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by Meguid El Nahas - Tuesday, 28 February 2012, 6:15 PM
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In this month issue of Nephron: Garcia  /Harden  /Chapman: The Global Role of Kidney Transplantation:

This review raises important issues and in particular the fate of those suffering from ESRD in Emerging countries. Limited healthcare and Nephrological resources makes long term renal replacement therapy by dialysis unavailable. Transplantation is often the sole option for those at risk of death due to ESRD. This year’s WKD raises issues related to transplantation in emerging countries including major and justifiable concern over organ commercialisation.

The authors state: “There remain major challenges to providing optimal treatment for ESRD worldwide and a need, particularly in low income economies, to mandate more focus on community screening and implementation of simple measures to minimize progression of CKD”

Whilst Detection and Prevention of CKD is a healthcare priority worldwide, general population screening is unlikely to be a universal option and targeted screening is likely to be more beneficial and cost/effective. Screening should focus on the two main causes of CKD: Diabetes and Hypertension! Most hypertensive individuals and those suffering from diabetes are often diagnosed very late in emerging countries and poorly controlled hence a higher rate of cardiovascular complication including CKD.

Also, it is important not to overlook the fact that the majority of those reaching ESRD in Emerging countries are seen within 90 days or less from starting RRT; Emphasis should therefore be on timely referral of those suffering from CKD to Nephrologists. Perhaps, screening and appropriate referral of those suffering from CKD3 should also be a priority.

  The authors state: “The recent  designation of renal disease as an important non-communicable disease at the UN High Level Meeting on NCDs is one step in this direction. But early detection and prevention programs will never prevent ESRD in everyone with CKD, and kidney transplantation is an essential, viable, cost-effective and life-saving therapy which should be equally available to all people in need. It may be the only tenable long-term treatment option for ESRD  in  low-income  countries  since  it  is  both  cheaper and provides a better outcome for patients than other treatment for ESRD”

Dialysis cost is unaffordable in Emerging countries and even in some developed countries where financial austerity and healthcare budget restrictions are a threat. So access to renal transplantation is an imperative but also post-transplant care provisions. Of note this is not even readily available some developed countries?!

The authors state: "The success of transplantation has not been delivered evenly across the world, and  substantial disparities still exist in access to transplantation, we remain troubled by commercialization of living donor transplantation and exploitation of vulnerable populations for profit."  

Commercialisation is unacceptable in healthcare. It is also a very emotive term. Organ exchange with incentives may be more acceptable and commonly practiced. Care has to be taken not to mix Western high ethical standards with the life of those deprived of dialysis and facing death unless they “find” a kidney. Ethics or Death can sometime clash…Most choose Life!

The authors state: "There are solutions available. These include demonstrably successful models of kidney transplant programs in many developing countries; growing availability of less expensive generic immunosuppressive agents; improved clinical training opportunities; governmental and professional guidelines legislating prohibition of commercialisation of transplantation."

Governments and legislation ban of organ exchanges for profit are fully justifiable but will only be effective if and when those Government and legislators offer alternative options for Life for those with ESRD. Until and unless this is made available to those dying from ESRD such legislation will only encourage and foster a growing black market in transplantation with dire consequences due to the worst possible medical practices. Government sponsored and organised organ exchange with incentives may be a viable alternative to ban!?


[ Modified: Thursday, 1 January 1970, 1:00 AM ]
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A review article by McCaughan and Courtney in NDT January 2012 reviews the situation relating to the apparaent increased incidence of PJP recipients of renal allografts. A number of recent reproted outbreaks in renal transplant recipients have raised concern about adequacy of prophylaxis strategies.  In general it is considered that PJP prophylaxis is justified and should be considered if the risk of disease is estimated to exceed 3%. The incidence of PJP infections in moderately immunosuppressed renal transplant recipients is usually <1%. Six renal centres reporting outbraks in Asia and Europe have all adopted the surveillance rather than prophylaxis approach based on the above assumptions. However, it is important toi appreciate that the risk is higher in:

1. High risk patients

2. Higher immunosuppression including use of ATG

3. Frequent rejection episodes

4. CMV infections

Currernt guidelines recommend 3-6 month prophylaxis with septrin (trimethoprim-sulfamethoxazole) from the time of transplantation. These guidelines may warrant review as most recent outbreaks took place more than 6 months after transplantation.

Therefore in higher risk and susceptibe individuals, it would be advisable to continue prophylaxis until the immunosuppression burden can be reduced.

Routine prophylaxis for all may be justifiable.

Prolonged immunosuppression may also be justifiable specially in the days of ever more agressive immunosupressive therapies.

Nephrologists need to inform their decision based on:

What is the justification of the Intervention?

Who is most susceptible to PJP and warrants prophylaxis?

Risk: benefit analysis; Septrin is not without its risks and side effects and PJP can be fatal!

Cost: benefit analysis.

McCaughan JACourtney AEPneumocystis jiroveci pneumonia in renal transplantation: time to review our practice? Nephrol Dial Transplant. 2012 Jan;27(1):13-5. Epub 2011 Aug 3.






[ Modified: Thursday, 1 January 1970, 1:00 AM ]
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The answer to this question is usually that ACE inhibitors and ARBs have a protective effect by slowing the progression of CKD.

Yet, in all studeis on inhibition of RAAS and CKD progression diabetic or otherwise, there hasn't been a single study that reported the impact of the intervention on GFR. Instead, all the studies on ACE inhibition and progression since that of Lewis et al in 1993 relied on surrogate markers of progression namely: serum creatinine, creatinine clearance, 1/Cr slopes against time or more recently estimatedGFR. Not a single study published to my knowledge solid data on the hard and relevant endpoint of measured GFR and changes with time???!!!!

Authors have overlooked that changes in serum creatinine and derived formulation can be due to one of 4 factors:

1. Impact on dietary intake of amino acids or creatine

2. Creatine/Creatinine metabolism

3. GFR

4. Tubular secretion

So changes upon ACE inhibition in serum creatinine could be due to any one of these 4 confounders; yet nobody seems to take that into consideration and equate changes in serum creatinine to changes in GFR only....Why I ask myself this oversight????

This, in spite of evidence to suggest that inhibition of the RAAS system impacts on :

1. Efferent arterioles; leading to vasodialtation

2. Increased peritubular capillary circulation secondary to improved efferent arteriolar blood flow

3. Increased tubular secretion of creatinine either indirectly through 1 and 2 or directly through an increase in its organic cationic transporters (OCT1 and 2) that affect creatinine secretion by the proximal tubules (ref 1,2).

In conclusion, the oberved effect of RAA system inhibition of the rate of decline of serum creatinine may be simply the reflection of increased tubular secretion of creatinine rather than anything to do with prevention of GFR decline as the latter has never been measured!? Clearly, this is a hypothesis as much as the assumption that inhibition of RAAS slows the decline of true GFR!

Isnt it intriguing that investigators studying the progression of CKD never reported measured changes in GFR....I wonder why????


1. Thomas MCTikellis CBurns WCThallas VForbes JMCao ZOsicka TMRusso LMJerums GGhabrial HCooper ME,Kantharidis PReduced tubular cation transport in diabetes: prevented by ACE inhibition.Kidney Int. 2003 Jun;63(6):2152-61.

2. Thomas MCJerums GTsalamandris CMacisaac RPanagiotopoulos SCooper MEMDNSG Study GroupIncreased tubular organic ion clearance following chronic ACE inhibition in patients with type 1 diabetes.Kidney Int. 2005 Jun;67(6):2494-9.
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by Meguid El Nahas - Wednesday, 15 February 2012, 10:42 PM
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Questions and answers put to Prof Glassock following his talk on the Management of Vasculitis:


Prof Salah Naga: Is there a role for CNIs in the management of ANCA associated systemic vasculitis?

Prof Glassock: CNIs do not seem to be very effective in the management of AASV. They certainly dont feature in the recognised effective therapeutic approaches.

Prof Sabry Gohar:  Is there a role for Infliximab in AASV?

Prof Glassock: No role and many reports of significant side effects including a high rate of infectious complications.

Prof Adel Afifi: IN the face of an increase in sCr, when would you rebiopsy?

Prof Glassock: Rebiopsying should be considered in the face of clinical, biochemical (CRP) or immunological (Autoantibodies) signs of disease activity.

Prof Afifi: How do you treat relapses?

Prof Glassock: I treat relapses of AASV with rituximab to avoid the toxicity of repeat courses of cyclophosphamide.

Prof Essam Nooreldin: How do you prevent hemorrhagic cystitis?

Prof Glassock: In more than 30 years of practice, I did not see a single case of hemorrhagic cystitis.

I tend to prescribe the cyclophosphamide to be taken at 9am

along with 4 glasses of water and I encourage th epatient to drink more water at bedtime (another 4 glasses).

Prof El Nahas: Do you think that Plasma exchange is beneficial outdside the indication for lung hemmorhage?

Prof Glassock: Whilst the MEPEX study showed some benfit at 12 months, follow up study over more than 3 years failed to show any advantage of plasma exchange of ESRD or death and was associated with increased toxicity/side effects (Walsh and Jayne, Personal Communication).





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by Arif Khwaja - Tuesday, 14 February 2012, 5:20 PM
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Interesting data published in this months JASN again challenges the ‘one-size fits all’ approach of many guidelines in nephrology. The Correction of Anemia and PRogression of Renal Insufficiency in Transplant patients (CAPRIT) study from Amiens France, was an open label RCT that randomised patients to receive epoietin-beta to achieve either a normal haemoglobin (13-15g/dl) or a lower haemoglobin (10.5-11.5g/dl). There was no difference in baseline characteristics of the 125 patients who were randomised to the study. At 6 and 12 months the normal haemoglobin group had improvements in quality of life scores compared to the lower haemoglobin group. At 2 years progression to ESRD and return to dialysis occurred in 3 patients (4.8%) in the normal haemoglobin group and 13 patients (21%) in the low haemoglobin group (P=0.01) The death-censored graft survival at 2 years was 94.6% in normal haemoglobin group compared to 80.0% in the low haemoglobin group (P=0.01). The primary outcome was difference in eCrCl by Cockroft-Gault. At year 2, the mean eCrcl decreased by 2.4±1.1 ml/min per 1.73 m2in the normal haemoglobin group and 5.9±1.1 ml/min per 1.73 m2in the low haemoglobin group (P=0.03). There was no increase in CV events in the normal haemoglobin group. Theese results contrast the epo studies in the CKD population where normalisation of haemoglobin was harmful – TREAT, CHOIR, CREATE.

So is this a practice changing paper? I don’t think so because the study was much, much smaller than the CKD trials with a lower prevalence of cardiovascular disease – therefore the study may simply have been underpowered to detect differences in adverse cardiovascular events. Postulated mechanisms by which epo may improve transplant outcomes include a possible immunomodulatory effect or correction of tissue hypoxia and clearly warrant further investigation. Furthermore the potential impact of epo on malignancy could not be evaluated.

What the study does do is highlight the need for a larger multicentre RCT to address the issue of optimal haemoglobin in a transplant patient and the problems of 'extrapolating' guidelines from one patient group to another.

See Correction of Postkidney Transplant Anemia Reduces Progression of Allograft Nephropathy

Gabriel Choukroun, Nassim Kamar, Bertrand Dussol, Isabelle Etienne, Elisabeth Cassuto-Viguier, Olivier Toupance, François Glowacki, Bruno Moulin, Yvon Lebranchu, Guy Touchard, Maïté Jaureguy, Nicolas Pallet, Yannick Le Meur, Lionel Rostaing, Frank Martinez, and for the CAPRIT study Investigators. J Am Soc Nephrol 2012;23 360-368

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by Meguid El Nahas - Tuesday, 14 February 2012, 4:49 AM
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I am attending the Annual meeting of the Egyptian Society of Nephrology and Transplantation (ESNT) in Marsa Alam, Egypt.

 On the 13 and 14 of February and Pre Congress CME meeting is held.

On day 1 of the CME meeting, I attended a lecture by Professor Richard Glassock, USA, in which he discussed arguments related to the timing of the initiation of renal replacement therapy. He showed very elegantly in his lecture how timing of starting dialysis has evolved over the last 30 years from those who in the 70s and 80s advocated early start of RRT at GFR levels of around 15 to 20 ml/min to those morte recent observations arguing that late start of HD may be more beneficial.

A number of reviews and analysis concluded that there was little advantage in starting RRT too early; GFR>15 ml/min.

Professor Glassock referred to his work and that of Rosansky (2010) showing that those starting HD at the highest quartile of eGFR (>15) had the highest mortality. Of interest, this was more specifically evident in those with higher GFR and serum albuminlevels >35g/l. He also referred to the IDEAL study by Cooper et al (2009).

Prof Glassock explained the possible confounder of the interpretation of such observation with emphasis on the value of low serum creatinine as a marker of somatic malnutrition whilst changes in serum albumin are more reflective of visceral malnutrition. Sarcopenia and wasting may therefore explain some of the observations linking poor outcomes to early initiation of HD based on calculated GFR derived from equations such as the MDRD. 

He also stressed the poor performance (imprecision and bias) of the MDRD formula in CKD stage 5. In fact, he showed data that eGFR calculated in CKD5 by such an equation considerably overestimates measured GFR. He suggested that the average of creatinine + Urea clearance may be a more accurate way of measuring GFR at this late stage of CKD.

It is also important to consider that timely referral of CKD4-5 patients to pre-dialysis care clinics and optimal preparation for RRT ar eas important in relation of the overall care of the CKD5 patient than the timing of the initiation of dialysis. Early referral to nephrologists is often not the case with patients presenting late and ill prepared for RRT. The setting up of pre-dialysis/low clearance clinics has been avocated in the UK to optimise the pre-RRT care of CKD patients. Optimal pre-ESRD care leads in many cases to prolong period of stable kidney function between eGFR of 10 and 15ml/min in asymptomatic patients. Many of the symptomas of these patients are alleviated by good anemia control as well as good control of their calcium and phosphorus metabolism as well as attention to their nutritional requirements. Pre dialysis clinics also allow for a better planning of vascular access as well as consideration/investigations for renal transplantation. Finally, good pre dialysis care involves social and psychological counselling for the patient and his family.

* See Review by Mustafa Arici in the OLA Libray on Timing of Start of RRT.


[ Modified: Thursday, 1 January 1970, 1:00 AM ]
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Oscar Wilde  wrote that " a cynic is someone who knows the price of everything but the value of nothing" ....... Over 100 years later the same might be said of Medicare's attitude to kidney transplantation. In a depressing critique of Medicare's funding of kidney transplantation in the United States, Gill and Tonelli ( see NEJM online first) point out the impact of a lack of a universal funding strategy on clinical outcomes in transplantation. The 10 year graft survival in the US of 43% contrasts with a graft survival of between 55-60% in Canada, Australia and the UK.  Whilst these differences maybe due to a multitude of factors it's worth noting that in the US itself the likelihood of graft failure is much higher in the Medicare-insured group than those not insured by Medicare. The risk of graft failure rapidly increases after 3 years in the Medicare group. So what happens at 3 years? At present those insured with Medicare have their funding for immunosuppressants stopped after 3 years unless they are over 65 or deemed to have significant disability. Of course one can't prove that the cost of drugs accounts for the poorer outcomes amongst the Medicare group but the authors point to a survey of US transplant program's in which 68% of centres reported deaths or graft failures related to cost-related non-adherence.

Whilst the clinical reasons to support transplantation are overwhelming the economic reasons are just as robust. The cost of transplantation is initially estimated at $110,000  but this cost falls rapidly after the first year - making transplantation a much more cost effective therapy that dialysis which costs $75,000 per annum with the cumulative cost of dialysis much more than transplantation.  However despite the fact that Medicare won't fund immunosuppressants after 3 years ( even though effective generics for Tacrolimus and MMF now widely available) they are able to fund lifelong dialysis. The economic modelling suggests that $200 million could be saved annually by providing universal coverage for lifetime immunosuppressive medication. An amendment to the the Social Security Act before the US Congress proposes to provide universal coverage for transplantation. A previous attempt to provide such coverage in 2009 failed. One can only hope that in the midst of a global economic crisis the policymakers can do their sums and come up with the right answer.

Penny Wise, Pound Foolish? Coverage Limits on Immunosuppression after Kidney Transplantation. John S. Gill, M.D., and Marcello Tonelli, M.D. February 1, 2012 (10.1056/NEJMp1114394)

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by Denise Smith - Wednesday, 1 February 2012, 12:06 PM
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'Ideal Criteria' for Starting Chronic Hemodialysis: Numbers, Symptoms or an Alerting 'Traffic Light' System? (Mustafa Arici, Ankara; Nephron Clin Pract 2012;120:c17-c24) Arici writes in this issue an "Opposite View" regarding the timing of starting renal replacement therapy (RRT). He cautions readers against the misinterpretation of recent data suggesting that late onset RRT is safe and that early initiation of dialysis can be harmful. He draws attention to the use of estimated GFR equations with their limitations and inaccuracies in CKD stage 5 as well as their misrepresentation of true GFR in wasted and sarcopenic CKD5 patients. He also stresses the importance of a more holistic approach to the initiation of RRT beyond a simple eGFR value. Finally, he makes the important distinction between late onset RRT and late referral of CKD4 and 5 patients. Suffice to say that in many emerging countries the great majority of those who start RRT are seen within 3 months from the onset of dialysis. The main question in my view is not when to start RRT, but instead when to refer patients with CKD3b and 4 to Nephrology centers to prepare for RRT. All too often the timing of referral is inappropriately late, thus being the main cause of poor outcomes.

Mechanism-Based Therapeutics for Autosomal Dominant Polycystic Kidney Disease: Recent Progress and Future Prospects (Chang and Ong, Sheffield; Nephron Clin Pract 2012;120:c25-c35) The authors provide readers with an up-to-date critical appraisal of mechanisms and treatment of autosomal dominant polycystic kidney disease (ADPKD). Lessons for nephrologists from the ADPKD story so far are: (1) translation from the laboratory to the bedside can, with concerted effort, take place relatively quickly in CKD, (2) animal models of disease do not always accurately reflect the human equivalent, and (3) biomarkers and surrogate markers of disease should not be the target of interventions; instead the hard endpoints of CKD progression and end-stage renal disease should be kept in focus. Finally, most clinical trials target a single ADPKD pathway. Perhaps progression in this condition will require a multitargeted approach. The ADPKD polypill combines a range of inhibitors of cell proliferation and transduction pathways: multitargeted therapy for a multigenetic disease?

Urinary Red Blood Cells: Not Only Glomerular or Nonglomerular (Poloni, Fogazzi and colleagues, Milan; Nephron Clin Pract 2012;120:c36-c41) This review reminds nephrologists of the lost art of urine microscopy. They go well beyond glomerular and non-glomerular hematuria as distinguished by the morphology and presence of dysmorphic urinary red blood cells. They describe urinary sickle cells, anisocytes, poikilocytes, dacryocytes and elliptocytes, and illustrate these urinary red blood cells' morphological alterations by the corresponding clinical conditions. The article reflects Professor Tita Fogazzi's passion for urine microscopy. He has turned urine microscopy into a rediscovered science and art. Practicing nephrologists, however, remain divided on the value of urine microscopy. Many hold it in high diagnostic esteem and some even raise it to the level of scientific art. Others, including myself, do not use urine microscopy for diagnostic purposes. I must confess that I have not looked at a single urine sediment in the last 25 years - whether this has affected my diagnostic ability may never be known!

Towards Erythropoietin Equations That Estimate Oxygen Delivery rather than Static Hemoglobin Targets (C.J. Diskin, Opelika, Ala.; Nephron Clin Pract 2012;120:c48-c53) The author argues that current inconsistencies in diagnosis and management may be the result of overlooking some basic physiological facts and the pathophysiology of anemia and oxygen delivery in CKD. Anemia in CKD is associated with changes in the oxygen-hemoglobin dissocation curve that is affected by variables such as acidosis, hyperphosphatemia as well as circulating/cellular urea levels. The review is a reminder to readers that simplistic therapeutic algorithms such as those currently in use for the management of anemia in CKD may cause more harm than benefit when they are not fully based on a better understanding of the pathophysiology of the underlying disease. Such understanding may become even more relevant when interventions to treat anemia of CKD are based on manipulations of hypoxia-inducible factors. Whether more complicated equations based on incorporating more modulators of anemia improve practice remains to be determined.

[ Modified: Thursday, 1 January 1970, 1:00 AM ]
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Semin Dial. 2012 Jan;25(1):9-14. doi: 10.1111/j.1525-139X.2011.01003.x. Epub 2011 Dec 6.


An Obituary for GFR as the Main Marker for Kidney Function?

This editorial review in NDT challenges the use of serum creatinine and derived eGFR to estimate kidney function in terms of glomerular filtration.
We forget all too often that serum creatinine is the result of creatinine homeostasis based on:
1. Intake, amino acids and creatine
2.Cr Metabolism  from creatine to creatinine; relying on muscle mass and related enzymes
3. Glomerular filtration
4. Secretion; renal tubular and intestinal
So any intervention that seemingly lowers serum creatinine or slow its rise may be the result of any of the above or a combination of some of them. Cionsequently, interventions pertaining to slow teh progression of CKD based on a slower rise in serum creatinine compared to control may be due to:
1. Decrease intake, metabolism and secretion as with Low protein Diet
2. Secretion as with ACE inhibitors and ARBs as they improve in CKD peritubular circulation and enhance the transport and secretion of Creatinine. This raise teh question as to whether the whole literature on ACE (RAAS) inhibition and CKD is a tubular secretion paraphenomenon of these agent... Not a single study bothered measuring or reporting GFR.
It is high time nephrologists go back to basics and remember how Creatinine is handling and stop equating changes in serum creatinine to changes in glomerular filtration alone... this is wrong and misleading!
[ Modified: Thursday, 1 January 1970, 1:00 AM ]
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by Meguid El Nahas - Saturday, 28 January 2012, 11:00 AM
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De Vriese and colleagues in Belgium argue in teh january issue of KI that all patients on RRT should be screened for coronary artery disease (CAD). This implies that symptomatic but also asymptomatic patients should be screened.

Their argument is based on the fact that a very high prevalence of CAD in chronic dialysis patients including up to 53% in asymptomatic patients and 83% in those with diabetes. Also higher prevalence in older dialysis patients. Consequently, the majority of dialysis patients with angiographically documented CAD are asymptomatic (Ohtake et al).

They show data confirming the good predictive value of a positive Myocardial Perfusion Scintigraphy (MPS) for CAD. Adenosine, dipyridamole or dobutamine stresss MPS  have all been shown to have high predictive values for CAD;  the presence of reversible ischemia upon stress MPS closely correlating with the gold standard of coronary angiography (Rabbat et al, 2003).

The question that comes to mnd is why screen asymptomatic patients as data in non CKD patients shows that survival in such patients is not affected by intervention and therefore investigations not recommended. Furthermore, there is a good body of evidence that medical therapy? The authors argue that dialysis patients are at much higher risk of CAD and related mortality thus justifying screening and intervention. The published data, albeit limited, suggest that in dialysis patients with CAPD treated with PCI or CABG have a survival advantage compared to those on medication only. 

The authors advocate screening all those on dialysis listed for transplantation arguing the high prevalence of asymptomatic patients justify such an approach rather than current guidelines recommending screening only in those with a histroy of revascularisation, a signficant reduction in LV function, or symptoms suggestive of CAD/CHF. Guidelines also recommend screening selected high risk patients which woukld automatically, in my view, include diabetic patients.

The authors advocate a large RCT that examines the incremental benefit of revascularisation in addition to medical therapy in asymptomatic dialysis patients.

I remain unconvinced on a cost/benefit analysis basis that all dialysis patients should be screened as their editorial review suggests a risk of asymptomatic CAD predmoninatly driven by diabetic patients on HD. It would therefore be more cost-effective to screen as currently recommended by international guidelines those at high risk: diabetics, history of CAD, those with an abnormal echocardiogram, etc...

It would be desirable to have a cheap and non invasive test/biomarkers that predicts the presence of subclinical CAD. Cartiac Troponins may prove to be such a test. Recent high sensitivity assays showed a considerable higher circulating levels in asymptoamtic CAD ESRD patients (Jacobs et al).  


De Vriese et al. Should we screen for CAD in asymptomatic chronic dialysis patients. Kidney Int. 2012;81:143-151.

Ohtake et al. High prevalence of occult CAD in patients with CKD at th einitiation of renal replacement therapy. JASN 2005;16:1141-1148.

Rabbat et al. Prognostic value of myocardial perfusion studies in ESRD patients: a meta-analysis. JASN 2003; 14:431-439.

Jacobs et al. Hemodilayusis patients longitudinally assessed  by highly sensitive  cardiac troponin T and commercial cardiac Troponin T and I assays. Ann Clin Biochem 2009;46:283-290.





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