Blogs from the 46th annual American Society of Nephrology Kidney Week 2013 Meetings in Atlanta, GA.


Contents

  1. President’s message – Open Plenary
    [blog] [Kidney Week Media Site] [twitter transcript]

  2. State of the Art Lecture: Regenerative Medicine
    [blog]
    [Kidney Week Media Site] [twitter transcript]

  3. State of the Art Lecture: Polycystic Kidney and Liver Diseases
    [blog] [Kidney Week Media Site] [twitter transcript]

  4. State of the Art Lecture: Marfan Syndrome
    [blog] [Kidney Week Media Site] [twitter transcript]

  5. Urinary Acidification
    [blog] [twitter transcript]

  6. Choosing the Right Dialysis Modality for Each Patient: PD versus HD
    [blog]

  7. Choosing the right targets in diabetic kidney disease
    [blog] [Kidney Week Media Site] [twitter transcript]

  8. Chymase and AGEs as targets in diabetic kidney disease
    [blog] [twitter transcript]

  9. Protein kinase C in diabetic kidney disease
    [blog] [twitter transcript]

  10. High Impact Clinical Trials: AKI during On-pump versus Off-pump CABG and Kidney Function One Year Later
    [blog] [twitter transcript]

  11. High Impact Clinical Trials: Bardoxolone in type 2 diabetics with CKD stage 4 — BEACON Trial
    [blog] [twitter transcript]

  12. High Impact Clinical Trials: Combined Angiotensin Inhibition for treatment of Diabetic Nephropathy — VA Nephron D
    [blog] [twitter transcript]

  13. High Impact Clinical Trials: Hypertension in Hemodialysis patients treated with lisinopril versus atenolol — HDPAL Study
    [blog] [twitter transcript]

  14. High Impact Clinical Trials: ZS-9
    [blog] [twitter transcript]

  15. Teaching and Evaluating Learners in Nephrology: The Win-Win of Simulation in Nephrology
    [blog]



President’s Opening Plenary Session
Speaker: Bruce Molitoris
[Kidney Week Media Site]
[twitter transcript]
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The 46th annual meeting of the American Society of Nephrology (Kidney Week, formerly Renal Week) started off with the customary opening address by the outgoing ASN President. This year, the president jumped right into the main issue facing nephrology today: decreased interest amongst young trainees. Currently, less than 32% of all nephrology fellowship positions are filled by US medical graduates: the lowest number ever. In previous years, fellowship programs have depended on internal medical graduates (IMGs) to fill these fellowship positions, but now even IMGs are showing less interest in the field. These trends have resulted in our current state, whereby the President anticipates a total number of applicants that will be less than the total number of positions available.


In 2010, an ASN-created task force looked at the reasons why interest in nephrology is declining. They found that a “lack of innovation” was a key cause of this decline (more on this later). The task force also determined that other MD-specialities are caring for kidney patients, leaving, primarily, only advanced CKD patients for the nephrologist (e.g., ICU and anesthesiologists managing fluids and electrolytes, hospitalists managing acute kidney injury, etc.).


To help mitigate this decline, ASN developed 2 new programs: Kidney TREKS (link) and Kidney MAPS. Both are intended to increase awareness of kidney disease amongst the public and young trainees. The ASN Kidney Week travel grant has been expanded; this year, 49 medical students and 117 residents were given grants to attend Kidney Week — the most ever.


Now back to the idea of “innovation”. The president tried to make the case that nephrologists must develop new diagnostic and therapeutic tools to treat kidney patients, and that these tools should be individualized to the patient and not to a group (e.g, for patients who are CKD stage 4). Innovative individualized care is needed to help raise interest in nephrology and would also be better care for kidney patients. He did not go into the specifics of “innovative individualized” care during his address.


Finally, some more bad news. The American College of Physicians has come out against the need for CKD screening (link): a step with which the president fully disagrees. To add insult to injury, the NIH’s total funding for kidney disease amounts to $28 per patient; in comparison, it’s $507 per cancer patient.


We’ve got a long way to go to increase awareness and appreciation for the ravages of kidney disease and convince young trainees that nephrology is a worthy field for them to enter.

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State of the Art Lecture: Regenerative Medicine
Speaker: Anthony Atala
[Kidney Week Media Site]
[twitter transcript]
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Dr. Anthony Atala gave the first State of the Art lecture for Kidney Week 2013 on Regenerative Medicine. He is well known for his research in growing tissues and organs in vitro. However, he isn’t the first physician to try such a feat: the field of regenerative medicine actually began in the 1930s and in 1981 physicians applied harvest skin to burn victims and saw that the wounds healed.


There have been few clinical advances of regenerative medicine since the 1930s because of 3 main reasons: 1) inability to grow cells outside the body, 2) problems with adequate vascularity, and 3) poorly developed biomaterials for scaffolds. He touched on each of these challenges briefly.


It has been very difficult to grow cells outside the body. While one thinks that simply adding a growth factor (e.g., VEGF) would stimulate cells to grow, such a simple mechanism does not exist. One must have the correct growth factors, in the correct proportions, delivered at the appropriate times, under specific environmental conditions, to name just a few of the variables required to grow cells in vitro. To date, Atala’s group has been successful in growing all cells in vitro except: 1) hepatocytes, 2) neurons, and 3) pancreatic cells (he didn’t mention if the difficulty is the growth of exocrine, endocrine cells, or both).


Once his team succeeded in growing cells in vitro, they realized that the amount of cells that they could grow was tremendous. While this feat was remarkable, it often led to poor results because of the inability to provide adequate vascularity to the majority of the cells. His team realized that vascularity required branching of the main vessel into smaller and smaller caliber vessels. Branching would be the only way that large sheets of cells could receive enough vascular supply to survive. This branching pattern is now found in most scaffolds that are used to grow cells.


Atala then turned his attention to the biomaterials used to create scaffolds. For small defects, simply regenerating cells in vitro and then transplanting them would be sufficient. For larger defects, however, both cells and scaffolding would be needed to repair the defects. In most of his experiments, he is able to successfully repair large defects using a cell/scaffold model. The scaffold is made of biodegradeable material that actually allows the cells to lay down their own native matrix (usually happens around 6 months post-implantation).


Finally, the issue of scalability arose. Atala and his team have been developing these organs/cells one at a time. This has presented a problem of scale as he cannot develop these cells/tissues/organs fast enough. His team is now looking at 3D printing to create the scaffolds that he needs to repair larger defects. This is the same 3D printing that we’ve heard about outside of medicine. 3D printing, however, is in its infancy and, probably for that reason, Atala did not expand on this idea in detail.


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Urinary Acidification
Speakers: L. Lee Hamm, Thomas DuBose, Eric Simon
[twitter transcript]
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This set of lectures started out with Dr. Hamm reviewing the basic processes of acid excretion along different portions of the nephron. In the proximal tubule (PCT), acid excretion primarily occurs through bicarbonate reabsorption (i.e., for every 1 bicarbonate anion that is reabsorbed, one proton is excreted). Bicarbonate absorption in the PCT heavily depends upon carbonic anhydrase (isoforms II and IV). Isoform II is intracellular and isoform IV is found on the brush border (luminal side). CA II is needed to convert carbon dioxide back to proton + bicarbonate anion; the latter is then reabsorbed back into the blood stream through a sodium-bicarbonate antiporter on the basolateral surface of the principal cell.


In the distal nephron, the main transport proteins that facilitate acid excretion are: 1) the H+-ATPase and 2) the H+/K+-exchanger (an antiporter).


Net acid excretion (NAE) can be defined by this simple mathematical equation:

NAE = urine TA + urine NH4+ – urine bicarbonate

The greater the titratable acid, more the NH4+, and the more bicarbonate reabsorbed, the greater the net acid excretion. In this equation, only 3 variables determine NAE, with NH4+ actually representing 2/3 of NAE.

Now we turn to the renal tubular acidoses (RTAs). Dr. DuBose spent about 1 minute explaining the “delta-delta” equation to identify an superimposed non-anion gap acidosis in the presence of an an anion-gap acidosis. [See our 10-Minute Rounds video to understand this concept (video 1 and video 2]. It is important to try to calculate the amount of urinary NH4+ that is excreted, since the kidney relies on this mechanism to “defend the body” against acidemia. While it is possible to directly measure urinary NH4+ levels, it is still cumbersome. Thus, we continue to use the urine anion gap (link) and the urine osmolar gap to estimate NH4+ excretion (UOSM gap /2 = ~ urinary NH4+ excretion).


A final note about RTAs: there has been recent talk disfavoring the use of the TTKG. Dr. DuBose did not dwell on the subject too much but was unequivocal in his statement that he continues to use the TTKG and teaches it to his residents and fellows. [See this 10-Minute Rounds video on why the TTKG was developed (link) and how to interpret its value (link)]



Dr. Simon concluded the session with a discussion of acidosis in CKD. It seems that in many studies, a bicarbonate level of < 22 leads to faster progression towards ESRD (in Wesson KI 2010, the higher bicarbonate group had a decline in GFR of -1.8 ml/min/year versus -4.8 ml/min/year in the lower bicarbonate group; link), greater damage to bone and muscle, and higher mortality (in one study whose reference I could not get, a 2.5x greater mortality for those patients with bicarbonate < 22).


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Choosing the Right Dialysis Modality for Each Patient: PD versus HD
Speaker: Joanne Bargman
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Patient populations:
Obese patients
Dr. Bargman’s experience is that they have less incidence of problems including hernia
​Considerations:
- Can use larger volumes at night when supine, smaller volumes in day to help prevent hernia development
- Is the Kt/V accurate in obese patients? The “V” or volume may be wrong due to the increased proportion of fat
- Don’t base adequacy decisions in the obese patient solely on the Kt/V
o Use clinical judgment!
• How do they look?
• How do they feel?
• Are they eating?
• How is their albumin?
• If u must use kt/v, use the fat free kt/v
- Consider use of pre-sternal PD catheters in the obese patient

Elderly patients
- In France, older they are more likely to do PD
- In North America we underuse PD in the elderly – a tragedy
o Keep them in their home, prevent falls, improve QOL, etc
o Doing PD may eliminate problem of hemodynamic instability and vascular access problems
• Elderly more than likely to get myocardial stunning with HD
• PD is not associated with myocardial stunning
• Elderly may be more prone to being “wiped out” after HD sessions
• Fistula failure is a problem in the elderly
o On the other hand, PD catheters seem to do fine in elderly
• Nessim, Clin J Am Soc Nephrol 2009 “Predictors of Peritonitis in Patients on Peritoneal Dialysis”
• Elderly seem to be no more predisposed to peritonitis (Hong Kong Experience and Sharon Nessim’s data from Canadian database)
o BOLDE: QOL in UK study looked at elderly patients on HD and PD
• PD pts had higher mental score on PD.
• Physical score was equivalent.
• In-center HD is more disruptive to their life than PD
o COST – if the elderly pt requires ambulance transport to in-center HD
• She tells a story of a US center describing a 200.00 cost of transporting a patient to in-center HD
• 6 transports a week x 200.00 = 1200.00 per week
• 1200.00 per week x 52 weeks/year = %62,400 per year!!

Myths and PD
- Low IQ is not a disadvantage
o Might be an advantage sometimes!
- Obese is not a contraindication (see issues above)
o One option would be to consider a pre-sternal catheter
o Colostomy patients could use a pre-sternal catheter
- Can still do PD with low socio-economic status
- Can still do PD in the setting of poor hygiene or a dirty domicile

SO WHO SHOULDN’T DO PD?
- End stage liver disease patient requiring regular paracenteses due to type II HRS
o They can get leak from the PD catheter
o They have massive protein losses
o They have large drain volumes
o BUT THIS DOES NOT INCLUDE patients with functioning liver transplant who have kidney failure due to CNI toxicity – they do ok
- Overweight, especially young pt, who needs to lose weight to get a transplant
o PD supplies 400 calories /day due to glucose in dialysate
- Previous surgical peritonitis from perforated bowel, multiple intra-abdominal abscesses, et cetera
o BUT THIS DOES NOT include history of other surgeries: cholecystectomy, hysterectomy, appendectomy (unless ruptured), colectomy for colon cancer, nephrectomy, AAA repair especially procedure involving intravascular stenting
- Recurrent diverticulitis is a risk
- Mental problems or emotional instability unless there is a caregiver
o But remember, patients may do better in home environment – in-center HD may not go well for these patients
- Living conditions may be a contraindication but not always!
o Tells story of PD patient where dialysis supply delivery team would not go into the patient’s house due to rats running around. This patient never had 1 episode of peritonitis!

Barriers to PD
- It’s just easier to start HD – schedule a tunneled dialysis catheter and come to the center – especially when there is an empty HD chair that just sucks the patient in…..
- Getting PD started takes more coordination with providers, patient and caregiver


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State of the Art Lecture: Polycystic Kidney and Liver Diseases
Speaker: Stefan Somlo
[Kidney Week Media Site]
[twitter transcript]
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Stefan Somlo is the 2013 ASN Homer Smith award winner. He has spent 25+ years studying polycystic kidney disease and among his many discoveries was the PKD2 gene; a defect in which accounts for about 15% of polycystic kidney disease in the world. PKD is the most commonly inherited kidney disorder, affecting all genders and races/ethnicities equally. Dr. Somlo presented a basic-science lecture discussing the role of genes in both PKD, polycystic liver disease (PLD), and the cilia (a crucial structure whose defect is thought to cause the polycystic phenotype).


One of the most interesting aspects of his talk was the concept of “gene dosage”. Though not explicitly mentioned, polycystic kidney disease is a disease in which the degree of the gene product directly correlates with the polycystic phenotype. Using mouse models, Dr. Somlo showed that the greater the reduction in the polycystin 1 (encoded by the PKD1 gene), the greater the polycystic phenotype and faster progression to ESRD. We are accustomed to correlating the word “dosage” with a drug but it was interesting to see how the level of a gene’s product (protein) could also act as a drug in its therapeutic effect.


Dr. Somlo focused on the role of the cilia in PKD. For the last 10 years, cilia have gained an increasingly important role in the development of cysts. While neither PKD1 or PKD2 gene products are needed to form cilia, their respective gene products (polycystin 1 and polycystin 2 proteins) are found within the cilia. In a series of mice knockout models, if you knockout the gene for cilia formation, you get the polycystic phenotype. The same is true if one knocks out PKD1 gene. If, however, you knockout both the gene for cilia and PKD1, you get a protective phenotype. This was an extremely interesting finding but gauging the audience’s lack of response, I don’t think many understood how antithetical this finding is. Dr. Somlo intimated that the protective phenotype had to do with the timing (or sequence) in which the genes were inactivated, but wasn’t able to go into greater detail during his State of the Art lecture.


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State of the Art Lecture: Marfan Syndrome
Speaker: Harry Dietz
[Kidney Week Media Site]
[twitter transcript]
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Most of the State of the Art lectures this year focused on gene discoveries and genomic studies. This theme was evident in the Marfan Syndrome talk as it had very little to do with the kidneys per se. Dr. Dietz discovered that fibrillin 1 is the gene whose defect results in the Marfan’s phenotype. This gene encodes fibrillin, a protein whose function (among many others) is to suppress TGF beta. TGF beta is thought to be the main culprit behind the Marfan’s phenotype. (Interestingly, TGF beta is also thought to be a culprit in diabetic kidney disease).


The most interesting and relevant information as it related to kidney disease was the use of the angiotensin receptor blockers (ARBs) as a treatment for Marfan’s syndrome. It is known that angiotensin II (Ang II) stimulates the production of TGF beta via the AT-1 receptor and inhibits its production via the AT-2 receptor. If you selectively block the AT-1 receptor with an ARB, you halt production of TGF beta. In mouse models who have a defect in fibrillin 1, treatment with ARBs (losartan) resulted in an elimination of the Marfan’s phenotype.


As a nephrologist, it is very interesting to know that TGF beta is a newly identified culprit in kidney disease. Perhaps ARBs exert their therapeutic effects against diabetic kidney disease through the suppression of TFG beta. We shall see.


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New targets in diabetic kidney disease
Speaker: Kumar Sharma
[Kidney Week Media Site]
[twitter transcript]
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This was an excellent introduction into the world of proteomics and metabolomics. Although not explicitly defined by Dr. Sharma, after sitting through the lecture one can get the idea of what proteomics and metabolomics are about. In a nutshell, the search for proteins and metabolites that are consistently present at altered levels in diabetic kidney disease patients is the foundation for this type of research. The hope is that we can identify proteins/metabolites whose altered levels indicate early diabetic kidney disease (earlier than microalbuminuria) and/or represent new targets for therapy. This type of research requires sorting through a large number of candidate molecules until one finds a molecule whose levels are altered (either too high or too low) in diabetic kidney disease. Needless to say, any study in proteomics/metabolomics will require a Bonferonni or Bonferonni-like correction because the problems of multiple hypothesis testing.


From among 273 urinary proteins measured, Dr. Sharma’s group found 12 proteins whose levels are consistently altered in diabetic kidney patients that they are candidates for further study. Almost all 12 of these proteins/metabolites are derived from the mitochondria, allowing him to postulate that, perhaps, diabetic kidney disease occurs through mitochondrial damage. Though he didn’t mention the specific metabolites (he did show a side but the names were too long and complex to jot down), he specifically mentioned AMP-kinase as a possible “common denominator” in the dysfunction of mitochondria, resulting in diabetic kidney disease.


Proteomics/metabolomics is an exciting area of research. The will likely be many new proteins/metabolites identified that could lead to an earlier diagnosis of diabetic kidney disease (DKD) and/or new therapies against DKD. However, given the sheer number of proteins/metabolites that are likely to be found, I wouldn’t be surprised if many of the studies we see in the next few years turn out to be negative. I wouldn’t lose hope in this area of research and wouldn’t allow these anticipated negative studies to dissuade researchers from searching for newer targets in DKD.


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Chymase and AGEs as targets in diabetic kidney disease
Speakers: Lisa Harrison and Gary Striker
[twitter transcript]
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Dr. Harrison started off this session by focusing on her work with chymase. Chymase is a serine protease that can cause fibrosis through it’s activation of TGF beta. Her initial studies showed a large amount of chymase-containing mast cells within diabetic kidneys. Further work showed that no matter the etiology of the kidney disease, the density of chymase-containing mast cells was increased. On the contrary, histologic examination of normal kidneys shows very few chymase-containing mast cells. Her early work has shown that chymase also increases angiotensins I and II activity, in a manner that is independent of angiotensin-converting enzyme activity. In a mouse model, the administration of a chymase inhibitor (not an ACE-inhibitor) actually decreased urine albumin excretion for up to 8 weeks. She did not mention why the results were only seen for 8 weeks, but this research is in the early promising stages of a potential new therapy.


Dr. Striker discussed AGEs (advanced glycosylation end-products). We know that lower AGE levels exert a protective effect against diabetic kidney disease. We also know that AGE levels rise as a result of: 1) decreased renal excretion, 2) increased intracellular conversion, and 3) increased enteral intake.



It turns out that much of the food in the Western and Asian Indian diet are rich with AGEs. It may not be the food itself that is rich with AGEs but rather the manner in which the food is prepared. Mediterranean diets are poor in AGEs but when prepared in certain ways (e.g., deeply fried), their AGE content dramatically rises. It’s the preparation methods, and not the foodstuff itself, that affects the AGE content.


Sevelamer carbonate is an excellent binder of AGEs in the duodenum. Metformin, on the other hand, is an excellent inhibitor of intracellular AGE formation. Perhaps these medications are potentially useful therapeutic agents in the fight against kidney disease, no matter what the etiology. Unfortunately, Dr. Striker did not mention any recent or ongoing clinical trials to assess these medications.


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Protein Kinase C and diabetic kidney disease
Speaker: Katherine Tuttle
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Dr. Tuttle started off her talk with mention of the drug ruboxistaurin (RTX). It’s an unfamiliar drug to most of us but has been shown to decrease rates of glomerular sclerosis and interstitial fibrosis in diabetic kidney disease. The mechanism of action is through an inhibition of protein kinase C (PKC), which she believes is the central player in the pathogenesis of diabetic kidney disease. Unfortunately, the drug has been tied up in abnormal “business practices” and isn’t available for clinical trials. Dr. Tuttle focused the rest of her talk on the values of inhibiting PKC, including reduced urinary albuminuria. However, with additional clinical trials, we are left wondering what is the future of PKC-inhibitory agents.


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High Impact Clinical Trials: AKI during On-pump versus Off-pump CABG and Kidney Function One Year Later
Speaker: Amit Garg
[twitter transcript]
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It is theorized that the risk for long-term kidney disease is increased in those patients that have suffered mild-moderate episodes of AKI. Many of us actually thought this was proven in a randomized controlled trial, but in fact is has not. The authors of this investigation wanted to prove, in a controlled trial fashion, if the onset of mild-moderate AKI had a detrimental effect on longer-term kidney function.


To accomplish this task, they randomized 3000 patients to either on-pump CABG or off-pump CABG procedures. Within each group, they defined AKI as a 50% increase in post-operative AKI and longer-term kidney dysfunction as a 20% decrease in eGFR at 1 year.


Patients in the on-pump CABG group had a greater risk of developing AKI (20.8% versus 17.5%, p 0.01). However, at one year of followup, the on-pump CABG group actually had a non-statistically lower rate of chronic kidney disease (15.3 versus 17.1%, p NS).


This investigation teaches us a few points. One: we need to rethink if the development of mild-moderate AKI actually has detrimental effects on longer-term kidney function. Two: is one-year actually a long enough duration to assess kidney function (i.e., would we have seen a difference at 2 or 3 years)? Three: simply believing something to be true doesn’t make it so; search for randomized data wherever possible to guide our clinical decision making.


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High Impact Clinical Trials: Bardoxolone in type 2 diabetics with CKD stage 4 — BEACON Trial
Speaker: Glenn Chertow
[twitter transcript]
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Coming off the positive results of the BEAM trial (link), the BEACON trial yielded significantly disappointing results. As a quick review: bardoxolone is a potent activator of NRF2. NRF2 decreases NFkB production, which in turn decreases oxidative stress. It is believed that oxidative stress is the main cause of kidney injury. After the successful results of the phase 2 BEAM trial, BEACON was undertaken to see its effects on the onset of ESRD and CV death (these were the primary endpoints).


Alas, there was no difference in either of the primary endpoints between the bardoxolone and placebo groups. While this could be explained away by faulty trial design (e.g., too short a follow up), the trial was actually terminated early for safety concerns. There was a greater percentage of side effects in the bardoxolone group, namely increased deaths, than the placebo group.


The audience seemed to be very appreciative of the authors for having conducted this study, pleased with the NEJM for publishing a negative study, but overall bummed at another negative clinical trial in nephrology.


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High Impact Clinical Trials: Combined Angiotensin Inhibition for treatment of Diabetic Nephropathy — VA Nephron D
Speaker: Linda Fried
[twitter transcript]
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Coming off the heels of ONTARGET and ALTITUDE (link), the VA Nephron D study looked at primary renal endpoints in type 2 diabetics who were given either an ARB alone versus combination ARB + ACEi therapy. Specifically, the primary endpoints were a a change in eGFR, Serum Cr, development of ESRD, and death. The study was initially slotted for 3 years but because of slow recruitment (not sure why, and the speaker didn’t comment further), enrollment was extended up to 4.25 years.


Unfortunately, the study was terminated early (2.2 years) with only 1448 patients recruited. The risks for severe hyperkalemia and severe AKI were increased in the dual-therapy group (HR 2.5 and 1.7, respectively; both significant results). Interim analysis of those patients that were enrolled showed a 12% decrease in the primary endpoint in the dual-therapy group; these results were not significant primarily because of the low sample size. And similar to the ALTITUDE trial, the dual-therapy group had a lower amount of albuminuria.


The audience was keen on knowing what the speaker felt about dual-renin-angiotensin-aldosterone blockade. In so many words, she basically said the concept is dead.


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High Impact Clinical Trials: Hypertension in Hemodialysis patients treated with lisinopril versus atenolol — HDPAL Study
Speaker: Rajiv Agarwal
[twitter transcript]
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In this study, the investigators wanted to know if the use of lisinopril versus atenolol would lead to a regression in LVH (a clinically-significant endpoint for untreated hypertension) in hemodialysis patients. Both drugs were dosed to a target BP of <140/<90. Thus far, 104 patients were available for analysis. After 3 months, there was a larger drop in BP in the atenolol group (about 5-6 mm drop greater than in the lisinopril group); this was sustained for at least 12-months of followup. Unfortunately, the study was terminated early because of higher adverse events in the lisinopril group. Both groups showed a decrease in LV mass index (LVMI) at 12 months but because the study was terminated early, these results are under-powered and have little meaning.


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High Impact Clinical Trials: ZS-9
Speaker: Stephen Ash
[twitter transcript]
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ZS-9 is the code name for a potassium-trapping molecule. The speaker was clear that it is not a resin like kayexalate, but didn’t elaborate as to what it is. While kayexalate is unselective for K+ (it also binds Ca++ and Mg++), ZS-9 has nine-times more K+-binding capacity. In a phase 2 trial (which was presented here), the 10 g and 3 g dosages of ZS-9 achieved excellent results with minimal side effects (the 0.3 g dosage did not achieve as great a reduction in serum K+).


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Teaching and Evaluating Learners in Nephrology: The Win-Win of Simulation in Nephrology
Speaker: Laura Maursetter
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Chicken Breast and Olive
- Chicken breast with olive inserted is a simulation model for kidney biopsy
- The “kidney”( =olive) is a bit echo dense so still experimenting with a more real life model
o Also looking at some sort of covering for the chicken breast to simulate capsule
- Dr. Alan Seigal at University of Vermont offered some comments about his program’s use of the Phantom Simulator http://www.bluephantom.com/product/Renal-Biopsy-Ultrasound-Training-Model.aspx?cid=531 ($3600.00)
o His learners had more difficulty explaining the procedure and putting the phantom at east than difficulty with the technical aspects of kidney biopsy
o However, when fellows moved on to do actual kidney biopsies, he found they had technical difficulties
 Surmised that the Phantom did not provide real-world simulation and fellows had trouble with
• Patients who were anxious
• Patients who could not hold their breath
• Phantom could not simulate these real-world challenges we experience with patients undergoing biopsy

Difficult Discussion
- the fellow participates in a “difficult discussion” simulation with a “trained patient” where there are specific professionalism and interpersonal skills/communication behaviours expected.
- The trained patient is scripted, and does an excellent job leading the fellow through the simuilation experience.
- Example of this could be end-of-life issues in a dialysis patient, dialysis initiation or other

Professionalism
- The fellow is contacted by a healthcare provider – example given is one of your charge nurses role playing as an outside facility where your patient is being seen and they are calling the fellow for advice about transfer to the fellow’s facility or assistance with management.
- The healthcare provider could be one of your charge nurses, staff nurses or really anyone that the fellow would not immediately recognize over the phone
- Need to make sure at the end of the simulation that the fellow realizes this was not a real situation

CRRT simulation
- Done when the fellow is on call
- Program director calls the fellow on call and presents them with a CRRT dilemma. A medical record is provided so that the fellow may look up the patient in the EPIC “playground” section – this is a mirrored EMR that does NOT contain real charts
- Fellow looks through the chart and data, and makes treatment decisions
- Needs to be checked and debriefed, but this can be done by the PD at a later time

Checking and Debriefing
- Always an important part of any simulation process


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