Saturday, February 25, 2017

Awesome HTN Trial Cheat Sheet and info for becoming an ASH Specialist in Clinical Hypertension
Nephrologists treat hypertension! And not just in our advanced CKD/ESRD patients.

For folks (including fellows in training) who are perhaps more interested in hypertension than the average nephrologist, certification from the American Society of Hypertension (ASH) can offer a greater understanding of hypertension physiology and management (through preparation) as well as a notch in your CV and expertise to advance your career. If you are intrigued, ASH offers some education materials online as well as an explanation of the certification process.

Trainees who have passed their ABIM boards and are enrolled in relevant fellowships (e.g. renal, cards, endo) are able to take the boards. You do not have to pass your nephrology boards first apparently.

If you are interested consider discussing this with your TPD.

Since hypertension is perhaps the most overwhelming area of nephrology, at least in terms of clinical trials, here is a quick cheat sheet of key trials. Not all encompassing but a good start.

Rob Rope, MD Nephrology Fellow, Stanford

Friday, February 24, 2017

ASN Communities Onconephrology Live Journal Chat

On Monday, February 27 at 9:00 pm EDT the Onco-Nephrology community is hosting a journal chat on immune checkpoint inhibitors and all ASN members are invited!

Here is how you can participate: 
  1. Join the Onco-Nephrology Community, if you haven't already
  2. Set your community notification settings for the Onco-Nephrology Community only to “Real Time”
  3. Read the Topic Summary on line or listed below.
  4. Watch your inbox on Monday for the discussion to start and participate in the chat
If you have any questions about setting up your notifications, please contact ASN Communities Associate Zach Cahill

Summary of topic by Mona Doshi, MD

The goal of any course of cancer treatment is to prevent and/or kill future growth of malignant cells. Sometimes this can be challenging as some cancer cells gain the ability to “trick” the immune system into thinking the cancer cells are normal healthy cells. Doctors are seeing promise in a group of drugs called immune checkpoint inhibitors, which actually “open up the immune system” and allow the immune system(T-cells) to recognize and attack the cancer. Two recent reviews published in early 2017 have summarized the effects of immune check point inhibitors (ICI) on the kidney.
We shall be discussing NEJM letter published on Jan 12th 2017. While effective in most cancer patients, this course of treatment has been less successful in kidney transplant patients because activating the immune system causes the patient’s body to start rejecting their donor kidney.  Five prior cases published in the literature of renal transplant patients getting PD-1 inhibitors have resulted in rejection. The rejections were mostly seen in PD-1 inhibitor based therapy compared to CTLA-4 therapy. In addition, the 2 cases of liver transplant where these agents were used and 1 case of heart transplant didn’t lead to a rejection episode.  But in the renal transplant patients, 5 cases have now been reported of leading to acute cellular and antibody mediated rejection when PD-1 inhibitor was administered. In a recent case correspondence in NEJM Jan 12th 2017 issue, the authors observed during the treatment of a patient living with cancer who had a kidney transplant that the combination of steroids and sirolimus (an immunosuppressant that has anti cancer properties),  could prevent a patient’s body from rejecting the organ during  cancer treatment with ICI.
In the case the authors observed the treatment of a 70 year-old Caucasian male who received a kidney transplant in 2010 and recently underwent treatment for small bowel cancer which had spread to the liver. The patient was given prednisone, a steroid, and sirolimus prior to incorporating an immune checkpoint inhibitor (nivolumab). The steroids were started 1 week prior to the starting of nivolumab and continued at a tapered regimen as mentioned in the manuscript to prevent the immune mediated reaction seen in prior cases. Steroids didn’t hinder the shrinkage of the cancer. There was significant response in tumor burden (as shown in the appendix) and the serum creatinine remained stable (as shown in appendix). There were no clinical or immunological signs of rejection.
In this forum discussion, as nephrologists, we can try to come up with ways to answer few questions for the oncologists.
1. What is the best treatment strategy for ICI induced AIN (dose, duration of steroids)?
2. What is the best preventive strategy for patients who have had ICI induced AIN and need to continue the targeted therapy?
3. Given the above single case report, can the above mTOR inhibitor+ steroid strategy be employed in all transplant patients receiving PD-1 inhibitors?

If you have questions about the content of the chat, contact any of the ONC leaders.

The Onco-Nephrology Leadership Team

Tuesday, February 21, 2017


I got an econsult this morning on a young patient with an incidentally-discovered lesion on her kidney which was consistent with an angiomyolipoma. It is not uncommon to see these on ultrasound and there are a few clinical pearls that I thought I would share:

  • Angiomyolipomas (AML) are benign tumors comprised of blood vessels, adipose tissue and smooth muscle. Very occasionally (more commonly in patients with tuberous sclerosis complex), they can be malignant. Malignant AMLs are more likely to be fat-poor, hypoechoic tumors (termed epitheliod AML).
  • The prevalence is about 2% in the general population and they are 4 times more common in women
  • The presence of multiple AMLs suggests the possibility of tuberous sclerosis complex and the possibility that patients have subclinical disease should be kept in the back of your mind.
  • Confirmation of the ultrasound findings should be done with CT or MRI as there are some renal cancers that can be hyperechoic on ultrasound.
  • The hyperechoic nature of these lesions on ultrasound is due to fat in the tumor rather than the vascularity.
  • For unkown reasons, more of these tumors are found on the right side
  • Most of these tumors are slow growing and do not require treatment (surgery or embolization) unless they are >4cm in diameter. mTOR inhibitors may be useful in some patients with unresectable tumors. Patients should be followed-up yearly with ultrasound.
  • Patients on estrogen therapy are more likely to have rapid tumor growth and should be followed up more often.
Image from:

Spontaneous Tumor Lysis Syndrome

A 70 year old Ghanaian man was recently admitted under our care.  He had been diagnosed with aggressive myelodysplasia 2 months previously after presenting with fatigue and abnormal blood results (WBC 50.3, platelets 130 and LDH 928 at the time of diagnosis).  A plan was made for palliative chemotherapy. One month after his diagnosis he developed a large pericardial effusion and had 1L of haemorrhagic fluid drained.  At this point his creatinine was 200 umol/L (2.26 mg/dL).  Routine and TB culture of the fluid was negative, as was cytology and immunophenotyping.
Image result for swissnephro uric acid
Two weeks after this admission he represented with abdominal pain.  A CT showed bilateral renal and bladder calculi without obstruction.  He was oliguric with a creatinine of 577 umol/L (6.5 mg/dL) rising to 709 umol/L (8 mg/dL) over the next 12 hours.  His uric acid level was 18.0 mg/dL, which had not been checked previously.  Phosphate was 1.86 mmol/L (5.75 mg/dL), Ca 2.1 mmol/L (8.4 mg/dL) and K 4.6 mmol/L.
Our diagnosis was of a spontaneous tumour lysis syndrome (TLS; see previous RFN posts here & here).  Nucleic acids released from tumour cell lysis are broken down into xanthine and then uric acid by xanthine oxidase.  Renal failure is caused by uric acid precipitating in renal tubules causing a mechanical obstruction and inflammatory reaction.  While TLS is typically seen following initiation of chemotherapy causing a rapid breakdown of cancer cells, a spontaneous form has been described in acute leukaemia and NHL.  Our patient was at high risk of converting into AML but had no rise in peripheral blasts to suggest this.
Interestingly, spontaneous tumour lysis syndrome is associated with hyperuricemia but often without the hyperphosphatemia (and hyperkalemia) seen in the classical form of the disease– thought to be because the released phosphorus is quickly used up in the generation of new tumour cells.  This would fit with our patients results.
Our patient was commenced on dialysis which gave reductions in uric acid levels of 50% per treatment, but they quickly rebounded.  He was no longer fit for treatment of his myelodysplasia making longer term management more difficult.  Given his African ethnicity, we checked his glucose-6-phosphatase levels, which were normal, before he received rasburicase (recombinant urate oxidase). Rasburicase reduces uric acid levels by converting it into allantoin.  It may cause severe oxidative hemolysis if glucose-6-phosphatase deficient. Uric acid fell to undetectable levels following this however he had an ongoing dialysis requirement (note that rasburicase retains in vitro activity in the blood bottle so sample should ideally go on ice).  Allopurinol as a longer term medication to reduce uric acid formation may be useful, but may not manage to suppress formation sufficiently.  
In addition to tumour lysis syndrome, acute urate nephropathy can be caused by other states of tissue catabolism such as seizures, in primary overproduction of uric acid or in cases of reduced urate reabsorption in the proximal tubule. Urinalysis can show uric acid crystals (birefringent with polarisation; see image) or can be normal (as in our patient) perhaps due to a lack of output from obstructed tubules. 
This case raised several points to me. Was his pericardial effusion also caused by a urate infiltration?  No clear cause was ever identified at the time and he did not appear ‘uremic’ despite his renal dysfunction.  Could any of this have been prevented if treatment for his hyperuricemia had been commenced earlier?  I also learned:
  • The nuances of spontaneous tumor lysis syndrome (often phosphate & K not hugely elevated).
  • Rasburicase is contraindicated if glucose-6-phosphatase deficient (approximately 20% of Africans).
  • The ‘undetectable’ result of urate after rasburicase administration appears to be due to in vitro activity of the drug in the blood bottle.

Image thanks to Florian Buchkremer @swissnephro

Post by Ailish Nimmo

Thursday, February 9, 2017

Should you use intravenous immunoglobulin (IVIG) in the treatment of BK nephropathy?

Nice debate on ASN Transplant Community about the use of IVIG for BK nephropathy.

Personally, I have used IVIG in a handful of patients with refractory BK nephropathy in the past. However, I have convinced myself that there is no data supporting that.

Most case series used IVIG in combination with reduction of immunosuppression (Sener et al. Transp 2006), preventing any conclusion on the matter. We had a nice debate with Jay Fishman (MGH Transplant Infectious Disease expert) on last AST Fellow's Symposium about this issue. 

The conclusion was that an effective viral response requires cytotoxic T cells to kill infected cells (Figure above). Antibodies against the virus may help neutralize circulating virus but alone are not capable of stopping an ongoing infection. In particular, prior immunity against BK (IgG BK positive prior to transplant) does not seem to protect against post-transplant BK infection (different than CMV exposure). However, one must keep in mind that there are at least 4 different BK genotypes and immunity against one genotype does not equal immunity to all genotypes, which may explain some of the controversies on the topic (Pastrana et al. PLOS Pathogens 2012).
Overall, reduction in immunosuppression remains the cornerstone of BK viremia treatment.
Remaining controversial topics: 
  • Should you give steroids if intense inflammation? Some data suggest it may not be good... 
  •  Should you stop or just reduce antiproliferative dose? Unclear on my view, but intensity of viremia and allo-immune risk must be balanced here. 
  • Should you switch to an mTOR inhibitor? Some interesting data suggesting that mTOR inhibitors suppress BK replication (similar to suppression to other virus like CMV) (Hirsch et al. AJT 2016)
More data still needed... 

Thursday, February 2, 2017

Cidofovir nephrotoxicity and Probenecid

I recently saw an interesting case. A woman was being treated with cidofovir for adenovirus which was presumed to be responsible for an acute cardiomyopathy. Concurrent with cidofovir, she was also receiving probenecid for renoprotection, which I was not familiar with.
Cidofovir is a nucleotide analogue used primarily to treat CMV retinitis in patients with AIDS. However, cidofovir is also used to treat a number of DNA viruses including adenovirus. The main toxicity of cidofovir is nephrotoxicity, which can manifest as AKI, proteinuria, or a Fanconi-type syndrome with proximal tubular dysfunction. Nephrotoxicity can be reduced by co-administration with iv fluids and probenecid (the dosing regimen for the latter is 2g po 3 hours prior to the dose, then 1 g po 2 hours and 8 hours after.
How does probenecid reduce cidofovir nephrotoxicity? Over 80% of cidofovir is excreted unchanged in the urine in 24 hours. Most of this occurs via glomerular filtration, but cidofovir is also actively taken up from blood by the kidneys via the "organic anion transporter" located on the basolateral side of renal proximal tubular cells, and is then more slowly secreted into the tubular lumen. Renal clearance of cidofovir therefore exceeds the corresponding GFR.
The relatively slow secretion of cidofovir into the tubular lumen, in comparison to uptake from the blood, results in a long intracellular half-life of the drug in the proximal tubular cells which appears to underlie the nephrotoxicity. Probenecid, by inhibiting the organic anion transporter, prevents tubular uptake and protects the kidneys. This was demonstrated nicely in a pilot study in HIV patients. Interestingly, and somewhat paradoxically, this means that probenecid reduces nephrotoxicity while also DECREASING the renal clearance of the drug and thus INCREASING serum cidofovir concentrations as much as two-fold.
Probenecid is a banned drug for athletes for a related reason - because it blocks entry of certain drugs into the urine, it has been used as a masking agent for other banned performance-enhancing drugs including steroids. 
Posted by David Leaf

Wednesday, February 1, 2017

Hyponatremia and ESRD

Hyponatremia can be seen in patients with end-stage renal disease (ESRD), often as a consequence of a patient’s increase in free water intake in the setting of the kidneys’ diminished ability to regulate sodium and water homeostasis. I recently received a question from a resident asking for some insight into the management of such patients.
To begin, it should be noted that uremic patients with chronic hyponatremia are thought to be protected from osmotic demyelination syndrome (ODS) after hemodialysis. In this situation, urea may act as an effective osmole, whereby the decline in blood urea nitrogen (BUN) levels during dialysis could offset serum hypertonicity.  Additionally, animal studies have shown that azotemic rats were protected from ODS due to a reaccumulation of organic osmolytes  such as myoinositol and taurine within two hours of correction of hyponatremia
Though rare, case reports of ODS in uremic patients with hyponatremia do exist. One case described a uremic patient who developed ODS after being initiated on hemodialysis with an initial serum Na of 100 meq/L that corrected to 121 meq/L after three hours against a dialysate sodium concentration of 140 meq/L. It is important to note that ESRD patients in other case reports who went on to develop ODS had other risk factors for the development of the disease, such malnutrition and chronic alcoholism.
I recently helped care for an ESRD patient who was admitted with probable sepsis. His serum sodium on admission was 122 meq/L.  Because we had no outside records available at the time, we assumed his hyponatremia had been present for at least 48 hours. The patient had no uremic symptoms and had no need for urgent small solute clearance or volume removal. Nephrology was consulted for routine dialysis needs.
In choosing our dialysis prescription, we attempted to limit the increase in sodium to no more than 1 meq/L/h, or 3 meq for a 3-hour treatment.  We elected to reduce the blood flow rate to 100 ml/min, use the lowest possible sodium concentration bath allowed in the dialysate (130 meq/L), and use a dialysate flow rate of 600 mL/min.  Cocurrent flows were not used.  After a 3-hour dialysis session, the patient’s serum sodium rose to 125 meq/L, and hourly measurements of serum sodium during dialysis revealed that the patient’s sodium had indeed risen by 1 meq/L/h.
Our calculation was derived from a helpful approach described by Wendland and Kaplan, which showed that the rate in rise of serum sodium could be estimated by the product of the concentration gradient between the patient’s sodium and the dialysate sodium multiplied by the clearance. To do this, we would begins with the following formula:
Change in total body Na = Clearance (L/h) * (dialysate Na – patient Na)
By minimizing the blood flow rate to 100 mL/min and maximizing the dialysate flow rate to 600 mL/min, we assumed that there would be near-total equilibration between the patient’s serum sodium and the sodium concentration of the dialysate bath.  Thus, clearance would be approximately equal to the blood flow rate.
Thus, using our patient as an example:
Change in total body Na = Blood flow rate (L/h) * (130 meq/L – 122 meq/L)
A blood flow rate of 100 mL/min = 6 L/h
Therefore, the change in total body Na after 1 hour of dialysis would be:
6 L/h * 8 meq/L = 48 meq/h
Our patient’s total body water was 48L.  If we add 48 meq Na to our patient’s initial total body Na of 5856 meq (48L * 122 meq/L), we obtain the new total body Na after 1 hour of dialysis: 5856 meq + 48 meq = 5904 meq.
Dividing this value by the patient’s total body water would give us the new serum sodium after 1 hour of dialysis, assuming no ultrafiltration or volume changes.
5904 meq/48L = 123 meq/L
Thus, the patient’s serum sodium would rise by approximately 1 meq/L after 1 hour.
It would be interesting to discuss other options are available for managing ESRD patients with chronic hyponatremia.  Assuming there is no urgent need for small solute clearance, would continuous renal replacement therapy be a safer option?  If uremia is indeed “protective” against ODS, should we avoid low dialysate flow rates and concurrent flows?  How would the prescription change if the patient were to need more aggressive small solute clearance?
It seems that there is more than one way to manage these patients, and factors such as co-morbidities and electrolyte abnormalities need to be taken into consideration when formulating a dialysis prescription.
Posted by Devika Nair, MD
Nephrology Fellow, Vanderbilt

Tuesday, January 31, 2017

February Renal Path Video - Wash U Nephrology Web Episodes!

For anyone wanting to unravel an unusual case and brush up on their renal pathology, check out the February episode of the Wash U Nephrology web series.

Tuesday, January 24, 2017

Point of Care Ultrasound for the Nephrologist at #SCM2017

Want to up your ultrasound game... Attend the point of care ultrasound for the nephrologist pre-course at the NKF Spring Clinical Meeting in Orlando, FL April 18 2017

click here to register

The nephrology consultant needs knowledge of lung ultrasound to determine volume status, renal and bladder ultrasound to evaluate for obstruction and knowledge of vascular access guidance to assist in placement of catheters. This course will focus on the above elements in point of care ultrasonography.
  • Image acquisition will be practiced on human models using high-quality ultrasound machines and supervised by experienced faculty. Training sessions give you practical, hands-on training with a 1:3 teacher-to-learner ratio, so you benefit from personal instruction.
  • Image interpretation during group sessions under the supervision of experienced faculty members offers relevant practice. Numerous ultrasound images demonstrating normal and pathologic findings will give you a comprehensive learning opportunity. As you improve your skills, you will be further challenged with unknowns and case-based image sets.
  • Knowledge base will be enhanced with lectures that focus on important aspects of point of care ultrasonography applicable to the renal consultant. Discussions will have immediate application within your practice. 
Learning Objectives:

Upon completion of this course, participants will be able to:
  • Discuss how to perform lung ultrasonography and ultrasonography of the renal system.
  • Identify appropriate uses of ultrasonography in renal practice.
  • Demonstrate appropriate image acquisition techniques required for renal ultrasonography.
  • Interpret image-based clinical cases to help identify abnormalities.

Tuesday, January 17, 2017

Renal Grand Rounds: Correlate Clinically

I recently presented the case of a middle-aged patient with ESRD secondary to Goodpasture syndrome. She presented with AKI 3 months after a kidney transplant. Her creatinine had normalized to 0.9mg/dl post-transplant. However, over the next few months she had multiple hospitalizations for infections, perinephric fluid collections and three episodes of AKI. Her creatinine finally stabilized at 1.5mg/dl. Due to concerns that she was overly immunosuppressed, her mycophenolate was discontinued during her last admission and her prednisone was stopped per weaning protocol. She was continued on tacrolimus. At her post-discharge follow up, she was found to have recurrent AKI with Cr 2 mg/dl She had 1+ blood on UA, but no proteinuria. GBM antibody was negative. She was admitted for a transplant kidney biopsy.

The biopsy demonstrated diffuse linear staining of the glomerular basement membrane. There was no evidence of active glomerulitis or crescent formation. Mild mesangial expansion and moderate thickening of the GBM were noted with no signs of cell-mediated or antibody-mediated rejection.

This prompted the million dollar question: Is this diffuse GBM staining early recurrence of anti-GBM disease or something else?

The inciting event of anti-GBM disease is still unknown (correlations with smoking, cocaine use, solvent exposure, and infections), however the pathophysiology is fairly well established - an insult causes a conformational change of the type IV collagen network in the GBM resulting in exposure of the non-collagenous portion of the alpha-3 chain which elicits an immune response. Based on multiple uncontrolled studies, these patients can be transplanted 6-12 months after their GBM antibody titers become negative and they have similar transplant outcomes when compared to other causes of ESRD.

But how often does it recur after transplant? In 2013, Tang et al retrospectively analyzed 58,000 patients in Australia and New Zealand started on RRT and found 449 diagnosed with anti-GBM disease, 224 of whom were transplanted. Of those transplanted, 2.7% developed biopsy proven recurrence. So... it recurs, but rarely.

What about a false negative GBM antibody titer? Our patient's titer was negative, and the reported false negative rate for the ELISA and western blot is 2-3% making it unlikely. However, there have been case reports of anti-GBM disease with negative ELISA and weakly positive western blot suggesting low or transient antibody production. In addition, alternative immunoglobulins not picked up by the ELISA, such as IgG4, and alternative GBM antigens have been proposed based on case reports.

What else could produce diffuse GBM staining? In monoclonal immunoglobulin deposition disease the physicochemical properties of the monotypic light chains result in high affinity for the GBM and diffuse linear staining. In addition, in diabetic glomerulopathy, there is thought to be a loss of negative charge in the GBM which allows negatively charged species such as immunoglobulin and albumin to collect in and expand the GBM. Our patients SPEP and SFLC were normal, and the donor didn't have a known history of DM. 

In the end, we couldn't answer the million dollar question definitively, but we decided to treat with plasmapheresis, rituximab, and restarting prednisone and mycophenolate. Rituximab was used instead of cyclophosphamide due to previous complications during her initial treatment.  She's currently doing well with Cr stable at 1.5mg/dl

Posted by Patrick Reeves

(Picture is Dr. Ernest Goodpasture who first described this condition while studying victims of the Spanish Flu in 1919)

Tuesday, January 10, 2017

Renal Grand Rounds - What Lurks in the Gap

I recently presented the case of a middle-aged man with a history of a remote Roux-en-Y gastric bypass, chronic diarrhea, and colon cancer on chemotherapy who initially presented with progressive fatigue and weakness in the setting of increased diarrhea. Shortly after admission he developed agitation that progressed to encephalopathy with dysarthria. His baseline labs from a month prior to presentation were notable for a chronically low serum bicarbonate of 15-17 with no anion gap. When he presented he was hypokalemic to 2.5 and his bicarbonate had dropped to 11 with a new elevated anion gap of 25 and normal L-lactate. Metabolic acidosis was confirmed on VBG. Interestingly, his urine electrolytes demonstrated a positive urine anion gap of 26.

He was ultimately diagnosed with D-lactic acidosis based on his clinical presentation which was confirmed with a serum D-lactate of 6.28. For the week prior to admission, he had been drinking 1.5 L of Gatorade (224 g of sugar!) daily to replace diarrhea losses.

This was a classic presentation of D-lactic acidosis in which overgrowth of gram positive anaerobes in the setting of short bowel syndrome is combined with a large carbohydrate load resulting in bacterial fermentation and D-lactate production.  He even had the classic neurologic findings!  His chronic non-gap acidosis likely represented chronic diarrhea and D-lactate production, and his rising anion gap when he presented was consistent with increased D-lactate production.

In D-lactic acidosis, the findings of hypokalemia and a positive urine anion gap can provide a helpful clue. With elevated serum D-lactate levels, the fractional excretion of D-lactate approaches 100%, i.e. everything that's filtered is excreted. This is because the stereospecificity of the sodium-L-lactate cotransporter in the proximal tubule results in poor reabsorption of D-lactate relative to L-lactate. The negatively charged D-lactate essentially drags positively charged sodium and potassium into the urine causing hypokalemia as well as a positive urine anion gap (Na + K - Cl) due to the increased urine sodium and potassium.

This patient did well after his Gatorade was cut off and he was treated with antibiotics to address gram positive anaerobic overgrowth.

Posted by Patrick Reeves

(Image taken from here - an educational blog for ED residents)

Monday, January 9, 2017

Nephrology Business Leadership University

See below for details on a very interesting looking course for Renal Fellows:
We are excited to introduce a new innovative program available to Nephrology Fellows -   Nephrology Business Leadership University (
NBLU is a unique week long program that brings together a diverse faculty of practicing Nephrologists, hospital and dialysis provider executives, and other healthcare professionals who will share their insights on leadership, the business of nephrology, and the evolving healthcare landscape.  Most sessions are held in a workshop format and are highly interactive and individualized.  

Fellows attending a NBLU rotation can expect to leave with:
1.Ability to evaluate potential employers for the ultimate fit
2.Enhanced leadership and business understanding to bring to potential employers
3.An understanding of the ever-changing payment / reimbursement landscape
4.The know-how to embark as a solo practitioner or as a high impact member of a group practice
5.Confidence approaching the interview process
6.Knowing you have the tools to start your career in the right direction

Topics Covered:
-Billing & Coding Workshop
-CV and Interview Tips
-ACOs, ESCOs Basics
-How to find the right job
-Growth Strategies for your practice
-Marketing 101
-Practice Management
-How to Review Employment Contracts
-Financial Planning
-Much Much More.......

NBLU will hold its second annual program from August 7th to August 11,2017 in Plano, Texas.
Since we would like to keep the sessions very interactive space is limited. 

Registration is free and can be done on the website

Travel support, hotel accommodations, and most meals are provided to all fellows that are attending.  There should be little to no out of pocket expenses to the fellow or their training program.

Program Organizers - University of California San Diego Division of Nephrology  & Dallas Renal Group (

Nephrology Business Leadership University

If you or your program director has any questions please feel free to contact me at

Wednesday, January 4, 2017

Renal Grand Rounds - A Chilling Case of Hyperkalemia

A 62 year old man with ischemic cardiomyopathy (EF 35%) and CKD (baseline Cr ~3 mg/dl) had a witnessed out-of-hospital cardiac arrest.  EMS arrived within 3 minutes.  He received CPR and was shocked out of ventricular fibrillation (VF).  He was intubated and therapeutic hypothermia was initiated in the field. He was admitted to the CCU, where therapeutic hypothermia was continued for 24 hours.  He received aggressive KCl repletion for hypokalemia (see graph below) and supraventricular arrhythmias.  On the second hospital day the patient was rewarmed, developed severe DIC (INR 10), worsening shock requiring 3 pressors, and renal was consulted for hyperkalemia and oliguric AKI on CKD.

Clinical pearls: Hypokalemia is a frequent complication of hypothermia for two major reasons: 
1) cold diuresis, which is believed to result from peripheral vasoconstriction, increased venous return, and increased ANP; 
2) catecholamine-induced shift of KCl into cells.  
Interestingly, the latter seems to depend on the type of protocol used to induce hypothermia.  Core cooling increases norephinephrine but not epinephrine, and therefore does not cause a shift of K into cells.  In contrast, external cooling (which was used in this case, with the application of cooling pads) increases epinephrine disproportionately to norepinephrine.  The B2 agonist actions of epinephrine cause a shift of K into cells.  It is therefore critically important to avoid KCl repletion during rewarming due to the risk of rebound hyperkalemia, particularly in oliguric patients such as this one who are unable to deal with the excess potassium load once it moves back out of the cells during rewarming.
Posted by David Leaf

Come to KIDNEYcon April 7-8 2017 for hands on learning

When- April 7-8, 2017
Where- Little Rock, Arkansas
Who should attend- Internal Medicine Residents, Pediatric Residents, Adult and Pediatric Fellows, Attending Nephrologists

**if you are an adult nephrology fellow and interested in coming please note that you should take the in-service exam  April 5 or 6. talk to your program director or coordinator

Travel Grants- Available to Adult and Pediatric Residents and Fellows (DUE DATE Feb 17th)


Mission Statement
KIDNEYcon is an annual two day educational event with a mission of fostering enthusiasm for careers in nephrology among residents and fellows and to provide educational updates on relevant kidney topics. An additional focus is to develop collaborative research projects between academic and private nephrologists.
Director- John Arthur, MD, PhD
Professor and Chief of Nephrology
University of Arkansas for Medical Sciences

Co-Director- Shree Sharma, MD
Arkana Laboratories, LIttle Rock, AR

Education Director- Matthew A. Sparks, MD
Assistant Professor and Associate Program Director
Duke University

KIDNEYcon is an annual conference designed to provide updates in the latest advances in kidney care in a hands-on collaborative format. A key component of KIDNEYcon's mission is to build enthusiasm for the field of nephrology among residents and fellows. We also aim to facilitate collaborative research projects among participants of the conference. The conference is a platform for nephrologists and medicine trainees to interact with experts from across the nation and learn about and discuss recent advancements in the diagnosis and treatment of kidney disease. The conference consists of Friday workshops targeted primarily to medicine residents, nephrology fellows and early stage nephrologists and a Saturday scientific and clinical conference with broader applicability.

KIDNEYcon 2017 will feature four interactive hands-on workshops
  1. The Kidney Biopsy Academy 
  2. Vascular Ultrasound for Assessment of Volume Status Workshop 
  3. Interventional Nephrology Workshop
  4. Social Media in Nephrology Workshop 
The Saturday session will be an educational meeting with multiple interactive sessions featuring case-based studies and audience response technology, followed by Q & A sessions with the expert panel.
One of the first duties of the physician is to educate the masses — Sir William Osler

Please consider coming to the conference. I am really excited about this years conference and our goal is to break the mold of the traditional conference. You will leave KIDNEYcon with more confidence and knowledge.

Matt Sparks

Monday, January 2, 2017

Wash U Web Episode - Kidney Pathology 101, "Welcome to 2017 Edition"

Happy New Year to all RFN visitors!  This month's nephrology web episode coming from Washington University is a primer on kidney histology.  Most of us can recognize the silver stain from the trichrome, but how many times have we looked at the H and E stain and confused it with the PAS?  Unfortunately, I have been guilty of this myself during many biopsy conferences.

Check out the video below:

Wednesday, December 28, 2016

Clinical Pearl - Bleeding and Liver Disease

Bleeding is a common complication of liver disease and given that we as nephrologists are sometimes asked to place lines or perform renal biopsies on patients with cirrhosis, it is important to know the physiology behind the reason for excessive bleeding in these individuals. Here is a nice clinical pearl from our Hematology colleagues at MGH:

Endogenous tPA is cleared by the liver and therefore circulating levels of tPA are elevated in patients with cirrhosis. This is the main reason that these patients bleed. Phrased another way, the main hemostatic defect in liver disease is not thrombin generation (defective production of procoagulant clotting factors) but rather accelerated clot lysis. Therefore, an antifibrinolytic treatment (like amiocaproic acid) that inhibits the binding of fibrinolytic molecules (plasmin, plasminogen) to fibrin and thus helps prevent breakdown of existing clots is an elegant and effective way to treat bleeding in cirrhosis. A reduced dose should be given in patients with renal dysfunction and it should be noted that this drug has been associated with AKI in some patients due to urinary tract obstruction and ATN.

Posted by Rebecca Karp Leaf MD and Walter Dzik MD.

Sunday, December 25, 2016

Top nephrology-related stories of 2016

2016 marks the 7th year of the Top Nephrology Stories post on RFN. When this list first started in 2010 it was more challenging to get the stories. Now 7 years later, everything has changed. In my mind the advent of Twitter and NephJC has changed all of that. We are more informed and better read on nephrology topics. All you need to do is go over to NephJC and look at what is being talked about. Everything is there. Discussion is deep and constant.


  • NephJC will host the #TopNephrology stories starting in 2017. 
  • We will use analytics from each of the chats throughout the year plus feedback from the NephJC team to create a #TopNephrology list. 
We hope these changes will result in an improvement and reflect the Top 10 stories that you need to be aware of. RFN is not going away and we have big plans for RFN. If you are a fellow and interested in posting to RFN please send me an email or DM.

Below are links to the last 6 years of the top nephrology stories hosted on RFN.


10. HLA-incompatible live kidney donation survival benefit in NEJM (5%)- Coming in as a tie for number 10 is a study reported in NEJM (March 2016) and covered by NephJC. It is well known that kidney transplantation is the best form of renal replacement therapy. However, there is a limited number of organs to meet the growing demand. Furthermore, patient related factors such as the presence of anti-HLA antibodies are another factor lengthening the wait time and often preventing transplantation. This study looked at matched patients (not a randomized trial).

  • One group of kidney transplant recipients undergoing a desensitization protocol with a live donor incompatible kidney transplant
  • A matched group who underwent deceased donor kidney transplant with a match or remained on the wait-list. 
The study looked at multiple kidney transplant centers between '97-'11 The results were striking. Patients who underwent a live incompatible kidney transplant with desensitization protocol had a significant survival advantage compared to wait-listed patients and wait-listed + deceased donor. However, it must be noted that the desensitization protocol itself has side effects and careful consideration is needed before using this method. This study is important because it represents a significant advance in generalizing the use of desensitization for patients unable to obtain a kidney transplant because of preformed antibodies.

10. ELAIN Trial of early versus late HD in the ICU in JAMA (5%)- This spring started off with a bang. Back to back presentations of renal replacement therapy in the ICU showing different results. First the AKIKI Trial (our number 3 story) was presented at the Critical Care meeting in San Diego and reported in NEJM and showed no difference in early versus late. A few weeks later came the ELAIN (Early vs Late Initiation of Renal Replacement Therapy in Critically Ill Patients With Acute Kidney Injury) Trial. This was a single-center randomized trial presented at the ERA-EDTA Congress in Vienna, and reported in JAMA. They found a significant reduction in 90-day all-cause mortality in the early initiation group. Some important caveats.

  1. This was a single center study (AKIKI was multicenter).
  2. Majority of patients were surgical ~80% (AKIKI ~80% medical) 
  3. 100% were CVVHDF (AKIKI ~30% CRT) 
  4. Only 4% in late group avoided RRT (~50% in AKIKI). 
Bottom line- these were very different studies and hence had very different results. Could a select group of patients with a more defined ischemic insult benefit from early RRT in the ICU? Jury is still out but the ELAIN Trial would suggest this to be true.

9. EuLite Trial of high cutoff dialysis in myeloma presented at UK Kidney Week (6%)- The long awaited results from the EuLite Trial were presented at UK Kidney Week this year. See Paul Phelan's post on RFN from way back in 2013. Unfortunately, the EuLite Trial isn't published just yet so we have is the live Twitter coverage from the meeting. The premise is that High Cutoff (HCO) Dialysis would provide benefit from removing toxic free light chains in myeloma cast nephropathy. HCO dialyzers employ high flux membranes with particularly large pores (up to 50kDa Vs 15kDa for conventional high flux) facilitating the removal of large plasma proteins such as FLC (kappa and lambda light chains have molecular weights of 22kD and 45kD respectively). The EuLite Trial is a randomized clinical trial testing the use of HCO dialysis versus standard dialysis  in patients with myeloma case nephropathy. Unfortunately, HCO Dialysis arm of the study had more mortality compared to the standard HD arm hinting at harm. We all eagerly await the full publication to be reported to we can really delve deep into this study. Looks like the early enthusiasm for HCO dialysis in myeloma cast nephropathy is fading as well.

7. Contrast nephropathy study in JASN (8%)- September brought a bombshell of a study. The Wilhelm-Leen, Montez-Rath and Chertow paper looked at the risk of acute kidney injury in the days following a dose of radiocontrast. And the researchers could find no hint of AKI. To say this counters nephrology dogma is an understatement. If Moses had brought down the Nephrology Ten Commandments, Thou shalt avoid radiocontrast would probably be in the top three, following only by Thou shalt monitor and control one’s blood pressure and Thou shalt not eat so much salt. The investigators used NIS, the largest publicly available all-payer inpatient care database, this covers 96% of the US population and used diagnosis and procedure codes to find exposures and acute kidney injury. Despite that limitation the result is so provocative that it begs relooking at this toxicity with open eyes. Of note similar findings have been published in the radiology literature for years: McDonald JS, Bruce RJ, while others have upheld the orthodoxy.

7. "Fistula First" survival benefit is due to patient factors in JASN (8%)- If contrast nephropathy is really just a figment of confirmation bias, then at least we know that fistulas are the best hemodialysis access and convey a true survival benefit. Or maybe we don’t know that. The same issue of JASN brought us the work of Robert Brown, Bhanu Patibandla and Alexander Goldfarb-Rumyantzev. The thread that triggered this investigation was the repeated observation that every study that revealed a survival benefit for starting with a fistula (all observational and retrospective data) also showed that catheter patients were different from patients starting with a fistula. Often the catheter patients were older, more urban, shorter pre-ESRD nephrology care, more diabetes, more cerebrovascular disease, and more heart failure that the patients starting with a fistula. The authors looked for a way they could separate fistula patients from these inherent biases that could explain the survival benefit these patients enjoyed. The authors divided elderly new starts to hemodialysis into three groups:
  1. Started dialysis with a fistula 
  2. Started dialysis with a central venous catheter, but had a fistula that was maturing when they started dialysis 
  3. Started dialysis with a central venous catheter 
If the fistula was driving mortality, group 2, that is dialyzed with a catheter, should have outcomes similar to group 3. If the patient characteristics were driving the survival advantage of the fistula, group 2 should look like group 1.

The money quote from the conclusion
although this study has confirmed the approximately 50% decreased mortality experienced by patients initiating hemodialysis with an AVF compared with a catheter, it showed that about two thirds or more of this mortality benefit is also seen in those initiating hemodialysis with a catheter but who had previously undergone unsuccessful fistula placement. Thus, these observational data suggest that the actual mortality attributed to the catheter itself is much less than previously considered and may be explained in large part by differences in patient factors. 
Similar conclusions were published in JASN this October using Canadian data. That team is planning on confirming these results with a randomized controlled trial of fistulas versus catheters (see this Medscape article, log in required). That will be amazing!

6. US Congress expands Medicare coverage for acute dialysis coverage (10%)->In June of 2015 the nephrology world suddenly became very interested in the Trade Preferences Extension Act of 2015. Because politics is hard, an important bill for acute kidney injury got stapled to this larger "Transporter bill". On June 29th President Obama signed the bill and section 808 became law.
Specifically, Section 808 of the law amends the Medicare statutes to provide coverage for “renal dialysis services furnished … by a renal dialysis facility or provider … to an individual with acute kidney injury.” 
This overturned a CMS ruling from 2012 that forbid medicare reimbursement to dialysis providers for the condition of acute kidney injury. This left lots of patients in a lurch. Patients unfortunate enough to develop AKI often would recover from their acute illness but they would have to remain in, or close to, the hospital as their acutely dtysfunctioning kidneys recovered or didn’t. Until a nephrologist was willing to give up hope and declare the patient ESRD, that patient would not be able to receive dialysis anywhere but the hospital. This esoteric bureaucratic red tape of where and when people could get dialysis hurt patients and it is nice to see this straightened out, even if it was passed in 2015 and doesn’t go into effect until January 1, 2017.

5. Nephrology societies embrace social media (11%)- Most of the nephrology societies have had a social media presence for many years (see this Twitter list from Joel Topf) however, 2016 marked some sort of a watershed in the seriousness, enthusiasm and effort taken by many of them to really engage with social media.

The American Society of Nephrology (ASN) has a very active Twitter presence, and actively tweets out the latest breakthroughs in research and other news in the nephrology universe. Along with ASN Kidney News and ASN Advocacy, the two flagship journals, JASN and CJASN, also have active Twitter handles, and are progressively using the medium effectively for communication. But two other initiatives stand out in all the things the ASN does on social media this past year: #askASN and ASN communities. Once every month, the ASN brings forward an expert for the #askASN chats (some of the featured guests include Richard Lafayette who runs Kidney News, POTASN Ray Harris and PEOTASN Eleanor Lederer, KidneyWk organizers Roy Zent and Patrick Nachman, and SPRINT investigators George Bakris and Bill Cushman) to answer questions from the nephrology Twitterverse. Secondly, a few months ago, spearheaded by Zachary Cahill, the ASN launched a forum, ASN Communities. It has gathered steam, and now boasts 8 separate communities (the Open Forum and Patient Care being most active, with Onconephrology, Transplant, AKI, Basic Science, Supportive Care, Training Program Directors being the others), with over 3,000 discussion threads!

The ERA-EDTA has been on Twitter for a while, but they publish two journals, and until recently didn’t have a social media presence. But they stepped nicely to a request, and @NDTsocial and @CKJsocial were born. Both have been actively tweeting out snippets of the latest nephrology literature (with CKJ continuing to be an #openaccess journal) over the last year.

The International Society of Nephrology (ISN) is ramping for the upcoming World Congress of Nephrology, scheduled to be held in Mexico in 2017. The ISN does have an active education committee and holds regular webinars, but for the WCN, they have established a WCN 2017 social media task force make up of 20 nephtweeters from around the world. We look forward to their coverage of the WCN2017.  Now only if someone could persuade Kidney International to join Twitter…

The National Kidney Foundation (@NKF) is also active on Twitter and actually sets the record for number of followers ~19,000. The NKF Spring Clinical Meeting (@NKFClinicals) was much more active this year and featured a live social media workshop. Next years meeting is featuring a social media ambassadors program at SCM17. Of course AJKD was an early adopter of social media and a leader in the space with AJKD blog,  NephMadess, and AJKDonline Twitter handle.

4. Empagliflozin approved for CV indication by FDA (13%)- A common refrain in the diabetes literature has always been a lack of benefit seen for hard outcomes with hypoglycemic agents, with metformin being a lone exception. This all changed with the EMPA-REG trial, which made it to the #TopNephrology stories in 2015 as number 2. At that time, we just had the late breaking trial to work on, but it was already huge news. The subsequent publication in NEJM was covered at a #NephJC session too. The need for this trial to be done is very interesting – until recently, showing a drug lowers blood sugar was the most important aspect of getting FDA approval. After the debacle behind rosiglitazone (avandia) and the possible risk of greater cardiovascular events despite lower blood sugar, the FDA mandated larger trials to demonstrate CV safety. EMPA-REG was one such trial, and demonstrated remarkable benefit in lowering CV outcomes. The FDA followed suit, and on Dec 2 announced a new indication for empaglifozin – for reducing cardiovascular death in patients with type 2 diabetes. The SGLT-2 inhibitors have indeed come a long way in a short period of time.

3. AKIKI Trial of early versus late dialysis in the ICU in NEJM (20%)- Coming in at #3 in this years poll is AKIKI. AKIKI was also the winner of the #NephJCKidneys at KidneyWk for Study of the Year. The timing of renal replacement therapy has been rated as a top priority for research in the AKI world. Indeed, in the last few years, clinical practice has slowly crept ahead of evidence, as it often does, and dialysis is being initiated earlier and earlier for acute kidney injury. And then came along the Artificial Kidney Initiation in Kidney Injury (AKIKI) trial, to do what IDEAL did for timing in the chronic dialysis field. In this trial, 620 patients with AKI were randomized to either early strategy (with RRT initiation at stage 3 AKI per KDIGO criteria) or delayed strategy, when a clinical indication occurred (eg hyperkalemia, pulmonary edema, or persistent oliguria > 72 hours). There was no difference in mortality, with only half the patients needing dialysis in the delayed group, who also had significantly less bloodstream infections. Check out the #NephJC coverage for more details.

2. PPI and CKD risk in JAMA Internal Medicine and JASN (22%)- This was big. Another important paper dropped in nephrology literature during springtime. We had AKIKI, ELAIN and now PPI causing CKD all Feb to April. The PPI leading to CKD story was first reported in JAMA Internal Medicine then in JASN. NephJC covered this and you can view the background and both chats here. While a rare association between PPI use and interstitial nephritis has been known for a while. Their association with chronic kidney disease had not been reported before. The JAMA Internal Medicine paper is an observational, prospective cohort study with two cohorts. The first is the Atherosclerosis Risk in Communities (ARIC) study, of which 10,482 participants were included. The second was the much larger Geisinger Health System Replication (GHSR) Cohort, with 248,751 participants. Participants using either PPIs or H2 antagonists were compared with each other to evaluate their respective risk of developing kidney disease. A propensity score-matched analysis was conducted to minimize confounding variables and identify whether baseline PPI use was associated with CKD. It is important to note that PPI users in both cohorts were more likely to have a high BMI, hypertension, cardiovascular disease, and exhibit polypharmacy (with antihypertensives, aspirin, diuretics and statins). They found that PPI use is associated with a higher risk of incident CKD. The JASN paper from Xie et al used a Department of Veterans Affairs national databases to build a primary cohort of new users of PPIs (173,321) and new users of H2 blockers (20,270) and followed these patients over 5 years to ascertain renal outcomes. In adjusted Cox survival models, the PPI group, compared with the H2 blockers group, had an increased risk of incident eGFR decline less than 60, incident CKD, and a graded association between PPI duration and risk of renal outcomes. Both of these studies point to a fundamental issue in medicine. Polypharmacy. We need to remain vigilant to remove medication that have no clear indication. PPIs once thought of as innocuous now have real risk associated with them.

1. suPAR from bone marrow myeloid cells in Nature Medicine (64%)- Coming in at # 1 this year is a basic science paper just published a few weeks ago in Nature Medicine. Just like the Gli1 story of 2014 we will also have to add an asterisks to this win. The suPAR aficionados really came out in force with heavy voting and it is not a surprise for us as suPAR has been a consistent story for the last 7 years. suPAR graced the TopNephrology stories in 2011. In fact, it hit the number 1 spot with the original Nature Medicine paper describing its potential link to FSGS. Then in 2015 suPAR was unable to crack the top 10 and landed at number 14 with the NEJM paper linking suPAR to CKD in a cohort of patients at Emory undergoing cardiac catheterization. Now in 2016, suPAR does it again. Our #1 story. The current study seeks to identify with cellular source of soluble urokinase plasminogen activator receptor (suPAR) which the above studies have implicated in CKD. Most notable is the fact that if a patient with FSGS receives a kidney transplant unfortunately their is a high chance of recurrence. Thus, implicating an extra renal "factor" like suPAR leading to kidney damage. Utilizing a combination of bone marrow chimera, ablation and cell transfer studies that suggest that Gr-1lo immature myeloid cells of bone marrow origin is the source of suPAR and a key contributor to glomerular damage. A very interesting observation that will no doubt lead to more studies on the link between bone marrow derived cells and kidney function.

Another busy and exciting year in the world of nephrology in 2016. Thanks to all of the contributors and readers in the nephrology online community for keeping nephrology fun, interesting and educational. Next year the #TopNephrology stories will be moving to NephJC.

Thanks for supporting RFN and NephJC. Happy holidays from the entire team.

Can't wait to see what 2017 has in store!

Don't forget to sign up for the NephJC email to keep up to date

Post by Matt Sparks, Swapnil Hiremath, and Joel Topf

Wednesday, December 14, 2016

Renal Grand Rounds: Fevers on Dialysis - Not always an Infection

At renal grand rounds this week, I presented a case of a gentleman who presented with fevers, confusion, and lower extremity pain during dialysis. The patient would spike low grade fevers pre-HD and then fevers up to 105 post-HD. He had a tunneled HD line, but blood cultures were negative, and his fevers persisted in spite of changing the line. We were initially concerned for a dialyzer membrane reaction, but the time course of fevers was not consistent with either type A or type B reaction, and his symptoms persisted even after switching to an Exceltra membrane. The patient was worked up further, and his serum electrophoresis revealed 2 M components, serum free light chains showed an elevated Kappa/Lambda ratio, and he had a positive urine Bence Jones protein. His CH50 and C4 levels were undetectable, but C3 was only mildly low. Cryocrit was sent, and was positive for a type 2 cryoprotein with a predominant IgM Kappa component.
It was unclear why the symptoms of cryoglobulinemia worsened with dialysis; it was hypothesized that hemoconcentration with ultrafiltration, along with exposure of blood to cooler temperatures within the dialysis tubing led to transient complement consumption and an inflammatory reaction. The symptoms of mixed cryoglobulinemia are typically nonspecific, and patients usually present with arthralgias, fatigue, palpable purpura, and peripheral neuropathy. C4 and total complement are usually dramatically low, as in this case.
Treatment of cryoglobulinemia usually involves the use of plasmapheresis to remove circulating cryoglobulins. Steroids are suppressive in some patients, and rituximab quells formation of new cryoglobulins.  There are no studies aside from case reports about the use of eculizumab for cryoglobulinemia. Trendelenburg et al analyzed the role of complement in glomerular inflammation using mice models, and showed that mice deficient in C5 had reduced glomerular infiltration by neutrophils. Eculizumab inhibits the conversion of C5a to C5b and subsequent formation of the membrane attack complex; it therefore be theoretically useful in treating cryoglobulinemia, which causes complement mediated renal failure.
The patient was treated with 2 doses of eculizumab and then rituximab for cryoglobulinemia, and is now doing well and tolerating dialysis.
Posted by Shruti Gupta, Renal Fellow MGH/BWH

Thursday, December 8, 2016

The Painless Guide to Mastering Clinical Acid Base

Apologies to Ben for the delay in posting about this.

Ben Abelow is an MD in New Haven who has long had an interest in teaching basic acid base physiology. In the late 1990s he published a primer for acid base that was very well received. Earlier this year, he published a new book, also on acid base physiology called "The Painless Guide to Mastering Clinical Acid Base". The purpose of this book is to help medical students and junior trainees grasp the basics of how to approach acid base problems while also give them the tools that they need to effectively teach acid-base in a simple and easy to understand way.

The first part of the book in particular very simply explains the basic chemistry behind acid base physiology and is very useful - I learned a few pearls that I will be using on rounds in the future. The rest of the book may be a little simple for renal fellows but it is short and very accessible so I think it is well worth reviewing at least once.

Ben's book is available on Amazon. He has also offered it for free to all first year renal fellows in the US. He is contacting program directors around the country to send them the book. If they are not responsive, he will be able to provide the books to individual fellows.

Thanks again Ben for this - students are always complaining that Renal Physiology is too complex but this really does make it simple

Green dialysis: what to do with discarded water used during dialysis?

Global warming is a growing threat to our health. Dialysis, while sustaining the lives of millions worldwide, has a significant environmental impact. Think of your last dialysis order. Perhaps the Kd was 500 ml/min for four hours. That’s 120 L. Dialysis units may waste up to 2/3 of the reverse osmosis (RO) water used for making dialysis. So add another 240 L. If you include additional saline used for used for priming and cleaning HD machines we may use between 400-500 L of water per 4-hour treatment. And that’s with a modest Kd of 500 ml/min.

Considering the global dialysis population, over 150 billion L of water are likely used every year with potentially 2/3 of that water discarded prior to dialysis. That’s about 40,000 Olympic swimming pools filled with wasted water. It should be noted that depending on your unit’s specific water system there may be less waste and increased recycling opportunities, but overall this remains a significant area of impact for dialysis on the world. And these concerns do not include the power and plastic needs generated by dialysis, which are also significant.

Does it have to be this way? RO “reject” water is more than just potable. It went through particulate filters, carbon filters, and water softeners prior to reverse osmosis. What emerges is practically expensive mineral water. It passes the WHO/EPA requirements for drinking water though is not legally considered potable.

Instead of going down the drain, RO reject water could be used for:
  • Steam generation for hospital sterilization 
  • Laundry services 
  • Sanitation services 
  • Landscaping 
  • Almost anything you already use water for 
Reusing dialysate is more challenging given the higher conductivity (salinity) and the requirement for either recurrent RO or sorbent therapy. This can be cost-prohibitive and technologically challenging.

How much RO water does your unit’s system reject?  
Is there a way to use that water if it is not already being used? 
Beyond that, can recycling be further emphasized for both in-center and home patients? 
Perhaps in some places solar-assisted hemodialysis is an option?

One day perhaps rejected RO water can grow fruit and veg on the roofs of dialysis units. Providing sustainable, affordable nutrition to those who need it most.

If you are intrigued, the following resources offer a starting point to making dialysis more environmentally sustainable.

Robert Rope, Nephrology Fellow- Stanford