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1 1370 Nephrol Dial Transplant (2010): Editorial Comments 8. Barker DJ, Forsen T, Eriksson JG et al. Growth and living conditions 21. Keller G, Zimmer G, Mall G et al. Nephron number in patients with in childhood and hypertension in adult life: a longitudinal study. J primary hypertension. N Engl J Med 2003; 348: 101108 Hypertens 2002; 20: 19511956 22. Hoy WE, Hughson MD, Bertram JF et al. Nephron number, hyper- 9. Horta BL, Barros FC, Victora CG et al. Early and late growth and tension, renal disease, and renal failure. J Am Soc Nephrol 2005; 16: blood pressure in adolescence. J Epidemiol Community Health 2003; 25572564 57: 226230 23. McNamara BJ, Diouf B, Douglas-Denton RN, Hughson MD, Hoy 10. Huxley RR, Shiell AW, Law CM. The role of size at birth and post- WE, Bertram JF. A comparison of nephron number, glomerular vol- natal catch-up growth in determining systolic blood pressure: a sys- ume and kidney weight in Senegalese Africans and African Ameri- tematic review of the literature. J Hypertens 2000; 18: 815831 cans. Nephrol Dial Transplant 2010; 25: 15141520 11. Lurbe E, Garcia-Vicent C, Torro I et al. First-year blood pressure in- 24. Hughson MD, Douglas-Denton R, Bertram JF et al. Hypertension, glo- crease steepest in low birthweight newborns. J Hypertens 2007; 25: merular number, and birth weight in African Americans and white sub- 8186 jects in the southeastern United States. Kidney Int 2006; 69: 671678 12. Whincup PH, Bredow M, Payne F et al. Size at birth and blood pres- 25. Rostand SG, Cliver SP, Goldenberg RL. Racial disparities in the as- sure at 3 years of age. The Avon Longitudinal Study of Pregnancy sociation of foetal growth retardation to childhood blood pressure. and Childhood (ALSPAC). Am J Epidemiol 1999; 149: 730739 Nephrol Dial Transplant 2005; 20: 15921597 13. Uiterwaal CS, Anthony S, Launer LJ et al. Birth weight, growth, and 26. Freedman BI, Hicks PJ, Bostrom MA et al. Polymorphisms in the blood pressure: an annual follow-up study of children aged 5 through non-muscle myosin heavy chain 9 gene (MYH9) are strongly associ- 21 years. Hypertension 1997; 30: 267271 ated with end-stage renal disease historically attributed to hyperten- 14. de Boer MP, Ijzerman RG, de Jongh RT et al. Birth weight relates to sion in African Americans. Kidney Int 2009; 75: 736745 salt sensitivity of blood pressure in healthy adults. Hypertension 27. Guyton AC, Coleman TG. Quantitative analysis of the pathophysiol- 2008; 51: 928932 ogy of hypertension. 1969. J Am Soc Nephrol 1999; 10: 22482258 15. Keijzer-Veen MG, Schrevel M, Finken MJ et al. Microalbuminuria 28. Fava C, Montagnana M, Rosberg L et al. Subjects heterozygous for and lower glomerular filtration rate at young adult age in subjects genetic loss of function of the thiazide-sensitive cotransporter have born very premature and after intrauterine growth retardation. J Am reduced blood pressure. Hum Mol Genet 2008; 17: 413418 Soc Nephrol 2005; 16: 27622768 29. Hoorn EJ, van der Lubbe N, Zietse R. The renal WNK kinase path- 16. Hallan S, Euser AM, Irgens LM et al. Effect of intrauterine growth way: a new link to hypertension. Nephrol Dial Transplant 2009; 24: restriction on kidney function at young adult age: the Nord Trondelag 10741077 Health (HUNT 2) Study. Am J Kidney Dis 2008; 51: 1020 30. Nesbitt SD. Hypertension in black patients: special issues and con- 17. Li S, Chen SC, Shlipak M et al. Low birth weight is associated siderations. Curr Hypertens Rep 2005; 7: 244248 with chronic kidney disease only in men. Kidney Int 2008; 73: 31. Schmidlin O, Forman A, Sebastian A et al. Sodium-selective salt sen- 637642 sitivity: its occurrence in blacks. Hypertension 2007; 50: 10851092 18. Vikse BE, Irgens LM, Leivestad T et al. Low birth weight in- 32. Grim CE, Robinson M. Blood pressure variation in blacks: genetic creases risk for end-stage renal disease. J Am Soc Nephrol 2008; factors. Semin Nephrol 1996; 16: 8393 19: 151157 33. Ritz E. Kidney damage in metabolic syndrome: nip it in the bud. Am 19. Zidar N, Cavic MA, Kenda RB et al. Effect of intrauterine growth J Kidney Dis 2009; 53: 726729 retardation on the clinical course and prognosis of IgA glomerulone- 34. Tishkoff SA, Verrelli BC. Patterns of human genetic diversity: impli- phritis in children. Nephron 1998; 79: 2832 cations for human evolutionary history and disease. Annu Rev Geno- 20. Na YW, Yang HJ, Choi JH et al. Effect of intrauterine growth retar- mics Hum Genet 2003; 4: 293340 dation on the progression of nephrotic syndrome. Am J Nephrol 2002; 22: 463467 Received for publication: 9.2.10; Accepted in revised form: 9.2.10 Nephrol Dial Transplant (2010) 25: 13701373 doi: 10.1093/ndt/gfq068 Advance Access publication 17 February 2010 Kidney and braina renal perspective of Les Liaisons Dangereuses Adalbert Schiller1 and Adrian Covic2 1 Nephrology Department, Emergency Clinical Hospital, Timisoara, Romania, and 2G. T. Popa University Hospital of Medicine and Pharmacy, Iasi, Romania Correspondence and offprint requests to: Adrian Covic; E-mail: [email protected] Chronic kidney disease (CKD) was identified as a major patients at high risk for CVD. Therefore, the American and independent risk factor for cardiovascular disease Heart Association recommends that all high CVD risk pa- (CVD) morbidity and mortality, CVD being also the leading tients should be screened for CKD [3]. Extensive informa- cause of death in CKD patients [1,2]. At the same time, the tion is now available about the relation between heart and prevalence of CKD is increased in CVD patients and even in kidney and about the impact on the heart and vessels of The Author 2010. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: [email protected]

2 Nephrol Dial Transplant (2010): Editorial Comments 1371 CKD complications (anaemia, mineral and bone disorders cunars cerebral infarction (LCI) or silent brain infarction is with vascular calcifications). Significantly less information a small and deep cerebral infarction induced by occlusion is available on the relation between CKD and the brain. of small penetrating cerebral arteries, identifiable by Cerebrovascular disease, considered by the Kidney magnetic resonance imaging (MRI) both in patients with Disease Outcomes Quality Initiative (KDOQI) group un- stroke and in healthy elderly persons. It seems that the prev- der the general terminology of CVD, includes quite var- alence of LCI in the general population ranges from 8 to ious disease entities of the brain vasculature [4,5]. Similar 28%, depending on age groups [14] and blood pressure; it symptoms and outcomes can be generated either by large is also significantly higher in CKD compared to non-CKD vessel (i.e. atherothrombotic cerebral infarction and other patients [15]. In a recent paper, Kobayashi demonstrated more rare causes of cerebral infarction) or small vessel that low eGFR is an independent risk factor for LCI and that diseases (i.e. intracerebral haemorrhage, silent brain in- the prevalence of LCI, as well as the number of lacunae, is farction, white matter lesions). The term stroke encom- inversely related to the level of eGFR. Most importantly, passes both atherothrombotic cerebral infarction and from a practical point of view, it seems that some of the con- intracerebral haemorrhage [4,6]. Stroke is now considered ventional risk factors for CVD (i.e. smoking, dyslipidaemia as the third leading cause of death after heart disease and and diabetes mellitus) are risk factors for stroke but not for cancer in developed countries [7]. LCI. High-sensitivity CRP (Hs-CRP), albumin, fibrino- In the general population, the incidence of stroke has the gen, haemoglobin, mineral metabolism parameters and tendency to double for each decade after the age of 55 years proteinuria (non-conventional CVD risk factors) are also [8]. In the 19992004 National Health and Nutrition not related to LCI. Only the presence of hypertension Examination (NHANES) survey, the prevalence of reported and the level of systolic blood pressure appear to be stroke in subjects over 55 years was 6%. This prevalence strongly related to LCI in CKD patients [6]. was, however, significantly higher in patients with de- Moreover, the prevalence of LCI was significantly lower creased eGFR below 60 mL/min/1.73 m2 (12.8%) and in pa- in patients with well-controlled blood pressure and in tients with increased Cr/Alb ratio over 30 mg/g (11.4%). those who used hypotensive drugs that potentially in- Furthermore, the prevalence of reported stroke seemed to crease angiotensin II (AT II) receptor activity [6]. White significantly increase with the severity of CKD. Various matter lesions [or hyperintensities (WMH)] demonstrated multivariate analyses consistently showed that older age, on MRI are also considered as markers of cerebral small the presence of hypertension, an elevated systolic blood vessel disease (i.e. hypertension-induced fibrohyalinosis pressure, coronary artery disease, low GFR and microalbu- and small vessel beta-amyloid deposition) mainly related minuria were all significantly associated with stroke [9]. to hypertension [16,17]. WMH seem to be associated The United States Renal Data System (USRDS) 2009 report with increased risk of stroke, cognitive alterations and de- analysed for stroke incidence, prevalence and mortality the mentia [1820]. Recent data showed that the prevalence data provided by two medical insurance systems: Medi- of WMH is independently associated with CKD even care (for people over the age of 65) and the Ingenix i3 when adjusted for age, sex, race-ethnicity, education (for a younger population). The incidence of stroke in and vascular risk factors (hypertension, diabetes, cardiac the Medicare database was 9% and, as expected, was lower disease and so on) [21]. in the Ingenix i3 population. The rates of incident stroke Small areas of signal loss detected on gradient-echo are 1.93.6 times higher for those with CKD than in sub- T2-weighted MRI images have been evidenced in patients jects without CKD from the Medicare older population with stroke as well as in normal elderly persons [22]. They and 4.67.6 times more frequent for CKD patients than seemed to be generated by previous extravasation of blood for non-CKD patients in the Ingenix i3 younger cohort [cerebral microbleeds (CMB)] and they have been attributed [10]. The incidence of stroke in CKD Stage 5 patients in- to bleeding-prone severe cerebral microangiopathy [17]. creases 3 months prior to renal replacement therapy (RRT) CMB have been found to indicate high risk of haemorrhagic initiation, peaks at initiation and then subsides thereafter stroke and are considered markers of severe cerebral small [10]. Overall, in CKD Stage 5D, in the Dialysis Outcomes vessel disease [23,24]. A recent study by Cho et al. sug- and Practice Patterns Study (DOPPS) study, the preva- gests that impaired kidney function is associated with the lence of cerebrovascular disease varied between 13% in presence of CMB in acute ischaemic stroke [25]. Accord- Japan, 14% in Europe and 18% in the USA [11]. ing to the data published in the current issue of Nephrology CKD is a strong, independent predictor of mortality and Dialysis Transplantation (NDT), pre-dialysis CKD and poor outcome in patients with acute stroke. The 1-year sur- CKD Stage 5D emerge as risk factors for CMB. In the paper vival rate in acute stroke patients is significantly lower in of Ikram et al., the prevalence of CMBs proved to be high in CKD patients compared to non-CKD subjects [12]. In the pre-dialysis CKD patients and increase with CKD progres- same 2009 USRDS report, the cumulative probability of sion [16]; low GFR emerged as an independent strong risk death 1 year after stroke in CKD patients is twice that of factor for the development of CMBs, along with high blood non-CKD patients [10]. Moreover, in a cohort of 1350 pressure and age. acute stroke patients, renal function on admission (AKI be- Shima et al. found the same relationship between CKD ing excluded from the study) seems to be a significant, in- progression and the prevalence of CMBs in pre-dialysis pa- dependent prognostic factor for long-term mortality and tients [26]; blood urea nitrogen (BUN), serum creatinine new cardiovascular morbidity over a long-term follow-up and low eGFR were significantly and independently associ- period of 10 years [13]. The data available on small vessel ated with the presence of CMBs. This study could indicate diseases of the brain are unfortunately less extensive. La- that decreased renal function is related to an increased risk

3 1372 Nephrol Dial Transplant (2010): Editorial Comments for clinical and subclinical stroke. The authors concluded Care and Outcomes Research Interdisciplinary Working Group. De- that CMBs in pre-dialysis CKD patients, assessed by T2*- tection of chronic kidney disease in patients with or at increased risk of cardiovascular disease: a science advisory from the American weighted MRI, would be a useful and feasible clinical mark- Heart Association Kidney and Cardiovascular Disease Council; the er for the prediction of future cerebrovascular events. Councils on High Blood Pressure Research, Cardiovascular Disease In CKD Stage 5D patients, Naganuma et al. described a in the Young, and Epidemiology and Prevention; and the Quality of high prevalence of CMBs, closely associated with other ce- Care and Outcomes Research Interdisciplinary Working Group: de- rebral small vessel diseases [27]. High blood pressure and veloped in collaboration with the National Kidney Foundation. Cir- age proved to be once again strong risk factors for CMBs. culation 2006; 114: 10831087 It has been suggested that the brain and the kidney pres- 4. Truelsen T, Begg S, Mathers C. The Global Burden of Cerebro- vascular Disease 2000 http://www.who.int/healthinfo/statistics/bod_ ent a common and unique way to react to fluctuations in cerebrovasculardiseasestroke.pdf blood pressure and flow due to similar small-resistance vas- 5. National Kidney Foundation. K/DOQI clinical practice guidelines for cular beds. High-pressure fluctuations that exist in the ca- chronic kidney disease: evaluation, classification and stratification. rotid, vertebral and renal arteries and the turbulent flow Am J Kidney Dis 2002; 39: S1S266 expose the small vessels of these two organs to pressure 6. Kobayashi M, Hirawa N, Yatsu K et al. Relationship between silent and flow fluctuations that explain the microvascular dam- brain infarction and chronic kidney disease. Nephrol Dial Transplant 2009; 24: 201207 age and the resulting renal failure and neurological and 7. Mackay J, Mensah G. The Atlas of Heart Disease and Stroke. cognitive alterations [28,29]. Thus, information about mi- World Health Organization (WHO) in Collaboration with the Cen- crovascular damage in one organ may provide information ters for Disease Control and Prevention 2004 http://www.who.int/ about damage in the other organ. For the kidney, the dam- cardiovascular_diseases/resources/atlas/en/ age markers proposed by KDOQI are albuminuria/protein- 8. Rosamond W, Flegal K, Friday G et al. American Heart Association uria and, for function decrease, eGFR, while for the brain, Statistics Committee and Stroke Statistics Subcommittee. Heart dis- ease and stroke statistics2007 update: a report from the American damage markers could be MRI-described small vessel al- Heart Association Statistics Committee and Stroke Statistics Sub- terationsi.e. the presence of LCI, WMH or CMB, as ap- committee. Circulation 2007; 115: e69e171[published correction propriate. Thompson and Hakim launched an intriguing appears in Circulation. 2007;115(5):e172], doi:10.1161/CIRCULA- hypothesis that small vessel disease is in fact a systemic TIONAHA/106.179918 condition that affects the brain as well as other systems, in- 9. Ovbiagele B. Impairment in glomerular filtration rate or glomerular duced by ageing and exacerbated by vascular risk factors. filtration barrier and occurrence of stroke. Arch Neurol 2008; 65 The authors used the term systemic arteriolar dysfunction 10. The 2009 USRDS Annual Data Report, Morbidity and Mortality, Vol.1 CKD, Ch 5, pg 92 http://www.usrds.org/2009 to delineate this condition. They suggest that one of the bi- 11. Goodkin DA, Young EW, Kurokawa K et al. Mortality among hemo- ological prices paid for the increase in our average life span dialysis patients in Europe, Japan, and the United States: case-mix (from around 40 to more than 70 years) is a widespread effects. Am J Kidney Dis 2004; 44: S16S21 dysfunction of arteriolar perfusion. According to them, 12. Yahalom G, Schwartz R, Schwammenthal Y et al. Chronic kidney we are literally outliving our biological means [28]. disease and clinical outcome in patients with acute stroke. Stroke Available data suggest that one logically central goal for 2009; 40: 12961303 13. Tsagalis G, Akrivos T, Alevizaki M et al. Renal dysfunction in acute prevention and treatment in both kidney and brain small stroke: an independent predictor of long-term all combined vascular vessel disease should be the reduction of central pulse events and overall mortality. Nephrol Dial Transplant 2009; 24: pressure. This means reduction of wave reflection by dila- 194200 tion of conduit arteries since drugs do not directly affect 14. Vermeer SE, Longstreth WT Jr, Koudstaal PJ. Silent brain infarcts: a the aorta and large arteries. Angiotensin-converting en- systematic review. Lancet Neurol 2007; 6: 611619 zyme inhibitors, angiotensin receptor blockers and calcium 15. Kobayashi S, Ikeda T, Moriya H et al. Asymptomatic cerebral lacu- nae in patients with chronic kidney disease. Am J Kidney Dis 2004; channel blockers could exert this effect [28]. 44: 3541 The relation between the kidney and the brain still needs 16. Ikram MA, Vernooij MV, Hofman A et al. Kidney function is related clarifications. Whether both are victims of perfusion fail- to cerebral small vessel disease. Stroke 2008; 39: 5561 ure or one is the aggressor and the other the victim is still 17. Fazekas F, Kleinert R, Roob G et al. Histopathologic analysis of foci not known. In the future to come, genetic and/or molecular of signal loss on gradient-echo T2*-weighted MR images in patients research may bring more light into this still grey mater. with spontaneous intracerebral hemorrhage: evidence of microangio- pathy-related microbleeds. Am J Neuroradiol 1999; 20: 637642 18. Vermeer SE, Hollander M, van Dijk EJ et al. Silent brain infarcts and Conflict of interest statement. None declared. white matter lesions increase stroke risk in the general population: the Rotterdam Scan Study. Stroke 2003; 34: 11261129 References 19. Au R, Massaro JM, Wolf PA et al. Association of white matter hy- perintensity volume with decreased cognitive functioning: the Fra- 1. Chobanian AV, Bakris JL, Black HL et al. The Seventh Report of the mingham Heart Study. Arch Neurol 2006; 63: 246250 Joint National Committee on Prevention, Detection, Evaluation, and 20. Prins ND, van Dijk EJ, den Heijer T et al. Cerebral white matter le- Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003; sions and the risk of dementia. Arch Neurol 2004; 61: 15311534 289: 25602572 21. Khatri M, Wright CB, Nickolas TL et al. Chronic kidney disease is 2. Go AS, Chertow GM, Fan D et al. Chronic kidney disease and the associated with white matter hyperintensity volume: the Northern risks of death, cardiovascular events, and hospitalization. N Engl J Manhattan Study (NOMAS). Stroke 2007; 38: 31213126 Med 2004; 351: 12961305 22. Kato H, Izumiyama M, Izumiyama K et al. Silent cerebral micro- 3. Brosius FC III, Hostetter TH, Kelepouris E et alAmerican Heart As- bleeds on T2*-weighted MRI: correlation with stroke subtype, stroke sociation Kidney and Cardiovascular Disease Council; Council on recurrence, and leukoaraiosis. Stroke 2002; 33: 15361540 High Blood Pressure Research; Council on Cardiovascular Disease 23. Viswanathan A, Chabriat H. Cerebral microhemorrhage. Stroke 2006; in the Young; Council on Epidemiology and Prevention; Quality of 37: 550555

4 Nephrol Dial Transplant (2010): Editorial Comments 1373 24. Kinoshita T, Okudera T, Toshio T et al. Assessment of lacunar hem- 27. Nakatani T, Naganuma T, Uchida J et al. Silent cerebral infarction in orrhage associated with hypertensive stroke by echo-planar gradient- hemodialysis patients. Am J Nephrol 2003; 23: 8690 echo T2*-weighted MRI. Stroke 2000; 31: 16461650 28. Thompson CS, Hakim AM. Living beyond our physiological means: 25. Cho A.-H, Lee S.B., Han S.J. et al. Impaired kidney function and small vessel disease of the brain is an expression of a systemic fail- cerebral microbleeds in patients with acute ischemic stroke. Neurol- ure in arteriolar function: a unifying hypothesis. Stroke 2009; 40: ogy 2009; 73: 16451648 e322 26. Shima H, Ishimura E, Naganuma T et al. Cerebral microbleeds in 29. O'Rourke MF, Safar ME. Relationship between aortic stiffening and predialysis patients with chronic kidney disease. Nephrol Dial Trans- microvascular disease in brain and kidney: cause and logic of therapy. plant 2010; 25: 15541559 Hypertension 2005; 46: 200204 Received for publication: 22.12.09; Accepted in revised form: 25.1.10 Nephrol Dial Transplant (2010) 25: 13731375 doi: 10.1093/ndt/gfq086 Advance Access publication 18 February 2010 Effects of icodextrin on the peritoneal membrane Raymond T. Krediet Division of Nephrology, Department of Medicine, Academic Medical Centre University of Amsterdam, Amsterdam, The Netherlands Correspondence and offprint requests to: Raymond T. Krediet; E-mail: [email protected] Fifteen years after the introduction on the market of a tent of glucose degradation products [11]. Studies on 7.5% icodextrin dialysis solution, its share in a state- biocompatibility have given different results. Icodextrin of-the-art dialysis prescription has become quite mean- incubation was associated with reduced viability of ingful. This is because of its superiority to induce fluid peritoneal mesothelial cells, while the phagocytosis ca- removal from the body during long dwells, compared to pacity of peripheral blood neutrophils was similar to solutions with low-molecular-weight osmotic agents, es- that of conventional glucose/lactate solutions [12]. Oth- pecially in patients with a fast solute transport status er studies have shown better phagocytosis [13,14], less [1,2]. Consequently, the use of icodextrin can effectively inhibition of cell growth [15] and reduced IL-6 mRNA reduce over-hydration [3,4]. Although the effects of ico- expression [16]. The general impression of these in vitro dextrin on fluid and solute kinetics are well-known studies is that most of them show no indication for [57], issues with respect to inflammation and mem- a deleterious effect of icodextrin on the peritoneal brane viability are still unclear. The outbreak of a cul- membrane. ture-negative peritonitis in 2001/2002, which was caused by contamination with peptidoglycans [8], raised suspi- Animal studies cion that icodextrin could increase susceptibility to local peritoneal inflammation. In a recent abstract presented at Experimental studies in rodents are often difficult to in- the congress of the American Society of Nephrology on terpret because these animals have very high plasma factors associated with encapsulating peritoneal sclerosis, and, therefore, also dialysateamylase activities. This the duration of icodextrin treatment was independently as- leads to a faster degradation of icodextrin into its me- sociated with this complication [9]. Although this observa- tabolites in the peritoneal cavity than in humans [17,18]. tion is preliminary and should be confirmed in other It explains the rise in dialysate osmolality during a studies, it was reason to review the old and recent litera- dwell with 7.5% icodextrin in rats [19]. It is unknown ture on possible effects of icodextrin on the peritoneal whether these locally formed oligosaccharides could membrane. have effects on peritoneal membrane morphology. An- other drawback of animal studies is that they are often performed in animals with normal renal function. These In vitro studies animals may, to some degree, be protected from accu- mulation of icodextrin degradation products because a Incubation of albumin with icodextrin leads to a re- part of these will be removed by glomerular filtration, duced formation of the advanced glycosylation end followed by uptake in the proximal tubule and further product pentosidine [10], probably due to its low con- degradation. The Author 2010. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: [email protected]

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