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Picture of Arif Khwaja
by Arif Khwaja - Friday, 27 March 2015, 4:00 PM
Anyone in the world

A few months ago I saw an 82 year old lady with very slowly progressive CKD4. She had T2DM, hypertension, a strong history of smoking and was referred by her GP as she had an eGFR of 29 mls/min ( compared to 35 mls/min 5 years ago). Her US showed slightly small kidneys and her dipstick was negative for protein and blood and immunology screen was negative. She was assumed to have ischaemic nephropathy as the cause of her CKD. She had been taking NSAIDs for 20 years for arthritis

Her BP was 152/90 and she was reasonably well - she lived independently with some support from her daughter. When I saw her her main problem was her arthritis - this was severe and she was racked with pain particularly in the morning. The nephrologist who saw her on her prevoius visit had understandbly told her to stop taking NSAIDs ( Ibuprofen 200mg tds) and instructed her family doctor to increase her anti-hypertensive medications by adding in a diuretic

The problems were two fold  i) she couldnt tolerate other pain killers ( nausea, constipation and hallucinations) so she was left taking paracetamol which didnt work. ii) She was already on a number of vasodialtors which left her with significant oedema and as she had an overactive, small bladder she found that taking diuretics meant that going out was difficult and so now had to stay at home as she was afraid of being incontinent in public.

What struck when me I saw here was that two very reasonable (from a nephrologists perspective) interventions (ie. stopping NSAIDs and increasing anti-hypertensive medication) had significantly worsened the quality of her life.... which got me thinking what was the actual 'value' we were adding to her quality of life or life expectancy by seeing her? Perhaps they were the following:

i) Reducing her risk of developing ESRD? This ladys risk of developing ESRD in her lifetime is miniscule.. as shown in the GLOMMS study women of this age with no albuminuria virtually never progress to ESRD and so if our goal is to try and reduce the risk of her developing ESRD then we are trying to reduce the risk of someting that is vanishingly unlikely to happen - even if she never sees a nephrologist. This was further brilliantly highlighted in a recent publication extrapolating the effect of a putative intervention that reduces the risk of ESRD by 30% in RCT to an elderly population with CKD. The reality was that the effect would be negligible for most of the elderly as few will progress - again highlighting the importance of interpreting RCT data in the context of the patient on front of you

ii) Stopping NSAIDs will reduce her risk of developing ESRD? Given the fact that she had been taking NSAIDs for 20 years with only a slow decline in kidney function the value of stopping NSAIDs in her case on either her life expectancy or quality of life are negligible - indeed her quality of life was significantly worse after stopping NSAIDs. So perhaps a better approach would have been to tell her to continue taking her NSAIDs (stopping only if she gets intercurrently ill) and to continue monitoring her kidney function regularly. And as a recent systematic review showed the impact of NSAIDs used at a normal dosage on GFR decline is negligible.

iii) Getting better control of her BP will reduce her risk of cardiovascular disease? Putting aside the fact that at the age of 82 with a lifetime of smoking, the dice in terms of CV risk has already been cast, would lowering lowering her blood pressure really improve her CV risk? - well there is increasing evidence that treating to a ‘target’ of less than 140/90 mmHg may not only have no benefit but may for some patients be harmful. In fact the evidence base from interventional studies to support a ‘tight’ BP target in this age group is negligible.

So what did I do…. well I stopped her diuretic, told her to go back on her NSAIDs - Her BP was 152/90 and her eGFR 30mls/min and most importantly she was now happy that she could get out of the house (without worrying about incontinence) and her pain was controlled. When I started talking about CV risk and salt in her diet, her eyes glazed, she leaned forward and said “you do know I’m 82 don’t you...?"

So what did I learn? well without sounding trite the clear learning message from this case is that treating risk is not the same as treating  a patient…What matters to us  ( e.g reducing proteinuria and BP, stopping NSAIDs) may not matter to the patient and whilst in some cases doing things like tightly controlling BP, reducing proteinuria and stopping NSAIDs will be incredibly important, in other situations they are at at best irrelevant and at worse counterproductive. 

This balance between the ‘evidence-based medicine’ and ‘patient-centred care’ has been articulated by a thought-provoking recent article by Ann O’Hare in NDT which continues on from an earlier article  stressing the importance individualised rather than disease-based care - a must read for anyone who actually practises medicine and sees real-world pateints.

In other words the certainties and value of guidelines and ‘evidence-based medicine’ are only realised if you can interpret them in the context, society, healthcare system and culture in which you practice and understand their relevance to the patient sitting in front of you. Real-life clinical medicine is still an art - a balance of risks, uncertainties, trade-offs and compromises.


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


    Anyone in the world


    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 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 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 interesting alliance...and welcomed 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 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 ILL INFORMED NEPHROLOGISTS ALL TOO KEEN TO BE SEEN ON PHOTOGRAPHS WITH A  GLASS OR BOTTLE OF WATER AND A HAPELESS GRIN...!!!


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


      Anyone in the world


      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.


      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 ]


        Anyone in the world


        IN aswer to the shortage of Nephrology trainees in US…/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 ]


          Picture of Meguid El Nahas
          by Meguid El Nahas - Monday, 15 December 2014, 4:03 PM
          Anyone in the world
          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.


          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.).


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



          Anti-Aldose Reductase (AR)



          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 ]


            Picture of Meguid El Nahas
            by Meguid El Nahas - Friday, 12 December 2014, 8:39 AM
            Anyone in the world
            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.


            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.


            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.


            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 ]


              Picture of Meguid El Nahas
              by Meguid El Nahas - Sunday, 16 November 2014, 3:48 PM
              Anyone in the world


              HALT-PKD- study a showed the a lower BP goal slows rate of increase of total kidney volume (TKV), reduces LVH, reduces albuminuria but has no effect on decline in eGFR (no mGFR reported.  Dual ACEi + ARB neither beneficial or harmful.  High uncertainty whether the short-term benefits on TKV change and LVH will have a benefit on Survival or ESRD.


              Disconnect between BP lower targets and reduction in LVH/albuminuria AND PKD progression in terms of decline of eGFR.

              This raises questions regarding the assumption (made for instance in mTOR inhibitors in  ADPKD) that a reduction in TKV (Total Kidney Volume) would translate into slowewr ADPKD progression.

              Also raises questions regarding the assumption that a reduction in LVH would imrpove CKD survival (by analogy here...a higher hematocrit improves LVH but doesnt survival...).

              Clinical trials in Nephrology are a huge challenge:

              1. Surrogate markers are unpredictable at best in terms of outcomes.

              2. Hard endpoints would take 5-10 years to reach.



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


                Picture of Meguid El Nahas
                by Meguid El Nahas - Saturday, 15 November 2014, 11:03 AM
                Anyone in the world

                eGFR has replaced true measured GFR in most nephrologists learned minds...

                We are told in epidemiological studies that those with eGFR higher than 100 ml/min have a higher mortality....

                We are told at ASN 2015 that those whose with CKD eGFR improves by >3ml/min/year have higher mortality...

                We equate higher eGFR to "Hyperfiltration"... a concept that was debatable in rats...but fully accepted without a shred of evidence in humans...

                We are told, and most believe, so many things in the name and at the altar of eGFR: estimated GFR....when in reality it is NEITHER ESTIMATED NOR is simply calculated based on dubious, totally unecessary and misleading equations that PRETEND TO REFLECT TRUE AND MEASURED GFR...!!!

                Therefore eGFR = iGFR: ILLUSION OF GFR...

                As it is mostly:




                in most general population studies:


                and it is totaly unrepresentative of TRUE GFR in those who have advanced CKD4-5. Where tubular secretion of creatinine makes up to 40-50% of the urinary excretion of creatinine.


                of course those with high eGFR have higher mortality...they are wasted...

                of course those with rising eGFR have worse prognosis and mortality...they are wasted....

                of course those starting RRT/dialysis at higher eGFR are worse off...they are wasted... 



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


                  Anyone in the world



                  La sclérostine est considérée comme un nouveau biomarqueur intéressant dans le cadre de la « santé osseuse ». La sclérostine est produite par les ostéocytes en réponse à différents stimuli dont les plus importants sont la PTH et le stress mécanique. En l’absence de stress mécanique (l’exemple le plus illustratif étant celui des astronautes en apesanteur), l’ostéocyte va produire de la sclérostine qui va elle inhiber la fonction ostéoblastique via un effet sur la voie Wnt-cathénine.
                  Certains points nouveaux ont été soulignés à l’ASN.
                  Il existe bien une corrélation entre l’expression de la sclérostine au niveau osseux par les ostéocytes et la concentration plasmatique de sclérostine. La sclérostine aurait aussi un effet autocrine sur la production de RANKL (et donc l’activité ostéoclastique). L’ostéocyte pourrait également interagir au niveau de la fonction musculaire. En cas de maladie rénale chronique (MRC), l’expression osseuse et la concentration de sclérostine sont augmentés. De manière intéressante, et cela reste un champ d’investigation, on ne retrouve pas de concentration augmentée de sclérostine chez l’enfant avec une MRC. En MRC terminale, la concentration de sclérostine semble influencée (concentration plus basse) chez les patients ayant encore une fonction rénale résiduelle. Le premières données en MRC terminale suggèrent un rôle de la sclérostine dans le diagnostique de l’os adynamique (associé à une concentration haute), mais les données sont contradictoires. La sclérostine permettrait aussi de prédire la perte de masse osseuse (mesurée par DEXA). Il y a également des données contradictoires sur le rôle de la sclérostine sur la survie du patient avec MRC.
                  Il existe encore bien des inconnues sur cette protéine et bien des limitations, notamment dans le dosage de la sclérostine plasmatique qui pose question. Néanmoins, nous entendrons de plus en plus parlé de cette protéine et la raison en est très simple et néanmoins importante : il existe en effet un traitement à base d’anticorps anti-sclérostine, traitement qui a déjà été testé et s’est révélé efficace chez la femme ostéoporotique.


                  Raised sclerostin levels in CKD

                  Good correlation between bone and plasma sclerostin levels.

                  PTH stimulates scelrostin

                  Scelrostin inhibits osteobalstic activity, favoring bone resorption

                  High plasma sclerostin levels correlate with decreased BMD.

                  Targetting sclerostin in CKD MBD: WATCH THAT SPACE...

                  Anti-sclerostin antibodies already tested for treatment of osteoporosis 

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


                    Picture of Meguid El Nahas
                    by Meguid El Nahas - Wednesday, 5 November 2014, 10:59 AM
                    Anyone in the world
                    BMJ. 2014 Oct 30;349:g6196. doi: 10.1136/bmj.g6196.

                    Co-trimoxazole and sudden death in patients receiving inhibitors of renin-angiotensin system: population based study.



                    To determine whether the prescription of co-trimoxazole with an angiotensin converting enzyme inhibitor or angiotensin receptor blocker is associated with sudden death.


                    Population based nested case-control study.


                    Ontario, Canada, from 1 April 1994 to 1 January 2012.


                    Ontario residents aged 66 years or older treated with an angiotensin converting enzyme inhibitor or angiotensin receptor blocker. Cases were those who died suddenly shortly after receiving an outpatient prescription for one of co-trimoxazole, amoxicillin, ciprofloxacin, norfloxacin, or nitrofurantoin. Each case was matched with up to four controls on age, sex, chronic kidney disease, and diabetes.

                    MAIN OUTCOME MEASURE:

                    Odds ratio for the association between sudden death and exposure to each antibiotic relative to amoxicillin, after adjustment for predictors of sudden death according to a disease risk index.


                    Of 39 879 sudden deaths, 1027 occurred within seven days of exposure to an antibiotic and were matched to 3733 controls. Relative to amoxicillin, co-trimoxazole was associated with an increased risk of sudden death (adjusted odds ratio 1.38, 95% confidence interval 1.09 to 1.76). The risk was marginally higher at 14 days (adjusted odds ratio 1.54, 1.29 to 1.84). This corresponds to approximately three sudden deaths within 14 days per 1000 co-trimoxazole prescriptions. Ciprofloxacin (a known cause of QT interval prolongation) was also associated with an increased risk of sudden death (adjusted odds ratio 1.29, 1.03 to 1.62), but no such risk was observed with nitrofurantoin or norfloxacin.


                    In older patients receiving angiotensin converting enzyme inhibitors or angiotensin receptor blockers, co-trimoxazole is associated with an increased risk of sudden death. Unrecognized severe hyperkalemia may underlie this finding. When appropriate, alternative antibiotics should be considered in such patients.



                    ACE inhibitors and Angiotensin receptor blockers (ARBs) have been promoted, to and amongst nephrologists, as the best thing since sliced bread...for the last 30 years, since Barry Brenner and his colleagues came up in Boston (1981-1982) with the Hyperfiltration-Hyperperfusion Hypothesis of progressive CKD:

                    Since, we , as nephrologists, have been dishing out RAAS (renin angiotensin aldosterone inhibitors) to our patients as smarties...regardless of the growing evidence that they are merely good anti-hypertensives with no added benefits:

                    This is also in spite of ignored evidence that RAAS inhibitions may accelerate/increase the risk of ESRD:


                    Now we are told that these agents, are potentially DANGEROUS and associated with:

                    1. Increaesd risk of AKI:

                    2. Increased risk of sudden death in older patients on certain antibiotics: Co-trimoxazole and quinolones (above abstract).

                    3. Increaased risk of CVD complications compared to beta-blockers on HD:


                    4. Increased risk of Cancer amongst smokers renal allograft recipients:


                    So from a wonder drug...based on limited and flawed evidence (not once was GFR measured in studies claiming that RAAS inhibitors slow CKD decline...???), to a potentially dangerous class of antihypertensives that accelerate renal functional decline in susceptible individuals, induce AKI in th elderly, may cause CVD complications in HD, associate with sudden death in older people on antibiotics, to respiratory cancer in allograft recpients....took 25 years...!!!!

                    25 years of flawed clinical trials in CKD and DN...

                    25 years of misinterpretation of published data...

                    25 years of ignoring the evidence...


                    25 years of good Pharma marketing...

                    25 years of Nephrologists gullibility...

                    25 years before we ask the question:

                    HAVE WE BEEN SOLD A PUP....????


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