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On average, the remaining renal function of kidney donors did not deteriorate more rapidly than what may be expected from ageing. However one-third of the female and half of the male donors developed hypertension and, approximately, 10% displayed proteinuria. Nevertheless, our study supports the continued use of living kidney donors if strict criteria are used for acceptance.

Abstract. Pentosidine is an advanced glycation end-product (AGE), formed by glycosylation and oxidation, that accumulates markedly in end-stage renal disease (ESRD). It has been speculated that AGE and carbonyl stress contributes to longterm complications such as cardiovascular disease (CVD) in ESRD patients. This study determined plasma levels of pentosidine as well as the presence of inflammation (CRP Ն 10 mg/L), clinical CVD (CVD clin ), and malnutrition (subjective global assessment [SGA] Ͼ 1) in a cohort of 191 ESRD patients, median age of 55 yr (range, 23 to 70 yr) and median GFR ϭ 7 ml/min (range, 2 to 17 ml/min), close to start of renal replacement therapy. Fifty-one elderly subjects, median age of 82 yr (range, 71 to 110 yr), with mild renal impairment, median GFR ϭ 67 ml/min (range, 38 to 113 ml/min), were also studied for comparative analysis of plasma pentosidine. The plasma pentosidine content was elevated in all patients compared with the levels in the elderly subjects and were negatively correlated with GFR both in the ESRD patients (Rho ϭ Ϫ0.24; P Ͻ 0.01; n ϭ 159) and in the elderly subjects (Rho ϭ Ϫ0.31; P Ͻ 0.05). Moreover, the plasma pentosidine content was correlated with age in the ESRD patients (Rho ϭ 0.26; P Ͻ 0.001) and in the elderly subjects (Rho ϭ 0.44; P Ͻ 0.001). The 63 malnourished ESRD patients (35%) had a significantly higher (P Ͻ 0.05) median plasma pentosidine than the well-nourished patients (39 versus 27 pmol/mg albumin). Similarly, 73 inflamed patients (38%) had a significantly higher (P Ͻ 0.001) median pentosidine content compared with 118 non-inflamed patients (37 versus 24 pmol/mg albumin). Also, the plasma pentosidine content showed weak but significant positive correlations with CRP (Rho ϭ 0.28; P Ͻ 0.0001), fibrinogen (Rho ϭ 0.23; P Ͻ 0.01; n ϭ 126), IL-6 (Rho ϭ 0.22; P Ͻ 0.01; n ϭ 169), and soluble vascular cellular adhesion molecule-1 (Rho ϭ 0.38; P Ͻ 0.001; n ϭ 74). On the other hand, no significant differences in plasma pentosidine content were noted between the patients with and those without CVD clin (32 versus 27 pmol/mg albumin, respectively). Analyses of all-cause mortality, by KaplanMeier, showed that mortality was not linked to the plasma pentosidine content. Moreover, survival analysis by the Cox regression model showed that age (P Ͻ 0.001), diabetes mellitus (P Ͻ 0.01), malnutrition (P Ͻ 0.01), and CVD clin (P Ͻ 0.01) independently predicted poor outcome, whereas an elevated plasma pentosidine content did not. The present study shows that an elevated plasma pentosidine content in ESRD patients is significantly associated with both inflammation and malnutrition and confirms that low residual renal function and high age further contribute to an increased plasma pentosidine content. However, in this small cohort, the plasma pentosidine content did not predict outcome. Thus, accumulation of plasma pentosidine is unlikely to be an appropriate clinically useful marker to predict mortality in ESRD patients.It is now well established that the extremely high cardiov...

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In all 0.5% of the donors developed ESRD. Due to high age of the uremic donors, there seems to be no increased incidence.

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GFR decreases by approximately 1.05 ml/min per year in very old persons. S-urea seems to be more sensitive than s-creatinine for indicating renal function in the elderly. The best formula for estimation of clearance is that of Levey. The Cockroft-Gault formula seems to underestimate GFR.

We investigated the phenotypic expression of factor H mutations in two patients with atypical hemolytic uremic syndrome (HUS). Factor H in serum was assayed by rocket immunoelectrophoresis, immunoblotting, and double immunodiffusion and in tissue by immunohistochemistry. Functional activity was analyzed by hemolysis of sheep erythrocytes and binding to endothelial cells. A homozygous mutation in complement control protein (CCP) domain 10 of factor H was identified in an adult man who first developed membranoproliferative glomerulonephritis and later HUS. C3 levels were very low. The patient had undetectable factor H levels in serum and a weak factor H 150 kDa band. Double immunodiffusion showed partial antigenic identity with factor H in normal serum owing to the presence of factor H-like protein 1. Strong specific labeling for factor H was detected in glomerular endothelium, mesangium and in glomerular and tubular epithelium as well as in bone marrow cells. A heterozygous mutation in CCP 20 of factor H was found in a girl with HUS. C3 levels were moderately decreased at onset. Factor H levels were normal and a normal 150 kDa band was present. Double immunodiffusion showed antigenic identity with normal factor H. Factor H labeling was minimal in the renal cortex. Factor H dysfunction was demonstrated by increased sheep erythrocyte hemolysis and decreased binding to endothelial cells. In summary, two different factor H mutations associated with HUS were examined: in one, factor H accumulated in cells, and in the other, membrane binding was reduced.