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Picture of Meguid El Nahas
by Meguid El Nahas - Monday, 15 May 2017, 12:11 PM
Anyone in the world

Obesity and new onset of CKD:

https://www.ncbi.nlm.nih.gov/pubmed/28187985

Obesity but not overweight increases risk of CKD (eGFR <60 and albuminuria) in the general population. A systematic review and Meta-analysis of 39 cohorts, 630,677 individuals showed an association between BMI >30kg/m2 and risk of low eGFR and albuminuria. Whilst many of the studies included adjusted the risk of CKD/Albuminuria to other risk factors associated with CD such as hypertension and smoking, the impact of obesity-related confounders remains unclear, in spite of adjustement for co-morbidities.

Limitations:

Concern has to be expressed over the use of MDRD eGFR estimation in the obese where it is poorly validated. Also, single measurement of eGFR does NOT define CKD...nephrologists seem to forget that a single eGFR value is not sufficient to label an individual as suffering from CKD as KDOQI recommends 2 of 3 positive values over a 3 months period as evidence of chronicity.

Finally, is BMI the best marker of obesity...as individuals with a high body weight due to a high muscle mass would have a higher serum creatinine than others and potentially a lower eGFR...whilst central obesity with a high abdominal fat content and a raised waist circumference/waist-Hip ratio seems a more accurate predictor of obesity-related outcomes...

This was recently highlighted in a study where there were no significant statistical interactions between WHR and obesity status (BMI) and central obesity was found to be associated with adverse cardiac dysfunction.

https://www.ncbi.nlm.nih.gov/pubmed/27307550

https://www.ncbi.nlm.nih.gov/pubmed/26337249

In other words, eGFR and BMI may be inaccurate parameters to evaluate the impact of OBESITY on RENAL FUNCTIONAL OUTCOMES; better studeis need to be divised with more accurate measurements of both renal function and central obesity and better validation of CKD!

 

 

 

 

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
Anyone in the world

April-May 2017

JASN 

Pregnancy outcomes in recovered AKI 

In a study of 105 pregnancies classified as rAKI (pregnant women with history of recovered AKI) were compared with 24640 control pregnancies-authors noted that “past episode of AKI, despite return to normal renal function before pregnancy, associated with meternal adverse outcomes in pregnancy”. Women with r-AKI were more likely to have preterm deliveries and deliveries by cesarean section compared with women without AKI (40% versus 27%; P=0.02). Also rAKI were more likely to have -preeclampsia, preterm preeclampsia, and early preterm preeclampsia (23%, 10%, and 7% versus 4%, 1%, and 0.4%; P<0.001). In offspring of mothers with r-AKI, 40% developed the composite adverse fetal outcome (preterm delivery, NICU admission, small for gestational age, or perinatal death) versus 19% in those without AKI (P<0.001). 

Clear message is -monitor young women with rAKI for maternal and fetal complications if they get pregnant. Don’t jump to the conclusion and blame past AKI for these complications though! Unlike other AKI outcome literature claiming host of bad outcomes associated with AKI in long run, authors of this paper (in addition to acknowledging limitations of  retrospective database analyses) make sensible conclusion,”We, therefore, hypothesize that the underlying metabolic milieu (or other shared risk factors) of these women confers risk for both preeclampsia and AKI.”

Hyponatremia: guidelines on guidelines

‘There are only two tragedies of human life…one, not to get what you want and other is to get it’ said Oscar Wilde. Had he been a nephrologist, he would have said,’there are only two tragedies in the management of hyponatremia…one not to correct it and other is to correct it!’

 Here and here are two guidelines on hyponatremia (european and american) and  this JASN article tries to compile them together. Whatever formula you choose, everyone except serum sodium obeys them.  I remember my residency days when more often than not serum sodium would either not change or change very little or change in opposite direction. Algorithms beginning with  assessment of volume status can only impress your board examiners as differentiation of euvolemic vs hypovolemic hyponatremia by clinical assessment can just be as accurate as toss of coin [sensitivity (50%–80%) and specificity (30%–50%)].

Only test that works at beside is repeated measurements of serum sodium and urine output trend-sudden onset of polyuria being the harbinger of dangerous overcorrection. In elderly, CKD, and for those on thiazides even urine Na can’t be relied upon. 

Some important points:

 -Safety limits have consistently decreased over last two decades from 14-16meq per day to 6-7meq per day given the dangers of overcorrection.

-Fractional excretion of uric acid >12% has the highest sensitivity and specificity to diagnose SIAD (i don’t know who does it)

-Coeptin which is one of the degradation products after prohormone is cleaved to form vasopressin and unlike vasopressin is more stable and can be assayed easily. May make our life easier if it becomes commercially available.

-In severely symptomatic acute hyponatremia, both guidelines prefer bolus 3% saline (100-150ml over 10-20min; can be repeated x3 if needed) over infusion (which is prevalent practice).

-Vaptans are NOT for severely symptomatic or acute hyponatremia; moreover if you overcorrect while using vaptans you lose DDAVP as an option to lower back. Urea on the other hand can be safer and effective option (i dont know how to get it)

CJASN 

“If you can measure it, you can associate it with something” and this issue of CJASN is full of such associations which only rarely turn out to be causal. Serum phosphorus and graft loss, TG/HDL ratio and mortality in dialysismonocyte count and risk of CKD/ESRDCRP and GFR decline to name a few. Time will be better used reading two nice reviews –IgA nephropathy and SGLT2 inhibition. 

SGLT2 inhibitors in addition to glycemic control, have been shown to lower your blood pressure, weight, uric acid, and are the only OHA that showed CV benefit. Also New onset of macroalbuminuria, new onset or worsening of DKD, doubling of serum creatinine and initiation of RRT was less in those treated with SGLT2i. EMPA-REG OUTCOME was funded by Boehringer Ingelheim and Eli Lilly-so lets wait for all of these to be confirmed in more studies. 

Another interesting article on symptom management in CKD: role of dialysis deals with an important puzzle that nephrologist face in patients with stage 4-5 CKD. “The interpretation of the literature is challenging, because the symptoms associated with uremia are often vague, difficult to quantify objectively, and difficult to distinguish from symptoms that can be attributed to conditions coexisting with advanced CKD or side effects of medications used to manage these conditions. Patients with stage 4 or 5 CKD are prescribed a mean of eight different medications” This is  one of the most symptomatic patient population and whether the given symptom complex will be benefited by dialysis is not always simple question to answer. This is especially so in elderly and frail population with multiple other comorbidities and calls for shared decision making involving patient and their caretakers.

Am J Nephrology

Interesting report of 477 patients from Germany who were identified as having euvolemic hyponatremia while on thiazide therapy. No single test could reliably differentiate SIAD from thiazide induced hyponatremia (TIH).  Its commonly believed to be hypovolemic hyponatremia due to saliuresis, but its not the case. Ever wondered why Gitleman’s which is a state akin to chronic thiazide use don’t develop hyponatremia?  Polydipsia and impaired urea mediated free water excretion  are the main drivers of TIH. So whatever may be the cause, be prompt in preventing/treating cerebral edema due to acute hyponatremia (3% saline) and osmotic damage due overcorrection (free water and/or DDAVP). Accompanying editorial nicely summarises the issue of TIH and practical difficulty in differentiating it from SIAD. Here is an excellent blogpost on use of DDAVP in safe correction of hyponatremia.

Nephrology Dialysis Transplantation

Every clinician who is committed to deliver best available care to his patients should  have basic understanding of the research methods to be able to make sense of the ever growing literature. I have found most lectures on research methods by statistician boring and sedating and best way to learn this is to apply/interpret them for articles published in your own specialty. This issue of NDT is devoted to clinical epidemiology and is worth archiving to your desktop. Prediction versus etiologysurvival analysisclinical versus statistical significancerelative versus absolute riskmeta analysis -all of them have examples from nephrology literature that makes it easy to understand the concepts. 

Sildenafil for glomerular disease

Erectile dysfunction turning out to be ‘blessing in disguise’ for patients with diabetic kidney disease! Here is a paper and an editorial (which I tried hard to read full). I was so disappointed when I noted that subjects of this experiment were rats and mice. Sildenafil seems to act via same pathways as pioglitazone which was once advertised as antiproteinuric. Abstract starts with this background “PPAR-γ agonists, like pioglitazone, appear antiproteinuric.” and probably even after human studies sildenafil will have the same place (?) as pioglitazone in the treatment of proteinuria. Meanwhile we can watch what happens to UPCR after somebody ‘gets started’ on Viagra. 

Tukaram Jamale
Associate Professor
Department of Nephrology
Seth GS Medical College and KEM hospital,
Mumbai, India 

 

 

 

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
Anyone in the world

http://www.nejm.org/doi/pdf/10.1056/NEJMp1608005

N Engl J Med. 2016 Nov 10;375(19):1817-1820.

Vitamin D Deficiency - Is There Really a Pandemic?

 
Prof Arif Khwaja quoted from the article:
A common misconception is that the RDA functions as a “cut point” and that nearly the entire population must have a serum 25(OH)D level above 20 ng per milliliter to achieve good bone health. The reality is that the majority (about 97.5%) of the population has a requirement of 20 ng per milliliter or less. Moreover, by definition of an average requirement, approximately half the population has a requirement of 16 ng per milliliter (the EAR) or less
 
This article may rebalance the debate suggesting that the majority of dark skinned individuals have native Vitamin D insufficiency or deficiency:
https://www.ncbi.nlm.nih.gov/pubmed/26643747
 
All too often norms are defioned in young, caucasian, western populations...and applied across the world's various and heterogeneous populations with different:
genetic background
different binding protein levels
different free and bound vitamin D levels
different activation levels to 1-25D
and
different VDR responses
 
Before we accept that there is a global pandemic of VitaminD deficiency causing all the world's ills...it may be judicious to examine the evidence critically....and temper the drive to over prescribe 25D to whole populations...
 
Big Pharma may want us to...we need to exert caution!
 
SEE MORE DISCUSSION ON OLA FORUM:
http://www.gkaonlineacademy.com/forum/ola-english/5922-native-vitamind-deficiency-in-emerging-countries-facts-and-fiction
 
 
 
[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
Anyone in the world


Am J Kidney Dis. 2017 Apr;69(4):552. doi: 10.1053/j.ajkd.2016.09.029.

Kidney Disease of Unknown Cause in Agricultural Laborers (KDUCAL) Is a Better Term to Describe Regional and Endemic Kidney Diseases Such as Uddanam Nephropathy.

Subramanian SJavaid MM1

MesoAmerican Nephropathy (MAN)
Chronic Kidney Disease of Unknown Etiology (CKDu)
chronic interstitial nephritis in agricultural communities (CINAC)
https://www.ncbi.nlm.nih.gov/pubmed/?term=sri+lanka%2C+CKD%2C+De+Broe
 
Now KDUCAL...
 
Are we looking for a name for renal insufficiency that affects labourers in extreme heat conditions...?!
 
Perhaps, we should call it...
CKDh (Chronic Kidney Disease heat induced...)
or even
CKDd (Chronic Kidney Disease dehydration induced...)
 
all these nephropathies observed amongst agricultural workers exposed to extreme heat conditions and who are chronically wasted and dehydrated include those noted amongst:
Sugar cane and other crop labourers in Central America
MesoAmerican Nephropathy
 
Including that observed in agricultural workers in India; Uddanam
https://www.ncbi.nlm.nih.gov/pubmed/27209444
 
In Cuba, Columbia, India, Sri Lanka, Egypt and elsewhere, those workers suffering form CKD may simply suffer from chronic dehydration in people exposed to long period of heat and related stress:
https://www.ncbi.nlm.nih.gov/pubmed/24717833
 
However, additional agricultural related factors have been raised by some, such as my good friend Prof Marc De Broe, who wrote:
https://www.ncbi.nlm.nih.gov/pubmed/?term=sri+lanka%2C+CKD%2C+De+Broe
 
"The heat stress and dehydration hypothesis, however, cannot explain: why the incidence of CINAC went up along with increasing mechanization of paddy farming in the 1990s; the non-existence of CINAC in hotter northern Sri Lanka, Cuba and Myanmar where agrochemicals are sparsely used; the mosaic geographical pattern in CINAC endemic areas; the presence of CINAC among women, children and adolescents who are not exposed to the harsh working conditions; and the observed extra renal manifestations of CINAC. This indicates that heat stress and dehydration may be a contributory or even a necessary risk factor, but which is not able to cause CINAC by itself."
 
In Sri Lanka, heavy metals, and trace elements including cadmium, strontium, etc... contamination of foodstuff has been raised:
https://www.ncbi.nlm.nih.gov/pubmed/26701260
as well as excessive high fluoride water content:
https://www.ncbi.nlm.nih.gov/pubmed/20853020
 
In the meanwhile...and until the etiology is settled....nephrologists will continue to look for a name...
 
same story as many decades ago when Balkan Nephropathy...was atributed to mycotoxins and ochratoxin...and it  became known as Aristolochic Acid Nephropathy (AAN)...
or is it?...
https://www.ncbi.nlm.nih.gov/pubmed/27871899
 
 
 
 
 
 
[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
Picture of Meguid El Nahas
by Meguid El Nahas - Wednesday, 8 March 2017, 5:50 PM
Anyone in the world

The 2017 WKD theme is OBESITY & CKD implying a link between the incidence, progression and outcomes of CKD and Obesity. Presumably a harmful link...?!

Whilst I am aware of links between Obesity and the Metabolic syndrome, and between the Metabolic Syndrome and microalbuminuria...,

I am not fully aware of strong evidence to suggest that there is a:

1. Higher incidence of significant CKD = CKD3b in Obese individuals

2. Faster rate of CKD progression from CKD3 to 5 in Obese individuals

3. Increased CKD Mortality in Obese in individuals

4. Increased CKD Cardiovascular morbidity/mortality in Obese individuals

In fact, there is considerable evidence to the contrary,

that OBESITY IS PROTECTIVE IN CKD against morbidity and mortality...

https://www.ncbi.nlm.nih.gov/pubmed/27190330

So, I ask myself are WKD themes a form of propaganda...fake news...to convey a message based on weak, flawed or even inaccurate information...as long as the message is populist; Obesity is BAD...so it must be BAD for the kidneys....BAD for CKD patients...BAD all round...as expected in popular discourse...TOTALLY UN-EVIDENCE BASED!

A few years ago...the WKD Theme was DRINKING WATER WAS GOOD FOR THE KIDNEYS....another fallacy based on no evidence and playing into the populist myth that drinking a lot of water is good for your kidneys...?! TOTALLY UN-EVIDENCE BASED!

So...in the era of post truth and fake news and conviction by propaganda, the Nephrology world and profession is giving into that trend...the trend of Trump...Brexit...and other propaganda and fake news driven messages...that aim to convince, without evidence...and convey false messages...as long as they serve a purpose?!

So why is WKD and those behind this noble annual initiative chosing misleading themes...is it out of ignorance...that would be unforgivable for such highly placed leaders in the field...or is it to purposely mislead and play on people's established conviction to reinforce them...albeit by misinformation...to raise the profile of CKD...?!

I AM CONFUSED AND DISAPPOINTED...PROPAGANDA SEEM TO BE EVERYWHERE...FACST ARE LOST...MISLEADING FACTS AND NEWS DOMINATE...OUR WORLD, EVEN THAT OF NEPHROLOGY AND WKD!

 

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
Picture of Meguid El Nahas
by Meguid El Nahas - Wednesday, 8 March 2017, 5:50 PM
Anyone in the world

The 2017 WKD theme is Obesity and CKD implying a link between the incidence, progression and outcomes of CKD and Obesity.

Whilst I am aware of links between Obesity and the Metabolic syndrome, and between the metabolic Syndrome and microalbuminuria...,

I am not fully aware of strong evidence to suggest:

1. Higher incidence of significant CKD = CKD3b

2. Faster rate of CKD progression from CKD3 to 5 in Obese individuals

3. Increased CKD Mortality in Obese in individuals

4. Increased CKD Cardiovascular morbidity in Obese individuals

In fact, there is considerable evidence to the contrary, that OBESITY IS PROTECTIVE IN CKD against morbidity and mortality...

https://www.ncbi.nlm.nih.gov/pubmed/27190330

So, I ask myself is WKD themes a form of propaganda...fake news...to convey a message based on weak, flawed or even inaccurate information...as long as the message is populist; Obesity is BAD...so it must be BAD for the kidneys....BAD for CKD patients...BAD all round...as expected in popular discourse...

A few years ago...the WKD Theme was DRINKING WATER WAS GOOD FOR THE KIDNEYS....another fallacy based on no evidence and playing into the populist myth that drinking a lot of water is good for your kidneys...?! TOTALLY UN-EVIDENCE BASED!

So...in the ear of post truth and fake news and conviction by propaganda, the Nephrology world and profession is giving into that trend...the trend of Trump...Brexit...and other propaganda and fake news driven messages...that convince, without evidence...and convey false messages and evidence...those unaware...

So why is WKD and those behind this noble annual initiative chosing misleading themes...is it out of ignorance...that would be unforgivable for such highly placed leaders in the field...or is it to purposely mislead and play on people's established conviction to reinforce them...albeit by misinformation...to raise the profile of CKD...?!

I AM CONFUSED AND DISAPPOINTED...PROPAGANDA SEEM TO BE BE EVERYWHERE...FACST ARE LOST...FAKE FACTS DOMINATE...OUR WORLD, EVEN THAT OF NEPHROLOGY AND WKD!

 

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
Picture of Meguid El Nahas
by Meguid El Nahas - Sunday, 19 February 2017, 6:29 AM
Anyone in the world
Prof Pierre Delanaye TWEETED: 
 
A cheap and (relatively) simple intervention to improve HTA in CKD! Don't forget it! This is a RCT!
 
 
Clin J Am Soc Nephrol. 2017 Feb 16. pii: CJN.01120216. doi: 10.2215/CJN.01120216. [Epub ahead of print]

A Randomized Crossover Trial of Dietary Sodium Restriction in Stage 3-4 CKD.

BACKGROUND AND OBJECTIVES:

Patients with chronic kidney disease (CKD) are often volume expanded and hypertensive. Few controlled studies have assessed the effects of a sodium-restricted diet (SRD) in CKD.

DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS:

We conducted a randomized crossover trial to evaluate the effect of SRD (target <2 g sodium per day) versus usual diet on hydration status (by bioelectrical impedance spectroscopy) and blood pressure (BP) between May of 2009 and May of 2013. A total of 58 adults with stage 3-4 CKD were enrolled from two academic sites: University of Michigan (n=37) and University of North Carolina at Chapel Hill (n=21); 60% were men, 43% were diabetic, 93% were hypertensive, and mean age was 61 years. Participants followed SRD or usual diet for 4 weeks, followed by a 2-week washout period and a 4-week crossover phase. During the SRD, dieticians provided counseling every 2 weeks, using motivational interviewing techniques.

RESULTS:

Whole-body extracellular volume and calf intracellular volume decreased by 1.02 L (95% confidence interval [95% CI], -1.48 to -0.56; P<0.001) and -0.06 L (95% CI, -0.12 to -0.01; P=0.02), respectively, implying decreased fluid content on the SRD compared with usual diet. Significant reductions in urinary sodium (-57.3 mEq/24 h; 95% CI, -81.8 to -32.9), weight (-2.3 kg; 95% CI, -3.2 to -1.5), and 24-hour systolic BP (-10.8 mmHg; 95% CI, -17.0 to -4.6) were also observed (all P<0.01). Albumin-to-creatinine ratio did not change significantly and mean serum creatinine increased slightly (0.1 mg/dl; 95% CI, -0.01 to 0.2; P=0.06). No period or carryover effects were observed. Results were similar when analyzed from phase 1 only before crossover, although P values were modestly larger because of the loss of power.

CONCLUSIONS:

In this randomized crossover trial, implementation of SRD in patients with CKD stage 3-4 resulted in clinically and statistically significant improvement in BP and hydration status. This simple dietary intervention merits a larger trial in CKD to evaluate effects on major clinical outcomes.

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
Picture of Meguid El Nahas
by Meguid El Nahas - Saturday, 14 January 2017, 12:54 PM
Anyone in the world

Prof Pierre Delanaye posted:

FISH OIL or ASPIRIN for AVF maturation: does not wok!
Written by Pierre Delanaye on Monday, 09 January 2017. Posted in OLA BlogJAMA Intern Med. 2017 Jan 3. doi: 10.1001/jamainternmed.2016.8029. [Epub ahead of print]
Effect of Fish Oil Supplementation and Aspirin Use on Arteriovenous Fistula Failure in Patients Requiring Hemodialysis: A Randomized Clinical Trial.
Irish AB1, Viecelli AK2, Hawley CM2, Hooi LS3, Pascoe EM4, Paul-Brent PA4, Badve SV5, Mori TA6, Cass A7, Kerr PG8, Voss D9, Ong LM10, Polkinghorne KR11; Omega-3 Fatty Acids (Fish Oils) and Aspirin in Vascular Access Outcomes in Renal Disease (FAVOURED) Study Collaborative Group.
 
Abstract

IMPORTANCE:
Vascular access dysfunction is a leading cause of morbidity and mortality in patients requiring hemodialysis. Arteriovenous fistulae are preferred over synthetic grafts and central venous catheters due to superior long-term outcomes and lower health care costs, but increasing their use is limited by early thrombosis and maturation failure. ω-3 Polyunsaturated fatty acids (fish oils) have pleiotropic effects on vascular biology and inflammation and aspirin impairs platelet aggregation, which may reduce access failure.
OBJECTIVE:
To determine whether fish oil supplementation (primary objective) or aspirin use (secondary objective) is effective in reducing arteriovenous fistula failure.
DESIGN, SETTING, AND PARTICIPANTS:
The Omega-3 Fatty Acids (Fish Oils) and Aspirin in Vascular Access Outcomes in Renal Disease (FAVOURED) study was a randomized, double-blind, controlled clinical trial that recruited participants with stage 4 or 5 chronic kidney disease from 2008 to 2014 at 35 dialysis centers in Australia, Malaysia, New Zealand, and the United Kingdom. Participants were observed for 12 months after arteriovenous fistula creation.
INTERVENTIONS:
Participants were randomly allocated to receive fish oil (4 g/d) or matching placebo. A subset (n = 406) was also randomized to receive aspirin (100 mg/d) or matching placebo. Treatment started 1 day prior to surgery and continued for 12 weeks.
MAIN OUTCOMES AND MEASURES:
The primary outcome was fistula failure, a composite of fistula thrombosis and/or abandonment and/or cannulation failure, at 12 months. Secondary outcomes included the individual components of the primary outcome.
RESULTS:
Of 1415 eligible participants, 567 were randomized (359 [63%] male, 298 [53%] white, 264 [47%] with diabetes; mean [SD] age, 54.8 [14.3] y). The same proportion of fistula failures occurred in the fish oil and placebo arms (128 of 270 [47%] vs 125 of 266 [47%]; relative risk [RR] adjusted for aspirin use, 1.03; 95% CI, 0.86-1.23; P = .78). Fish oil did not reduce fistula thrombosis (60 [22%] vs 61 [23%]; RR, 0.98; 95% CI, 0.72-1.34; P = .90), abandonment (51 [19%] vs 58 [22%]; RR, 0.87; 95% CI, 0.62-1.22; P = .43), or cannulation failure (108 [40%] vs 104 [39%]; RR, 1.03; 95% CI, 0.83-1.26; P = .81). The risk of fistula failure was similar between the aspirin and placebo arms (87 of 194 [45%] vs 83 of 194 [43%]; RR, 1.05; 95% CI, 0.84-1.31; P = .68).
CONCLUSIONS AND RELEVANCE:
Neither fish oil supplementation nor aspirin use reduced failure of new arteriovenous fistulae within 12 months of surgery. 

COMMENTSVery interesting study: prospective RCT, large sample, adequate randomisation, relevant question, clear and practical endpoints and clear conclusions!!Oif fish fir native AVF maturation: costly and useless

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
Picture of Meguid El Nahas
by Meguid El Nahas - Wednesday, 4 January 2017, 12:42 PM
Anyone in the world
Am J Transplant. 2016 Dec 27. doi: 10.1111/ajt.14186. [Epub ahead of print]

Early conversion from calcineurin inhibitor- to everolimus-based therapy following kidney transplantation: Results of the randomized ELEVATE trial.

Abstract

In a 24-month, multicenter, open-label, randomized trial, 715 de novo kidney transplant recipients were randomized at 10-14 weeks to convert to everolimus (n=359) or remain on standard calcineurin inhibitor (CNI) therapy (n=356; 231 tacrolimus; 125 cyclosporine), all with mycophenolic acid and steroids. The primary endpoint, change in estimated GFR from randomization to month 12, was similar for everolimus versus CNI: mean (SE) 0.3(1.5)mL/min/1.732 versus -1.5(1.5)mL/min/1.732 (p=0.116). At month 24, mean (SD) estimated GFR was 62.5(22.4)mL/min/1.73m2 with everolimus and 57.4 (19.9) mL/min/1.73m2 with CNI (p=0.005), and 59.7(20.5)mL/min/1.73m2 and 53.0(18.0)mL/min/1.73m2 , respectively, for the tacrolimus- and cyclosporine-treated CNI subgroups. BPAR at month 12 was more frequent under everolimus versus CNI overall (9.7% versus 4.8%, p=0.014) and versus tacrolimus-treated patients (2.6%, p<0.001) but similar to cyclosporine-treated patients (8.8%, p=0.755). Reporting on de novo donor specific antibodies (DSA) was limited but suggested more frequent anti-HLA Class I DSA under everolimus. Change in left ventricular mass index was similar. Discontinuation due to adverse events was more frequent with everolimus (23.6%) versus CNI (8.4%). In conclusion, conversion to everolimus at 10-14 weeks post-transplant was associated with similar renal function to standard therapy overall. Rates of BPAR were low in all groups, but lower with tacrolimus thaneverolimus. This article is protected by copyright. All rights reserved.

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
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by Meguid El Nahas - Wednesday, 23 November 2016, 5:52 AM
Anyone in the world

Prof Richard Glassock wrote:

I went to a session on Onco-Nephrology at the ASN meeting yesterday. 

Two randomized controlled trials of high-cut off (HCO) membrane intermittent hemodialysis compared to standard membrane hemodialysis for established AKI secondary to biopsy-proven Myeloma Cast Nephropathy  (MCN) were presented (the French  MYRE and the New Zealand EuLITETrials). 

The primary endpoints were similar (short-term freedom from need for dialysis), but the entry criteria and the basic chemotherapy for Multiple Myeloma administered  in conjunction with dialysis were different in the two trials. 

Both studies were well powered (n= about 100 cases) but only the MYRE trial had a positive result.

The EuLITE trial  failed to show any benefit for HCO dialysis for MCN.  Patient survival was not affected in either trial. The differences in the outcomes may well have been due to the trial design characteristics and/or the type of Myeloma chemotherapy utilized. It seems likely that HCO will remain as a controversial therapy for MCN.

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