User blog: Meguid El Nahas

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by Meguid El Nahas - Sunday, 7 June 2015, 2:23 PM
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Blog based on a lecture by Professor Samir Mallat at the Global Kidney Academy Master Class held in Prague on 7 June 2015.

SIMPLICITY HTN3 showed no effect of renal sympathetic denervation (RSD) on the control of hypertension.

Subgroup analyses of SIMPLICITY3 suggest that the effect may not be as negative as initially thought:

1. Those <65y may respond to RSD

2. Non African Americans may respond to RSD

3. Those NOT on alpha blockers may respond to RSD

4. The number of ablation bursts >10 may be beneficial

5. The circumferential denervation may be most effective

http://www.ncbi.nlm.nih.gov/pubmed/25744017

Consequently, more studies are planned.

http://www.ncbi.nlm.nih.gov/pubmed/?term=Simplicity+3+study%2C+resistant+hypertension

Is that good clinical research, following leads from posthoc and subgroup analyses, to establish new evidence?

or

is it the perseverance of the medical industrial complex that has invested heavily in that technology and doesnt want to ditch it...?

along with

medical practitioners who saw a potential source of income and private practice and dont want to give it up...?

The verdict is out...

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
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JAMA. 2015 May 29. doi: 10.1001/jama.2015.6731. [Epub ahead of print]

An Age-Calibrated Classification of Chronic Kidney Disease.

 
COMMENTS:

 The most practical way to separate age-related decline in eGFR from that associated with bona-fide kidney disease might be a persistent dipstick proteinuria of > 1+. While somewhat lacking in sensitivity it has reasonable specificity.  One needs to be careful about use of urine albumin to creatinine ratios (UACR) in the elderly as the expected decline in creatinine excretion with age (and frailty) leads to overestimation of albumin excretion, and thereby mis classification when one uses a KDIGO advocated schema.

 
The effect of ancestry and ethnicity on the age related changes in measured GFR or eGFR are not well studied.  Fitness and frailty, independent of ancestry or ethnicity, probably have a greater effect on eGFR (based on serum creatinine values). To my knowledge, the age-related decline in eGFR is seen in all ancestries, ethnicities but the rate of decline may vary, perhaps a consequence of the baseline nephron endowment at birth. The frequently cited Baltimore Longitudinal Study of Aging (BLSOG) was not a study of GFR per se, it was a study of true creatinine clearance and an unstated # of Type 2 diabetics were included-- it is not a useful study to examine the decline in eGFR in "healthy aging".  The findings of the BLSOG are frequently misquoted.  The cross-sectional data in very healthy subjects (living donors) strongly suggests that a decline in the functioning nephron population and whole kidney GFR is a fundamental biological phenomenon intimately entangled with organismal aging (organ senescence).  To designate an isolated decline in eGFR (using any equation you choose) to values less than 50% of that present in a healthy 20 year old without any other features of kidney damage as a disease per se is a mistake, in my judgement.
 
Richard Glassock
 
[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
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J Am Heart Assoc. 2015 Apr 20;4(4). pii: e001599. doi: 10.1161/JAHA.114.001599.

Persistent High Serum Bicarbonate and the Risk of Heart Failure in Patients With Chronic Kidney Disease (CKD): A Report From the Chronic Renal Insufficiency Cohort (CRIC) Study.

Abstract

BACKGROUND:

Serum bicarbonate varies over time in chronic kidney disease (CKD) patients, and this variability may portend poor cardiovascular outcomes. The aim of this study was to conduct a time-updated longitudinal analysis to evaluate the association of serum bicarbonate with long-term clinical outcomes: heart failure, atherosclerotic events, renal events (halving of estimated glomerular filtration rate [eGFR] or end-stage renal disease), and mortality.

METHODS AND RESULTS:

Serum bicarbonate was measured annually, in 3586 participants with CKD, enrolled in the Chronic Renal Insufficiency Cohort (CRIC) study. Marginal structural models were created to allow for integration of all available bicarbonate measurements and proper adjustment for time-dependent confounding. During the 6 years follow-up, 512 participants developed congestive heart failure (26/1000 person-years) and 749 developed renal events (37/1000 person-years). The risk of heart failure and death was significantly higher for participants who maintained serum bicarbonate >26 mmol/L for the entire duration of follow-up (hazard ratio [HR] 1.66; 95% confidence interval [CI], 1.23 to 2.23, and HR 1.36, 95% CI 1.02 to 1.82, respectively) compared with participants who kept their bicarbonate 22 to 26 mmol/L, after adjusting for demographics, co-morbidities, medications including diuretics, eGFR, and proteinuria. Participants who maintained serum bicarbonate <22 mmol/L had almost a 2-fold increased risk of renal disease progression (HR 1.97; 95% CI, 1.50 to 2.57) compared with participants with bicarbonate 22 to 26 mmol/L.

CONCLUSION:

In this large CKD cohort, persistent serum bicarbonate >26 mmol/L was associated with increased risk of heart failure events and mortality. Further studies are needed to determine the optimal range of serum bicarbonate in CKD to prevent adverse clinical outcomes.

COMMENTS:

The Nephrology community has been led to beleive with weak evidence that increased serum bicarbonate levels slows CKD progression (1-3). Whilst little doubt exists in Nephrologists' mind that metabolic acidosis in CKD is harmful, increased emphasis has been over the last 5 years on aiming for higher than normal serum bicarbonate levels to slow CKD progression and delay ESRD (1-3).

Now data published this month from a CRIC cohort seems to confirm that impression with patients with CKD and serum bicarbonate levels >26mmol/l have a significant decrease incidence of adverse renal events including ESRD compared to those with sBic <22mmol/l. However, the same cohort study shows an alarming increase in congestive heart failure and death rate in those whose serum bicarbonate levels exceeds 26mmol/l...!!!!

Previous NHANES III observations suggested that low serum Bicarbonate levels <22mmol/l are associated with increased mortality in CKD patients (3).

So it seems to me that optimal serum bicarbonate levels in patients with CKD may be between 24-26mmol/l, thus aiming at minimising CKD progression whilst avoiding metabolic alkalosis and its negative effects on the myocardium resulting in congestive heart failure and death. In other words, keeping serum bicarbonate levels within the middle of the normal range (24-26mmol/l) may prove that moderation is the best option for CKD patients!

References:

1. de Brito-Ashurst I, Varagunam M, Raftery MJ, Yaqoob MM. Bicarbonate
supplementation slows progression of CKD and improves nutritional status. J
Am Soc Nephrol. 2009;20:2075–2084.
2. Raphael KL, Wei G, Baird BC, Greene T, Beddhu S. Higher serum bicarbonate levels within the normal range are associated with better survival and renal outcomes in African Americans. Kidney Int. 2011;79:356–362.

3. Raphael KL, Zhang Y, Wei G, Greene T, Cheung AK, Beddhu S. Serum bicarbonate and mortality in adults in NHANES III. Nephrol Dial Transplant. 2013;28:1207–1213.

 

 

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
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The Gap between Theoretical and Practical/Clinically relevant Nephrology Knowledge grows with the type of teaching and conferences given in emerging countries and elsewhere...

Endless lectures...when the speaker shows off his/her knowledge and doesnt care about how much is useful or retainable by the audience...IT IS HIGH TIME THESE USELESS CONFERENCES STOP AND/OR CHANGE....

It is high time that lectures and conferences are audience centered rather than speakers centered...

Does anybody ask the DELEGATES what they would like to listen to...what their educational needs are...??? NO, instead they are given a form of education that is not targeted to their needs...but instead to the needs...promotion...recognition...of the SPEAKERS...!!!!!

I remember at a meeting, convdentional lecture loaded meeting, asking the delegates on Day 2 questions relating to ALL the lectures they listened to on Day 1...hardly one remembered anything meaningful...????

PASSIVE and UNTARGETED teaching is a waste of time for the delegates...and more so to the patients they meant to treat and translate their knowledge to benefit from...

So WHY is it going on...because of the CHRONIC AND HABITUAL SPEAKERS MAFIA... because of ACADEMIC EGOS...because of the HIDDEN AGENDAS OF NATIONAL AND INTERNATIONAL LEARNED SOCIETIES...because of the NOT SO HIDDEN AGENDA OF BIG PHARMA...

Therefore, this may not change but what can change is the way we perceive and receive these teachings....WITH A CRITICAL MIND...WITH A REFLECTIVE MIND...that allows us to filter the MEANINGFUL from the MEANINGLESS...

And always ask the speaker the 5 WHATS:

1. What is the clinical NEED and need for your lecture?

2. What is the EVIDENCE upon which you base your statements?

3. What is the RELEVANCE of what you teach to MY PATIENTS?

Then..

4. What is the risk versus benefit of what you are teaching us?

5. What is the cost versus benefit of the approach you are recommending?

LETS START THIS PROCESS AND CHALLENGE THE SPEAKER!

(give her examples that you have come across of bad teachers!)

 

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
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by Meguid El Nahas - Saturday, 18 April 2015, 11:48 AM
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Growing evidence is implicating a genetic absis for CKD in African-Americans linked to mutations in the APOL1 gene. A genetic mutation that served sub-saharan Africans well some 10,000 years ago as it confered trypanolytic activity against trypanosoma brucei...but now comes to cost them a susceptibility to non diabetic CKD including primary and secondary FSGS (1).

More recently, it has also become apparent that such mutations in the APOL1 gene may confer increased susceptibility to renal allograft failure; not as much in black recipients but in relation to balck donors. Renal allografts with APOL1 G1 and G2 mutations variants have considerably shorter allograft survival (2).

Consequently, the question is now raised as to whether Blacks with such AOPL1 mutations should donate their kidneys or not? In two respects, first whether such allograft will have a poorer outcome, second, whether the donor, if young, would be susceptible later in life to a nephropathy on his/her remaining kidney. Those may develop the unfavorable CKD/FSGS phenotype later in life.

This concern applies to both living as well as deceased donors. Two (G1 and G2) APLO1 risk variant kidneys may be avoided or used where expanded criteria donor kidneys are considered, as they have a greater probability of early allograft failure.

In the era of rapid sequencing and PCR based genotyping, time may have come for a better genetic evaluation of kidney donors (3).

However, such  approach whilst affordable and applicable in high economies is unlikely to be either practical or affordable in low and middle economy countries where most black individuals and those of African ancestry live...all too often medical guidelines and recommendations made in Western countries and Western publications overlook the fact that the world is not confined to the West, but also East and South...in those, genotyping of any kind is not an option, whilst renal transplantation may be a survival option in the absence of other forms of renal replacement therapies such as dialysis. Instead, a more careful clinical and laboratory evaluation of black donors is warranted, with careful family history (of CKD) souhgt, a careful evaluation of their kidney function and microalbuminuria, as well as more cautious, or agressive, management of these potentially higher risk of failure kidneys. 

References:

1. Genovese et al. Science 2010;329:841-45.

2. Reeves-Daniel et al. Am J Transpl 2011;11:1025-30.

3. Freedman and Julian. Kidney Int 2015; 87:671-73.

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
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WORLD KIDNEY DAY 2015 AND KIDNEY HEALTH FOR ALL....

Seemed intricately linked to drinking water....every WKD celebration showed people...doctors...nurses...kidney patients...volunteers...shifting case after case of drinking water...bottled of course...mineral some time...and drinking it...photographed drinking water....smiling with a bottle of water in hand...as if at last we have found as a profession the answer to kidney disease....the holy grail...of Nephrology...DRINKING WATER...BOTTLED OF COURSE...!!!!

What is that all about I ask myself...????

Had WKD 2015 addressed the global CKD challenge of kidney stones, I would have understood...some logic then behind drinking a lot...and diuresing a lot to dilute urinary salts and minerals and prevent their precipitation in the millions of worldwide sufferers of kidney stones...

But...KIDNEY HEALTH....and WATER DRINKING...is a different story. No evidence, other than old wives tales, linking kidney health to excessive fluid intake...NO EVIDENCE, as far a I know, linking increased fluid intake with CKD prevention or slowing its progression or improving kidney function in the communities...we target through WKD celebrations!

I am also aware that excessive water intake, aloing with that of salt, in patients with advanced CKD is harmful as it could exacerbate hypertension and precipitate heart failure.

Then, comes an intriguing association/partnership... Danone one of the main ISN and WKD sponsors, and at the same time the greatest producer and exporter of bottled water worldwide...an interesting alliance...and welcomed one...as long as facts are not distorted to link KIDNEY HEALTH to WATER CONSUMPTION...and obviously selling more BOTTLED WATER...

I would like to be proved wrong...that increased water intake...improves kidney health...as this would be the most signifiacnt breakthrough in Nephrology and the cheaper...BUT I COULD FING NO TANGIBLE EVIDENCE.

In the meanwhile, I remain skeptical....and even concerned about our professional society promoting "old wives tales"...and falsehoods...all too easily adopted by global communities...and more concerning still...by ILL INFORMED NEPHROLOGISTS ALL TOO KEEN TO BE SEEN ON PHOTOGRAPHS WITH A  GLASS OR BOTTLE OF WATER AND A HAPELESS GRIN...!!!

HAPPY WORLD KIDNEY DAY...I WILL NOT RAISE A GLASS OF WATER!

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
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IN THE LANCET THIS WEEK:

What is high quality science? Rigorous, accurate, original, honest, and transparent were the words selected by scientists who took part in the UK Nuffield Council on Bioethics' project to assess the ethical consequences of the culture of research. The project surveyed 970 scientists and held several discussion events in the UK as well as meetings with funding bodies, publishers, editors.

Scientists reported that they were motivated to do research to make discoveries that benefit society and to improve their own knowledge and understanding. However, they raised concerns that their working environment did not support their goals and visions. Worryingly, for some, the culture of research in the UK was such that it even encouraged poor quality research practices, such as rushing to finish and publish research and employing less rigorous research methods. High levels of competition for funding and jobs and promotions were noted as driving factors for these behaviours.

The Research Excellence Framework (REF) results (to be released on Dec 18), which inform allocation of core funding to higher education institutes, were a key issue for those surveyed. Despite a change in format since the last such exercise (eg, REF assessment panels were instructed not to make any use of journal impact factors in assessing the quality of research outputs), REF still causes researchers much anxiety, and misperceptions and mistrust about the system exist. Scientists still think that publishing in high-impact journals is the most important element in determining funding, jobs, and promotions, along with article metrics such as citation numbers.

The Lancet Series on Research: increasing value, reducing waste also noted problems with reward systems—they incentivised quantity more than quality and novelty more than reliability. “Research rewards and integrity: improving systems to promote responsible research” is the theme of the 4th World Conference on Research Integrity (May 31–June 3) in Rio de Janeiro, Brazil, 2015. Critical examination of rewards systems is warranted by all those involved in the research enterprise since existing approaches are putting immense pressure on scientists and could be damaging the very practice of science itself.

COMMENTS

Research culture based on pressurising scientisits to produce results, most often positive results, as many perceive a negative result as a failure...,  is most harmful. Such pressured environment has been, and remains, the essence of biomedical research in the UK and elsewhere. Publish or Perish...type of philosophy is destructive and dangerous.

It leads to short termism in research endaveours., with lack of continuity and longterm perspective...

It leads to a rush to publish preliminary findings that many misinterpret as definitive...and that are often contradicted by more in depth research and analysis...

It also leads, most importantly, to fraud...scientific fraud is common in such a pressured research environement where lack of publication, means lacks of subsequent funding, which in turn means loss of livelihood...all too often scientists cheat and manipulate their results to prodcue positive findings that allows publications and garantee their job security...Castles built on Sand...


 

 
[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
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ROFESSOR KIM SOLEZ (CANADA) WROTE:

IN aswer to the shortage of Nephrology trainees in US

http://ajkdblog.org/…/a-new-nephrologic-syndrome-acute-fel…/ 

Highly significant and related to what I have been writing and saying about the need for further engagement between nephrology and regenerative medicine! 

To put the situation succinctly, the stem cell generated kidney is the "moon shot" of regenerative medicine, substantially harder to pull off than the stem cell generated liver or heart. Nephrologists possess the unique knowledge that can make this "moon shot" happen, but they are running scared from regenerative medicine because their leaders are telling them "this will make everything we do redundant"! They need to embrace renal regenerative medicine as a logical extension of what they are already doing, and once they do that the best and the brightest young people will once again be competing to enter the field! I can think of no bigger issue than this right now in nephrology.

 

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
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by Meguid El Nahas - Monday, 15 December 2014, 4:03 PM
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N Engl J Med. 2014 Dec 11;371(24):2277-2287. Epub 2014 Nov 13.

Thrombospondin Type-1 Domain-Containing 7A in Idiopathic Membranous Nephropathy.

Abstract

Background Idiopathic membranous nephropathy is an autoimmune disease. In approximately 70% of patients, it is associated with autoantibodies against the phospholipase A2 receptor 1 (PLA2R1). Antigenic targets in the remaining patients are unknown. Methods Using Western blotting, we screened serum samples from patients with idiopathic membranous nephropathy, patients with other glomerular diseases, and healthy controls for antibodies against human native glomerular proteins. We partially purified a putative new antigen, identified this protein by means of mass spectrometry of digested peptides, and validated the results by analysis of recombinant protein expression, immunoprecipitation, and immunohistochemical analysis. Results Serum samples from 6 of 44 patients in a European cohort and 9 of 110 patients in a Boston cohort with anti-PLA2R1-negative idiopathic membranous nephropathy recognized a glomerular protein that was 250 kD in size. None of the serum samples from the 74 patients with idiopathic membranous nephropathy who were seropositive for anti-PLA2R1 antibodies, from the 76 patients with other glomerular diseases, and from the 44 healthy controls reacted against this antigen. Although this newly identified antigen is clearly different from PLA2R1, it shares some biochemical features, such as N-glycosylation, membranous location, and reactivity with serum only under nonreducing conditions. Mass spectrometry identified this antigen as thrombospondin type-1 domain-containing 7A (THSD7A). All reactive serum samples recognized recombinant THSD7A and immunoprecipitated THSD7A from glomerular lysates. Moreover, immunohistochemical analyses of biopsy samples from patients revealed localization of THSD7A to podocytes, and IgG eluted from one of these samples was specific for THSD7A. Conclusions In our cohort, 15 of 154 patients with idiopathic membranous nephropathy had circulating autoantibodies to THSD7A but not to PLA2R1, a finding that suggests a distinct subgroup of patients with this condition. (Funded by the French National Center for Scientific Research and others.).

COMMENTS:

More and more autoantibodies are being identified in patients with idiopathic membranous nephropathy:

anti-PLA2R1

Anti-SOD

Anti-Aldose Reductase (AR)

Anti-Enolase

Anti-NEP

http://www.ncbi.nlm.nih.gov/pubmed/22773590

http://www.ncbi.nlm.nih.gov/pubmed/23643301

and now 

Anti-Thrombospondin Type1 D7A (abstract above)

These anti-Podocytes antibodies, mostly IgG4, are most likely to represent, in my opinion, a paraphenomenon of podocyte injury with subsequent damage of the podocyte and exposure or enhanced antigenecity of these cytoplasmic and cell surface proteins and enzymes with a secondary auto-immune response.

It would be most unlikely that all these, overlapping and often correlating auto-antibodies are the primary auto-immune event in IMN. This would be the first disease, toi my knowledge, that is triggered simultaneously by 4 or 5 auto-immune antibody...the hypothesis that I put forward that these are events secondary to a primary podocytic insult/injury with subsequent injurious amplification loop is more plausible.

Unless, as suggested by the author of the publication above, there are different and distinctive subgroup of patients with IMN initiated by different auto-antibodies...seems less likely to me!

 

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
 
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by Meguid El Nahas - Friday, 12 December 2014, 8:39 AM
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Am J Kidney Dis. 2014 Nov 5. pii: S0272-6386(14)01363-8. doi: 10.1053/j.ajkd.2014.09.023. [Epub ahead of print]

The Future Burden of CKD in the United States: A Simulation Model for the CDC CKD Initiative.

Abstract

BACKGROUND:Awareness of chronic kidney disease (CKD), defined by kidney damage or reduced glomerular filtration rate, remains low in the United States, and few estimates of its future burden exist.

STUDY DESIGN:We used the CKD Health Policy Model to simulate the residual lifetime incidence of CKD and project the prevalence of CKD in 2020 and 2030. The simulation sample was based on nationally representative data from the 1999 to 2010 National Health and Nutrition Examination Surveys.

SETTING & POPULATION:Current US population.

MODEL, PERSPECTIVE, & TIMELINE:Simulation model following up individuals from current age through death or age 90 years.

OUTCOMES:Residual lifetime incidence represents the projected percentage of persons who will develop new CKD during their lifetimes. Future prevalence is projected for 2020 and 2030.

MEASUREMENTS:Development and progression of CKD are based on annual decrements in estimated glomerular filtration rates that depend on age and risk factors.

RESULTS:For US adults aged 30 to 49, 50 to 64, and 65 years or older with no CKD at baseline, the residual lifetime incidences of CKD are 54%, 52%, and 42%, respectively. The prevalence of CKD in adults 30 years or older is projected to increase from 13.2% currently to 14.4% in 2020 and 16.7% in 2030.

LIMITATIONS:Due to limited data, our simulation model estimates are based on assumptions about annual decrements in estimated glomerular filtration rates.

CONCLUSIONS:

For an individual, lifetime risk of CKD is high, with more than half the US adults aged 30 to 64 years likely to develop CKD. Knowing the lifetime incidence of CKD may raise individuals' awareness and encourage them to take steps to prevent CKD. From a national burden perspective, we estimate that the population prevalence of CKD will increase in coming decades, suggesting that development of interventions to slow CKD onset and progression should be considered.

 

COMMENTS:
We are mystified and deeply troubled by what appears to be a "fear mongering" simulation of the life-time risk of developing what is unreasonably called "CKD" recently published on-line in the AJKD (Hoerger, TJ; Simpson, SA; Yarnoff, BO; Pavkov, ME; Ríos Burrows, N; Saydah, SH; Williams, DE; Zhuo, X. The Future Burden of CKD in the United States: A Simulation Model for the CDC CKD Initiative Am. J. Kidney Dis., 2014- on-line- December 6, 2014). Both the authors and the reviewers of this paper clearly accept the notion that as humans age the GFR falls. They must also realize that the application of a fixed, absolute and arbitrary threshold of GFR as a definition for "CKD", without reference to other manifestations of kidney disease (such as overt albuminuria) will always and predictably lead to an increase in "CKD" as one grows older and GFR falls. Thus, it is expected and unsurprising that as populations and individuals age the incidence and prevalence of "CKD", defined in this fashion, will rise in a commensurate fashion. Does this mean that life expectancy is curtailed to any significant extent by this age-related" and artificially-created "pseudo-CKD"?  No!  Does this mean that the new label imposes any special burden on the person so labeled?  No!, except for the anxiety and fear that it engenders and the resulting “medicalization” of ageing and associated events such as falling GFR.

This publication, by suggesting that individuals can all look forward to a 1:2 chance of developing "CKD" over our lifetimes and that our societies can anticipate a secular increase in the prevalence of "CKD",  carries with it a deep responsibility to explain the origins of these phenomena to the reader in a clear and unequivocal way.  After all, the lifetime chance of dying is 1:1 and we all intrinsically understand what this means; namely, that death is inevitable, the process is biological and begins at the time of birth. Similarly, the decline GFR, in those who survive over 65 years of age, is also a biological process that will affect an increasing percentage of the ageing population. In addition, no cogent explanations are offered for the huge gaps in prevalence of “CKD” between Category 2 and Category 3A and Category 3B—if the CKD Categories represent some kind of naturall progression why do these discrepancies occur?

It is disappointing that the extremely worthwhile aspects of the CKD concept are being twisted in such an unhelpful way that obfuscates the real  risks of meaningful (treatable) CKD.  An obvious solution would be to age-calibrate the thresholds of eGFR used for defining CKD (in the absence of other disease defining features), in the first place.  One might anticipate that if this were done the frightening characteristics of the simulation would take on a more subtle, less dramatic hue. Only then will life-time risks of CKD assume meaningful significance to individuals, populations and societies.

 Richard J. Glassock

Meguid El Nahas

Pierre Delanaye 

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