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by Meguid El Nahas - Thursday, 21 December 2017, 12:48 PM
Anyone in the world

Hand grip strength (HGS) is a key measurement in the assessment of frailty phenotype in haemodialysis patients. However, the measurement is not very standardized, and notably, current data on the potential impact of a haemodialysis session on the results are both limited and controversial. In the present analysis, we compared HGS results before and after a haemodialysis session in 101 patients.
In the current observational study, HGS has been measured in adult haemodialysis patients on the same day, first before connection to the dialysis machine and then just after disconnection. At each timing, measurements were repeated three times with an interval of 5 s between measurements and the higher value was used for analysis.
One hundred and one patients (64% men) with a median (interquartile range, 25th percentile; 75th percentile) age of 66 (46; 76) years were included. In the whole population, a significant decline in HGS was observed after dialysis, with an absolute median decline of − 4 (0; −6) kg and a relative median difference of −11 (0; −20)%. These differences were observed in both genders and were independent of the baseline HGS value.
Our results suggest that the timing (before or after the dialysis session) of hand grip assessment is clinically relevant and should be taken into account in clinical practice and also in epidemiological and clinical studies.
Author's comments:
A very simple and pragmatic study. Hand grip strength (HGS) is a very simple tool to assess muscle strength. It is a functional test and this test is more predicitive of mortality than muscle mass measurement by DEXA. HGS is used in the evaluation of sarcopenia (or dynapenia) and frailty. We simple measured HGS with a classical dynamometer before and after the dialysis session. The data were discrepant in the literature. Some authors says that HGS is stable after dialysis session and other says it was decreasing. We clearly showed that HGS was decreasing after one single session. The decline was both statistically and clinically significant. The decline was significant both in men and women and both in patients with normal HGS at baseline and in patients with low HGS at baseline. As every measurement in medicine, HGS measurement must be standardized and obviously, the timing of the measurement is important. Even if we have no definitive proofs, we would recommend to measure before dialysis. Further reseach is now needed to better identify parameters that are associated with decline of HGS during the session.
[ Modified: Sunday, 27 May 2018, 11:51 PM ]
Picture of Meguid El Nahas
by Meguid El Nahas - Wednesday, 20 December 2017, 11:37 AM
Anyone in the world

At XMas time and the end of every year, one reflects on the year that has passed.

2017, has seen the explosion of fake news...false news....made up news...truth and reality dont seem to matter any more but instead, whoever shouted louder and repeated it often could promote any idea false or true...

This brought to mind a similar phenomenon in Nephrology...

Over the years, fake news, fake data, falsehoods, and semi truths permeated our profession. They became accepted out of ignorance of the facts, disrespect for the truth and propaganda like marketing of ideas based on half-truths and flawed any! The propaganda of these fake nephrology facts has been promoted intensively and aggressively by those who have vested interest in these semi-truths, falsehhoods and fake news...some went as far as bullying the nephrology community and nephrologists to accept these promoted falsehoods...I once witnessed a correspondance openly threatening a colleague who was rejecting one such falsehoods by one of the promoters of the propaganda...the subject was the classification of CKD...

  Many examples of such fake Nephrology permeate our thinking...

Here are some examples,

"One third of the world population suffers from CKD"...more propaganda than facts!

"Hyperfiltration causes progressive CKD"...more propaganda than facts!

"Albuminuria is not only a marker of progressive CKD, but a maker of CKD progression".... more propaganda than facts!

"ACE inhibitors have unique nephroprotecting properties other antihypertensives dont have"....more propaganda than facts!

"eGFR is a valuable marker of kidney function"....more propaganda than facts!

"The Lower the BP, the slower CKD progression"...more propaganda than facts!

These fake information have been peddled long become realities many if not most nephrologists beleive in...and have adopted blindly without questionning...or without a minimum of critical thinking!?

The herd instinct dictates that following the herd dictats and propaganda is safer than standing up and questionning the direction the herd is often feels safe to be a sheep than a shepherd...

Like fake news, repetition and mass media promotion and propaganda, make these fake facts, nephrology realities...even though they are not subject to scrutiny, critical thinking or even credible and substantiated evidence...

So as with fake news and social media promotion of fake news, it is high time Nephrologists and the Nephrology community as a whole takes a critical stand of what it is been fed...and start filtering facts from fiction!

I urge in 2018 Nephrologists worldwide to start asking questions and critically analyse what they are told...sold..what they are encouraged to beleive....and be more discerning regarding the fake facts propaganda that doesnt spare medical information, news or publications...

Also beware of those who try to manipulate us by providing shallow and unsubstantiated information dressed up as facts...dont let them bully you to beleive them...and beware they will repeat them often enough for you to beleive them...without a shred of evidence provided...



[ Modified: Thursday, 1 January 1970, 1:00 AM ]
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by Meguid El Nahas - Friday, 8 December 2017, 8:59 AM
Anyone in the world

Comments by Professor Neveen Soliman, head of EGORD (Egypt Group for Orphan Renal Diseases):

It is actually a pilot study where Gharavi and his coauthors tested the clinical utility of WES in 92 adults with undiagnosed/familial CKD.
They identified many known or undiagnosed genetic disorders in 22 of 92 cohort patients (24%).
Among these theyidentified PARN mutations (implicated in lung fibrosis) in 2 probands with tubulointerstitial fibrosis,
thereby extending the phenotype of PARN mutations to renal fibrosis.
They also confirmed the variable phenotypic expression of type IV collagen gene (previously reported by our group and others)
as they identified AR and XL forms of Alport syndrome among patients with the clinical diagnosis of FSGS.
This again supports the categorization of FSGS ad pathological and not an etiological diagnosis. As such WES had immediate clinical implications:
i) for surveillance for extrarenal manifestations; and ii) avoidance of unnecessary immunosupressive therapy in cases misdiagnosed as FSGS.
 My comments:
This work lends support to Prof Soliman own work in collaboration with Prof Hildebrandt in Boston on the value of application of WES to CKD, as they investigated genetic mutations in patients with CAKUT and detected recessive mutations in nine known disease-causing genes: ZBTB24, WFS1, HPSE2, ATRX, ASPH, AGXT, AQP2, CTNS, and PKHD1 notably, when mutated, these genes cause multiorgan syndromes that may include CAKUT as a feature (syndromic CAKUT) or cause renal diseases that may manifest as phenocopies of CAKUT. None of the above monogenic disease-causing genes were suspected on clinical grounds before this study. Follow-up clinical characterization of those patients allowed them to revise and detect relevant new clinical features in a more appropriate pathogenetic context.
They concluded that applying WES to the diagnostic approach in CAKUT provides opportunities for an accurate and early etiology-based diagnosis and improved clinical management.
Also, one of the most exciting associations between CKD and genetic mutations has been that involving the UMOD loci coding for Uromodulin (Tamm-Horsfall protein), that showed an association between such mutation and the incidence as well as the progression of CKD. 
In addition, rare mutations in UMOD seem to be major causes of autosomal dominant tubulointerstitial kidney disease, a condition that leads to CKD and ESRD.
In summary new and streamlined genetic approaches to the diagnosis and management of CKD are well underway and may unravel genetic mutations associations that shed light onto the mechanism of underlying nephropathies as well as open the way to the genetic manipulations of such abnormalities.
[ Modified: Thursday, 1 January 1970, 1:00 AM ]
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by Meguid El Nahas - Sunday, 5 November 2017, 3:06 PM
Anyone in the world

It is impossible to capture the "leading news" from the ASN meeting -  it is simply too immense-

In my field of glomerular disease, I would gave to pick out the CARDINAL and MENTOR trial findings

CARDINAL is a randomized placebo controlled study of the effects of Bardoxolone  methyl on GFR and profession of CKD in patients with Alport syndrome.  This agent was demonstrated to significantly increase GFR on a sustained basis.  Adverse events were minimal.  We do not know yet if it will prevent or delay ESRD.

MENTOR is a randomized controlled comparison study of Rituximab vs Cyclosporine A in patients with Nephrotic Syndrome due to presumed Primary Membranous Nephropathy (MN). At 24 months (12 months after stopping CsA) Rituximab therapy was non-inferior ( and likely to be greatly superior) to CsA therapy in terms of sustained complete or partial remission.  We will have to wait for an analysis of the impact of PLA2R antibody levels on these outcomes- but Rituximab has been elevated in the hierarchy of drugs used for treatment of MN as a consequence of this well designed and conducted study.

Richard Glassock

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
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by Meguid El Nahas - Thursday, 26 October 2017, 1:36 PM
Anyone in the world

The majority of RCTs in Nephrology are flawed and invalid for a range of reasons:

Having said that, Nephrology journals continue to publish such trials and mostly small, underpowered, Proof of Concept (POC) clinical trials without a WARNING SIGN!

Whist such trials often justify and stimulate future research, most readers without critical knowledge accept them as final proof of efficacy and go on applying their recommendations to their patients...

Small POC clinical trials (Phase2 trials) are hypothesis generating and not proof of efficacy. Thus they require confirmatory studies and larger RCTs to justify their conclusions.

Authors and their accomplice, the Journal Editors, not to mention the ill informed reviewers accept their conclusions and publish them as definite findings, thus misleading the unaware reader!

I encourage EDITORS to put a WARNING SIGN OR BOX....reminding such readers that this Clinical Trial is a POC and NOT A FINAL STUDY; it thus warrants caution and confirmatory studies.

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

the MAPEC spanish propsective study of ~5,000 individual showed that sleep-time hypertension rather than casual-clinic BP or 24h ABPM was the independent risk factor for incident CKD.

Previous studies highlighted the prognostic relevance of sleep time systolic BP to the development of CVD; Consistent evidence of numerous studies substantiates the asleep blood pressure (BP) mean derived from ambulatory BP monitoring (ABPM) is both an independent and a stronger predictor of cardiovascular disease (CVD) risk than are daytime clinic BP measurements or the ABPM-determined awake or 24-hour BP means.

More attention needs therefore to be paid timely and adequate measure of BP in the population at a whole but also those at risk of CVD and CKD; the older population.

Consequently, more attention needs to be paid to the timely, evening, administration of anti-hypertensive medication. Chronotherapy improves hypertension management and its complications.

Nephrologists and general practitioners need to shift their management paradigm to a focus on bedtime, sleep BP monitoring as well as evening, bedtime, ingestion of the full daily dose of at least one antihypertensive agent.


[ Modified: Thursday, 1 January 1970, 1:00 AM ]
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by Meguid El Nahas - Friday, 29 September 2017, 7:05 AM
Anyone in the world

The World Kidney Day (WKD) theme for 2018 is:"Kidneys & Women's Health"...

I am not sure what this i to expect the theme in 2019 to be... "Kidneys & Men's Health...

then what?!..."Kidney's & Africans' Health" or "Kidneys & Native Americans' Health"... all real issues but pointless focuses and even distractions for an annual World Kidney Day event!

The obsession of those who organise WKD of "Having a Theme"... is making a mockery of this very important annual event; choosing unfounded and meaningless themes such as "Kidneys and Women's Health"... We had "Drinking Water" before...When there is NO NEED TO HAVE A THEME!

Why have a theme that focuses every year on a single aspect in Nephrology when "KIDNEY DISEASES"  and "KIDNEY HEALTH" are overwhelming justifying messages that suffice to hold a WKD event every year...

Others who organise an annual focus day such as World Diabetes Day...World Hypertension Day...AIDS Day...etc, dont seem compelled to find a theme beyond the obvious one of reminding the world and raising awarness of the condition under focus. There is no need to have Diabetes & Women's Health Day...or AIDS and Women...for instance! or "Diabetes and Retina or Foot Health Day"...

So I urge those who choose a theme for WKD to drop that urge every year to come up with a theme...and come to appreciate that WKD suffice by itself to focus every year minds, and hopefully raise funds, to fight KIDNEY DISEASE FOR ALL...Men and explain how devastating kidney disease can be...their causes...their prevention...their societal impact...their human cost...

Kidney Diseases are so devastating that having an annual World Kidney Day is a fully justifiable and great initiative started in 2006.

To have a theme every year is a damaging and pointless diversion.

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

 N Engl J Med. 2017 Aug 24;377(8):745-755. doi: 10.1056/NEJMsa1616035.

Cost-Effectiveness of Intensive versus Standard Blood-Pressure Control.


In the Systolic Blood Pressure Intervention Trial (SPRINT), adults at high risk for cardiovascular disease who received intensive systolic blood-pressure control (target, <120 mm Hg) had significantly lower rates of death and cardiovascular disease events than did those who received standard control (target, <140 mm Hg). On the basis of these data, we wanted to determine the lifetime health benefits and health care costs associated with intensive control versus standard control.


We used a microsimulation model to apply SPRINT treatment effects and health care costs from national sources to a hypothetical cohort of SPRINT-eligible adults. The model projected lifetime costs of treatment and monitoring in patients with hypertension, cardiovascular disease events and subsequent treatment costs, treatment-related risks of serious adverse events and subsequent costs, and quality-adjusted life-years (QALYs) for intensive control versus standard control of systolic blood pressure.


We determined that the mean number of QALYs would be 0.27 higher among patients who received intensive control than among those who received standard control and would cost approximately $47,000 more per QALY gained if there were a reduction in adherence and treatment effects after 5 years; the cost would be approximately $28,000 more per QALY gained if the treatment effects persisted for the remaining lifetime of the patient. Most simulation results indicated that intensive treatment would be cost-effective (51 to 79% below the willingness-to-pay threshold of $50,000 per QALY and 76 to 93% below the threshold of $100,000 per QALY), regardless of whether treatment effects were reduced after 5 years or persisted for the remaining lifetime.


In this simulation study, intensive systolic blood-pressure control prevented cardiovascular disease events and prolonged life and did so at levels below common willingness-to-pay thresholds per QALY, regardless of whether benefits were reduced after 5 years or persisted for the patient's remaining lifetime. (Funded by the National Heart, Lung, and Blood Institute and others; SPRINT number, NCT01206062 .).


As the only beneficial effect shown by SPRINT is a reduction in fluid overload and the associated mortality due to Heart Failure; Cost effectiveness would be even higher with better use of DIURETIC THERAPY in those at risk.

This was shown in the ALLHAT study where treatment with the thiazide diuretic Chlorthalidone had a similar life year gain at a much lower cost!

Authors and Researchers of SPRINT will carry on trying to misguide the medical community that lower'"intensive"BP is life saving, whilst the findings of their study is that lower-intensive BP does NOT reduce the risk of CAD or Strokes in their study. This, is in fact at odd with the bulk of the literature; as SPRINT in the only study that showed that reducing BP does not prevent or reduce the incidence of strokes...

All the SPRINT study shows is that more appropriate and effective use of diuretic therapy prevents fluid overload and decreases the associated mortality (Heart Failure).

And, by clever statistical manipulation involving combined endpoints including heart failure as well as overall mortality...the heart failure-diuretic effect gives the misleading impression that mortality is primarily decreased, when in reality it is linked to heart failure and the beneficial effect of diuretics on heart failure, heart failure-associated CVD mortality and "all cause" mortality (that includes heart failure-CVD mortality!).

Effective diuretic therapy is key to prevention of Heart Failure and minimising its complications, including hospitalisations, morbidity and mortality. They are often poorly prescribed and mismanaged.



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

Are Nephrology Guidelines fit  for purpose or are they:

1. Too US Centric like the latest KDIGO Kidney Donors Guidelines

2. Too overlooking of low and middle economies healthcare priorities...

3. Too Pharma Friendly...

4. Too "KOL" friendly...

5. Too "One size fits all"...

Read the fascinating discussion on OLA and share your views:

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
Picture of Meguid El Nahas
by Meguid El Nahas - Wednesday, 26 July 2017, 11:46 AM
Anyone in the world

A Myth is a widely held but false belief or idea.

Nephrology is full of Myths that are peddled and believed without valid supporting evidence; some are based on animal experimentation without supporting evidence in man. Some are simply unsubstantiated and unvalidated but repeated often enough for beleive!?

Here is a list of 10 such Myths:

1. CKD progresses relentlessly....FALSE, many CKD patients stages 1-3a, seldom progress in a meaningful fashion...

some stay at CKD4-5 for months without progressing!

2. CKD progression is linear....FALSE, CKD progression has many patterns with non-linear progression in some and even regression in some...

3. Renal Hyperfiltration accelerates CKD...FALSE, no evidence from animal or human data; in animals hyperfiltration per se is irrelevant but glomerular hypertension is more important, but may all be related to systemic blood pressure levels and its transmission to the glomeruli (see Bidani and Griffin:

4. Proteinuria worsens the progression of CKD....FALSE, no evidence for that... and many examples were proteinuria/albuminuria is reduced and progression worsens...example: ONTARGET were albuminuria comes down with dual RAAS blockade and CKD progression worsens (

also treatment with Aliskiren decrease proteinuria but has no effect on CKD progression (!

5. Uric Acid is nephrotoxic...FALSE, no clinical evidence...(, and reduction by allopurinol is confounded by the drug hypotensive effect!

6. ACE inhibition slows the progression of CKD beyond BP control...FALSE, as meta-analysis of data do not support a specific Reno- or Cardio- protective effect of RAAS inhibition in CKD (see previous Blogs).

7. RAAS beneficial in Diabetic Kidney Disease (DKD) independently of BP lowering...FALSE, no evidence that this effect is independent of a better BP lowering as 24h BP was never measured and GFR itself never measured...

8. Low BP slows CKD Progression...FALSE, most studies addressing this issue failed to show benefit from aggressive BP reduction; ABCD, REIN2, AASK, SPRINT, etc...(See previous Blog on the topic). In fact, there is anecdotal evidence that raising BP may delay ESRD in advanced CKD...

9. Lipids are nephrotoxic and may accelerate CKD progression (, as lipid lowering (SHARP study) had no impact on CKD progression...(

10. Glifozins is Cardio- and Reno- protective in Diabetes Mellitus....FALSE, the observed cardioprotection with SGLT2 inhibitors in DM is due to a reduction in BP secondary to the powerful osmotic diuretic effect of these agents...(see previous Blog on the topic)

Sadly, many of these MYTHS are taken for proven FACTS by the Nephrology Community at large without any critical analysis to find the supportive evidence.

They are often based on indirect animal experimentation of little relevance to the clinical situation...or animal experimentation that has not been substantiated in humans. Others are accepted as fact with little scrutiny of the background information or evidence of supporting data...

A critical analysis of these Myths leaves many unanswered questions! 

Also knowledge evolves and evidence is challenged leading to challenges to some of these dogmas and myths...


[ Modified: Thursday, 1 January 1970, 1:00 AM ]
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