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Rapid Responses: Rapid Responses published:
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Effective Screening strategy ought to be adaptable to the type of community
- Emeka Anthony Nwankwo (7 November 2006)
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Who put CKD in the new GP contract?
- Des Spence (8 November 2006)
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Chronic kidney disease screening and blood viscosity
- Les O Simpson (8 November 2006)
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Another screening strategy for chronic kidney disease
- Ronald T. Gansevoort, Paul E. de Jong (12 December 2006)
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Re: Another screening strategy for chronic kidney disease
- Stein Hallan, Friedo W. Dekker (22 December 2006)
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Emeka Anthony Nwankwo, nephrologist umth maiguri 60001
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Dear Editor, Hallan et al reported that the screening of patients with hypertension, diabetes and age greater than 55 years old was the most effective strategy to detect chronic kidney disease in Norway(1). The matter of what strategy to use in detecting asymptomatic chronic kidney disease in a community remains controversial mainly because of the costeffectiveness considerations. In the developing countries the incidence of kidney failure is rising against the backdrop of inadequate healthcare resources and as a result, those countries may actually benefit more than developed countries from prevention, early detection and treatment of chronic kidney disease interventions. Targeted screening which Hallan et al recommend probably, best suits communities in Norway and elsewhere with very high standards of living and well developed healthcare systems. Whereas kidney function deteriorates with age and as a result it is sensible to focus on the elderly in a screening exercise, the reports from the developing countries are that both the mean and median age of incident kidney failure patients are less than 45 years (2-4). In other words targeting efforts at screening to the >55 years age group for example will certainly miss the objective in those areas. Diabetes ranks high among the risk factors for chronic kidney disease but again in the developing countries especially in sub Saharan Africa the contribution of diabetes to the chronic kidney disease burden is only recently beginning to rise but still remains relatively low. Both hypertension and diabetes in the developing countries remain largely undetected and untreated with several of such patients presenting for the first time with complications of the diseases. Besides the contribution made by the well known risk factors for chronic kidney disease in the developing countries, there probably exists a high prevalence of kidney failure of uncertain cause similar to the findings in people of Asian descent resident in the UK (5). It therefore appears that for certain communities like those in sub Saharan African, untargetted general population screening remains relevant if not the optimum. I believe that these issues are to be put into consideration in recommending a screening strategy of a universal application. Reference: 1. Hallan SI, Dahl K, Oien CM et al. Screening strategies for chronic kidney disease in the general population: follow-up of cross sectional health survey. BMJ, doi:10.1136/bmj.39001 2. Nwankwo EA, Ene AC. HIV infection in patients requiring dialysis in Maiduguri, Nigeria. Int J Artif Organs 2004; 27: 1000-2 3. Nwankwo EA, Wudiri WW, Bassi A. Practice pattern of haemodialysis vascular access in Maiduguri, Nigeria. Int J Artif Organs 2006 29: 956-60 4. Kher V. End stage renal disease in developing countries. Kidney Int 2002; 62:350-62 5. Ball S, Llyod J, Cairns T et al. Why is there so much end stage renal disease of undetermined cause in UK Indo-Asians. Q J Med 2001; 94: 187-93 Competing interests: None declared |
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Des Spence, GP Glasgow G20 9DR
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“Bonkers” said my Registrar. I smiled as she was picking some of evidenced-based terminology I’d taught her. Yes she was right the paper reinforces clearly that the inclusion of CKD in the New GP contract , is well –“nuts” . The paper for the first time sets out the natural history of CKD. It seems that about 5% of the population have CKD stage 3 or worse. However, in this paper out of the population of 3069 patients with CKD 3 or worse - only 38 developed end stage Renal Failure after 8 years (1.2% of the at risk population or just 0.15% per year) What we do not know is the percentage of these 38 people who would have be prevented from end stage renal failure by optimal antihypertensive, lipid lowering and control blood sugar intervention. ( I have searched for this through the usual sources - only to find the UK guidelines whose stark lack of real evidence has been crudely camouflaged by over 500 references). But for arguments sake lets assume that 50% of the 38 were delayed from end stage Renal Disease - which is a huge leap of faith on the available evidence. This would only prevent 0.075% per year, of the at risk population from end stage disease, with annual NNT of 1333. Lets leave aside the goggling opportunity cost of this exercise and reflect on the needless medical mayhem that we have unleashed on 5% of the population. Told they have a chronic kidney disease, scans, annual checks, polypharmacy , referral and doctors blind to the treatment paradox – much misery I fear. “Bonkers” unfortunately seems about right. 1. Renal Association Guideline on CKD – March 2006 Competing interests: None declared |
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Les O Simpson, retired medical research worker Dunedin, New Zealand, 9077
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Hallan et al concluded that only a small proportion of those with chronic kidney disease went on to develop end stage renal disease. However, it is possible that some cases considered to have chronic kidney disease might have had chronic renal dysfunction. The point of difference is that any screening programme which fails to take into account the role of blood viscosity on kidney function may be a waste of resources. When blood with increased viscosity passes through the afferent arteriole it will influence glomerular filtration pressure and alter both the nature and the volume of the glomerular filtrate. Furthermore, because of the effects of filtration, blood entering the efferent arteriole will be hyperviscous and will adversely affect the rate of blood flow in the peritubular plexus. Thus, the efficiency of tubular re- absorption will be compromised. So increased blood viscosity interferes with urine formation at two points in the process. Although Hallan et al noted the involvement of aging, hypertension and diabetes, there is no indication that they recognised that all three factors share the common feature of increased blood viscosity. Ajmani & Rifkind (1) described the role of increased blood viscosity in the aging process. There are many published reports of increased blood viscosity playing a causal role in hypertension (2). The first of many reports on blood viscosity in diabetes was published in 1966 (3). The relevance of these observations is that viscosity-related changes in urine composition may be a dysfunctional rather that a disease-related situation. Therefore it may be possible to reduce the level of dysfunction by dietary and lifestyle changes which have been shown to reduce blood viscosity References. 1. Ajmani RS, Rifkind JM. Hemorheological changes during human aging. Gerontology 1998;44:111-20. 2. Letcher RL, Chien S, Pickering TG, et al. Direct relationship between blood pressure and blood viscosity in normal and hypertensive subjects. Am J Med 1981;70:1195-202. 3. Skovberg F, Nielsen AAV, Schlictkrull J, et al. Blood viscosity in diabetic patients. Lancet 1966;i:129-31. Competing interests: None declared |
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Ronald T. Gansevoort, Internist-nephrologist Dept. Nephrology, UMCG, P.O Box 30.001, 9700 RB Groningen, The Netherlands, Paul E. de Jong
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Dear Sir / Madam, Hallan et al compared various strategies for detecting patients with chronic kidney disease (CKD), defined as an eGFR<60 mL/min/1.73m2 (1). They concluded that a strategy targeting screening at people with diabetes, hypertension, or age > 55 was the most effective. Patients thus identified with CKD had an increased risk for cardiovascular (CV) disease, but a low absolute risk for end-stage renal disease. When following this strategy, still a relatively large proportion of the general population will have to be screened, being 37.1%. The authors therefore questioned whether such screening will be cost-effective. We would like to draw attention to a screening strategy that has not been investigated. Presence of CKD can also be assessed by demonstration of an increased urinary albumin excretion (UAE). High levels of UAE have consistently been shown to be associated with known and yet undiscovered hypertension and diabetes, and to predict unfavourable CV and renal outcome. We recently described that subjects found by population screening to have only a low eGFR showed on average little renal function deterioration during 7.2 years of follow-up, whereas subjects with increased UAE showed rapid renal function decline and increased CV risk (2). We therefore propose screening for CKD to take place by screening subjects for UAE. Although such an approach will identify other subjects than screening for low eGFR, we hypothesize that the yield with respect to CV and renal risk identification will be at least similar. Screening for UAE can be done by subjects at home at low costs using urine dipsticks, or by sending by post a vial containing a portion of a first morning void urine to a central laboratory. Only those subjects found positive for micro-or macro-albuminuria are to be invited to visit their general practitioner for further clinical and laboratory investigations. In our study this proved to be only 7.2% of the general population (3). Newly discovered hypertension and diabetes can be treated in an early stage. In our study this proved to be 33 and 5% of the albuminuric subjects. Furthermore, in case micro-albuminuria is confirmed subjects could be treated with ACE inhibition to prevent renal as well as CV disease progression, even when diabetes and/or hypertension is absent (4). We recently showed that such an approach is likely to be cost-effective (5). Since in the HUNT II study in a considerable percentage of subjects information was obtained on UAE, we hope that it will be possible for Hallan et al to examine also the yield of a screening programme based on screening for increased UAE. References: 1. Hallan SI, Dahl K, Oien CM et al: Screening strategies for chronic kidney disease in the general population: follow-up of a cross-sectional health survey. BMJ 2006;333:1047-1052 2. Halbesma N, Kuiken DS, Brantsma AH, Bakker SJ, Wetzels JF, De Zeeuw D, De Jong PE, Gansevoort RT: Macroalbuminuria is a better risk marker than low estimated GFR to identify individuals at risk for accelerated GFR loss in population screening. J Am Soc Nephrol. 2006;17:2582-90 3. Hillege HL, Janssen WM, Bak AA, Diercks GF, Grobbee DE, Crijns HJ, Van Gilst WH, De Zeeuw D, de Jong PE: Microalbuminuria is common, also in a nondiabetic, nonhypertensive population, and an independent indicator of cardiovascular risk factors and cardiovascular morbidity. J Intern Med 2001:249;519-526 4. Asselbergs FW, Diercks GF, Hillege HL et al: Effects of fosinopril and pravastatin on cardiovascular events in subjects with microalbuminuria. Circulation. 2004;110:2809-16 5. Atthobari J, Asselbergs FW, Boersma C et al: Cost-effectiveness of screening for albuminuria with subsequent fosinopril treatment to prevent cardiovascular events. Clin Ther 2006:28;432-44. Competing interests: None declared |
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Stein Hallan, Associate professor / consultant NTNU / St Olav Hospital, Friedo W. Dekker
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Dear Sir / Madam, We thank Gansevoort and de Jong for stressing the importance of albuminuria. Albuminuria has expanded from being a test for diabetic nephropathy to a test for all kinds of kidney disease, and it probably also is a very important risk factor for cardiovascular disease in general. We therefore fully agree that albuminuria will be an important test for improving screening strategies regarding progression to end-stage renal disease (ESRD). Estimated glomerular filtration rate (GFR) has been the main screening tool in current suggestions for chronic kidney disease screening, and to evaluate these guidelines we focused on GFR (1). Gansevoort and de Jong’s suggestions are indeed interesting, and although we do not have too much people with available data, there are some interesting results. Among 2,525 random subjects from the general population with three albumin creatinine ratios available, microalbuminuria was found in 186 (7.4%) and macroalbuminuria in 21 (0.8%), which is comparable to the PREVEND data. Only one person progressed to dialysis during eight years of follow-up, and this was a patient with macroalbuminuria and GFR 21 ml/min/1.73m2. At best this would equal a number needed to treat of 207 (or at least 37, upper limit 95% confidence interval). We have previously shown that indications for renal replacement therapy are similar in Norway and the US (2), so the result can probably be generalized to other Western countries as well. Although Halbesma etal found that GFR <60 ml/min/1.73m2 was not a predictor for falling GFR during a six year period while albuminuria was a major predictor for progression (3), initial screening for albuminuria seems not to be an efficient screening strategy for future ESRD in our population. Screening in other high risk groups could perhaps be more efficient and this has to be explored. Based on our current knowledge we think that both albuminuria and GFR should be used if screening is to be considered, but better screening tools for predicting progressive kidney disease are clearly needed. Sincerely, S Hallan
F W Dekker
References: 1. Hallan SI, Dahl K, Oien CM, Grootendorst DC, Aasberg A, Holmen J, Dekker FW: Screening strategies for chronic kidney disease in the general population: follow-up of a cross-sectional health survey. BMJ 2006;333:1047-1052 2. Hallan SI, Coresh J, Astor BC, Asberg A, Powe NR, Romundstad S, Hallan HA, Lydersen S, Holmen J. International comparison of the relationship of chronic kidney disease prevalence and ESRD risk. J Am Soc Nephrol. 2006 Aug;17(8):2275-84 3. Halbesma N, Kuiken DS, Brantsma AH, Bakker SJ, Wetzels JF, De Zeeuw D, De Jong PE, Gansevoort RT: Macroalbuminuria is a better risk marker than low estimated GFR to identify individuals at risk for accelerated GFR loss in population screening. J Am Soc Nephrol. 2006;17:2582-90 Competing interests: None declared |
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