalcemia? What work-up is required and just how concerning is this Ca level in the context of its etiology? Does it even need “treatment”? ASN Communities offers expert opinions in this interesting thread. How would you approach this patient?
Summary provided by Roger Rodby, MD, MS


Contraception in CKD
What is the role of contraception discussions for women with CKD? What are the risks of pregnancy in CKD, and are some of these risks disease dependent that may dictate just what form of contraception may be preferred? How much does CKD affect fertility and should they be aware of that so that they do not delay trying to get pregnant as their CKD may progress and affect fertility even further. These topics are often an overlooked. What is your practice?
Summary provided by Roger Rodby, MD, MS

Sodium Bicarbonate in Respiratory Acidosis
What should you do with a patient with a moderately severe mixed metabolic and respiratory acidosis that needs dialysis? What are the acid base concerns related to the treatment? What is the physiology behind these concerns? This discussion gets to the basics of buffer function as well as CO2 production and excretion. It is never a bad time to review basic physiological principles. If they were easy everyone could be a nephrologist!
Summary provided by Roger Rodby, MD, MS

AA Amyloidosis with Crescents in Rheumatoid Arthritis Patient
Adding insult to injury, AA amyloidosis is a devastating complication that may appear after years of a similarly devasting chronic inflammatory illness. Add crescentic GN to this mix and you really have yourself a real diagnostic and therapeutic quandary. Are these two independent glomerular processes? Either way, what are the options for treating AA amyloid in RA whether the crescents are related or not? The pros opine in this illuminating discussion. How do you treat your patients with these conditions?
Summary provided by Roger Rodby, MD, MS


RRT for Patient with Cerebral Aneurysm
A 63-year-old female presents with an intracranial hemorrhage (with subdural and intraventricular extension and a saccular aneurysm) is found to have renal failure from previously undiagnosed polycystic kidney disease and requires renal replacement therapy (RRT). Concerns about RRT induced acute blood pressure changes or disequilibrium syndrome bring up the discussion of what is the safest method of RRT to minimize the risk of cerebral hypoperfusion or cerebral edema: CRRT, gentle hemodialysis, or even peritoneal dialysis. The pros and cons of each of these options are discussed in this interesting thread.
Summary provided by Roger Rodby, MD, MS

Organ Donor Pool
With the expanding list of patients requiring kidney transplants, there is acknowledgement by the medical community that we have yet to identify the most optimal way of allocating/utilizing many of our donor organs. The discard rate is unacceptably high. In 2013, OPTN/UNOS revised existing policies for Public Health Service’s increased risk (PHS-IR) donors and nucleic acid testing (NAT) helped identify which PHS-IR donors were at highest risk for transmission of hepatitis B, C and HIV. Underutilization of these organs continues. Use of high KDPI kidney­­s and better distribution of available kidneys remain two areas in need of improvement. Identifying ways to more effectively utilize and distribute these resources remains a goal of the transplant community. Read the thread to learn more and comment about these ideas.
Summary provided by Mark Lerman, MD


Post Parathyroidectomy Hospital Stay
A simple question is posed: “Do patients get discharged on the same day or stay for several days after the surgery? What is your protocol? How long do patients usually stay as an inpatient?” This is an important question because many patients develop “Hungry Bone Syndrome (HBS) following parathyroidectomy for severe secondary or tertiary hyperparathyroidism. It is important to appreciate that HBS can be a dangerous but accepted immediate or delayed outcome of parathyroidectomy. Risk factors, natural history, and treatment options for HBS, and proposes strategies that may even be used to prevent this disorder are discussed in length. Opinions span the globe from West Virginia to Singapore.
Summary provided by Roger Rodby, MD, MS

Dialysis Decisions in Pregnancy Pre-ESRD
We recently had two dialysis-in-pregnancy posts: “Pregnant Transplant Patient with Poor Renal Function” and “Pregnant Patient With CKD 4”. Clear guidelines exist on managing the rare ESRD pregnant patient, but there is less known about how to manage pre-ESRD CKD and pregnancy. In the former, renal replacement therapy (RRT) is increased to target a weekly KT/V as high as 6-8 and a BUN as low as <20 mg/dl. But when do you start RRT on a non-ESRD CKD pregnant patient, and given that for any level of BUN and creatinine, that patient should healthier than an anuric patient on dialysis, should the BUN target be different? These important questions are pondered in these posts.
Summary provided by Roger Rodby, MD, MS

Natural History of AKI
Acute kidney injury – how good are nephrologists in predicting AKI recovery, and how long is it going to take until the recovery process is complete? Does it continue to improve in some cases over a year or more? Is delayed recovery from AKI now being increasingly recognized? Many outpatient dialysis facilities are now excepting patients with acute kidney injury that are dialysis dependent. Is delayed recovery in these patients being missed? What is the impact of different drug regimens? Do you know the baseline kidney function prior to AKI? What additional research is needed? Join the conversation to learn how your peers answered these questions and to tell us how you would answer them.
Summary provided by Mark Lerman, MD, FASN

Hypertensive Donors
An otherwise healthy 34-year-old man wants to donate a kidney. He has HTN for 2 years only, and is controlled (127/87 as measured using ABPM) with only perindopril 4 mg/day. His BMI is 23 kg/m2, he has no proteinuria and his creatinine is 0.95. He has no target organ damage. Should he be considered for donation? What are the risks of mild HTN on a solitary kidney going forward knowing he should have many years of life ahead of him. Can “do no harm” go too far? The experts do not agree with each other on this ethical and medical dilemma. What is your opinion?
Summary provided by Roger Rodby, MD, MS

ARBs and Lung Cancer
RAAS inhibitor use (ACEi and ARBs) is fairly ubiquitous in cardiology, nephrology and general medicine. Over the last year we have seen FDA warnings on three different generic ARBs finding trace amounts of various carcinogens in them. We hear about one, and change our patient to a different ARB, only to find that it later is also reported to contain a carcinogen! And around the same time a report comes out linking ACEi use to lung cancer. What do we make of these issues? Is this prudent information we should act on or “Chicken Little”? You will need to form your own opinion and approach as the Discussants struggle with this dilemma. What approach(es) have you taken?
Summary provided by Roger Rodby, MD, MS

What Degree of Hemodynamic Instability Will Preclude Even CRRT
The question posed “What degree of hemodynamic instability will preclude even CRRT”? Realizing that CRRT was developed precisely for patients too unstable for intermittent hemodialysis, some patients still seem too hemodynamically tenuous to tolerate any form of RRT. What are the considerations that give us concern about isovolemic CRRT in these most unstable patients? Are these concerns warranted? Is there a point of futility? What is the role of PD in AKI and what are the special considerations that may make it less or more desirable means of RRT in this setting? Hopefully this discussion will illuminate your management or at least stimulate thought about this ICU AKI unstable patient population.
Summary provided by Roger Rodby, MD, MS

Advising Junior Faculty on How to Publish
Junior faculty who are not involved in research are often challenged to get their work published. It’s not just that they are unknown but they don’t know how to approach the process. To which journal should they submit their case reports, reviews, or quality improvement projects? How should they start and on what topic? How can they learn from rejection letters? What skills must be mastered to become an effective scientific writer? The discussion participants, all from different stages in their careers and all of whom have published, have offered some terrific feedback that anybody looking to publish should read. It’s not too late to join the conversation in the Career Advancement Community and add your recommendations and feedback.
Summary provided by Kambiz Kalantari, MD, MS

Foamy Urine
We are all taught that “foamy urine” is classic for nephrotic syndrome. But just how specific is foamy urine for predicting proteinuria? Is proteinuria alone enough or do you need accompanying lipiduria? And how does proteinuria cause foamy urine in the first place? Is foamy urine different than urine with bubbles? This Discussion delves into this interesting and perhaps whimsical topic. Read it if for no other reason than to learn some trivia on what makes beer foam.
Summary provided by Roger Rodby MD, FACP, FASN

Supporting the Mission
Studies have indicated that how we deliver nephrology education may improve interest in nephrology as a future career for trainees. Kidney educators are reviewing and evaluating new and unique methods for teaching and sharing of information. Do different tools lend themselves to different specialties or disease conditions like Acid Base and Electrolyte issues? What is the role of social media in training? Do Concept Maps work? Are small group learning sessions effective? Should educators consider the development of a nephrology toolbox that would contain unique tips and techniques? Are Flipped Classrooms the answer? Read the thread to learn more about these and other ideas. What innovative ideas have you implemented, or would you recommend?

Summary provided by Anna Burgner, MD

Puzzling Hyponatremia
A 72 year old man with a history of a pituitary tumor presents with seizures and a serum Na of 125 meq/l. He appeared hypovolemic and his UNa was <20 meq/l. He was given normal saline, and his PNa increased to 130 meq/l, but his UNa remained <20 and he developed edema. He was subsequently found to have hypopituitary hypocortisolism. He was given hydrocortisone alone and his PNa eventually normalized. The discussion focused on how hypocortisolism can cause hyponatremia and it being a SIADH like syndrome, realizing the difficulties in this diagnosis when the patient initially developed edema as he was clearly in a Na and Water retaining state, something that would rule out SIADH. The discussants expressed their own ideas on whether or not the hyponatremia seen in hypoadrenalism qualifies as a form of SIADH, or has its own pathophysiology. Is this just a matter of semantics? Read the thread and form your own opinion.
Summary provided by Roger Rodby MD, FACP, FASN

Uncontrolled Blood Pressure in HD Patient
A 45 year old male on hemodialysis has uncontrolled blood pressure despite seven blood pressure medications to the point that he requires frequent admissions to the intensive care unit. Medication compliance is not the issue since he takes these medications when admitted but usually ends up requiring an IV nicardipine drip to control his blood pressure. What is the cause of “resistant” hypertension in this patient and the many just like him? Is there a role for bilateral nephectomy or vascular radio frequency ablation? Is this simply a volume issue and if so what is the best approach to get him to a lower dry weight? Is there a role for online hematocrit monitors, IVC diameter measurements, fluid status by bioempedance measurements, BNP levels and low sodium dialysates. This discussion is strengthened by being full of opinions and experiences from nephrologists that have been practicing for many decades.
Summary provided by Roger Rodby MD, FACP, FASN

Calciphylaxis in PD Patient
A 68 year old female with ESRD on peritoneal dialysis (PD) develops calciphylaxis (calcemic uremic arteriopathy CUA). She is poorly compliant with any attempts at medical treatment for her CUA. The treating doctors want to give her sodium thiosulfate (STS). But while STS is typically given intravenously after hemodialysis (HD) to patients before they leave the HD unit, STS administration is a patient receiving PD is logistically very different. Should the patient be temporarily converted to HD specifically for STS treatment? Can STS be given intra-peritoneally and if so how often and at what dose? Can it be given orally? Very different opinions and experiences are expressed in this international discussion.
Summary provided by Roger Rodby MD, FACP, FASN

Proteinuria/Nephrotic Syndrome in Pregnancy
A 30 year old woman develops progressive proteinuria in the third trimester of an otherwise uncomplicated pregnancy. Her blood pressure and renal function are normal and she has no edema. Many questions arise. Should a biopsy be done? Should she be delivered early? What blood tests should be done? Are diuretics safe? Is an empiric trial of steroids indicated? Should she be anticoagulated? Could this be preeclampsia? How should we define hypertension in pregnancy since so much weighs on this finding. Will we someday be measuring sFlt and PIGF ratios to help us with that diagnosis and will we have targeted therapies to make that ratio more favorable for a successful term pregnancy? Many questions are proposed and many differing opinions abound in this lively discussion.
Summary provided by Roger Rodby MD, FACP, FASN

Tubulointerstitial Nephritis in a Young Patient

A 19 year old woman presents with hypertension and CKD. Her urinalysis is entirely normal and her kidneys are slightly echogenic. A renal biopsy has only 3 glomeruli, 2 of which are globally sclerosed, and there is extensive acute and chronic interstitial inflammation. What has caused this severe renal disease in such a young woman? Can hypertension alone explain these findings? What other work-up should be considered? Should genetic testing be done for autosomal dominant interstitial nephritis or nephronophthisis? Should she receive an empiric trial of steroids? Is there a role for another biopsy? Read the thread to see what the discussants decide.
Summary provided by Roger Rodby MD, FACP, FASN