Increased aortic stiffness is a major factor responsible for the high cardiovascular mortality in patients with end-stage renal disease, but the impact of kidney transplantation on recipient aortic stiffness remains poorly defined. The use of expanded-criteria kidney donors is associated with decreased recipient survival compared with the use of standard-criteria donors, although the underlying mechanisms are incompletely understood. It was hypothesized that donor characteristics may affect recipient aortic stiffness, which may contribute to cardiovascular mortality in these patients. Aortic stiffness was evaluated by measurement of carotid-femoral pulse wave velocity in 74 cadaveric kidney recipients at 3 and 12 mo after transplantation. At 3 mo, aortic stiffness was associated exclusively with recipient-related factors: Age, gender, and mean BP. At 12 mo, age of the donor kidney emerged as an additional determinant. The change in aortic stiffness between 3 and 12 mo strongly correlated with donor age; stiffness improved in recipients of young kidneys (first tertile of donor age) and worsened in recipients of older kidneys (upper tertile of donor age). At 12 mo, the carotid-femoral pulse wave velocity was Ͼ1 m/s higher in recipients of the oldest kidneys than in the recipients of younger kidneys. The association between donor age and aortic stiffness was independent of recipient age, gender, mean BP, pretransplantation dialysis duration, conventional cardiovascular risk factors, medication, posttransplantation events, and GFR. These results demonstrate that the impact of kidney transplantation on recipient aortic stiffness is dependent on donor age and suggest that ongoing damage to large arteries might contribute to the mechanism underlying the association of old-donor kidneys and increased cardiovascular mortality. 19: 798 -805, 200819: 798 -805, . doi: 10.1681 Successful renal transplantation confers significant survival advantage compared with dialysis. 1 An important component of this benefit is long-term reduction of cardiovascular (CV) progression and mortality. 2 Nonetheless, the annual risk for CV death in transplant recipients remains 50-fold higher than in the general population. 3 Premature CV death with a functioning graft is one of the leading factors in reducing long-term graft survival overall. Thus, reduction in CV mortality would dramatically improve longterm results of kidney transplantation. J Am Soc NephrolLarge-artery damage is one of the most important factors responsible for the high prevalence of

SUMMARY Effects of hemodialysis on extracellular fluid volume distribution, left ventricular volumes, and cardiac output were determined In patients with end-stage renal disease (n = 19). Distribution of extracellular fluid loss from hemodialysis differed widely among patients, so that weight change correlated weakly with contraction of total blood volume (index of determination 29%, p < 0.05). End-diastolic volume (EDV) decreased from 150 ± 49 ml (mean ± SD) to 118 ± 42 ml, p < 0.001; stroke volume (SV) decreased from 108 ± 36 to 86 ± 33 ml (p < 0.001) without change in ejection fraction (from 0.73 ± 0.09 to 0.74 ± 0.11).A significant correlation was found between total blood volume (TBV) and EDV before (r = 0.66, p < 0.005) and after dialysis (r = 0.61, p < 0.01). The correlation between TBV and SV was highly significant before (r = 0.78, p < 0.001) and after dialysis (r = 0.66, p < 0.005), but there was no correlation between change in TBV and change in EDV or in SV. The ratio of EDV to TBV (EDV/TBV X 100) was reduced significantly from 3.49 ± 0.92 to 3.06 ± 0.97, p < 0.001). There results suggest that, although intravascular volume was the major determinant of cardiac output in dialyzed patients, the postdialysis reduction in cardiac output might be related more to the relocation of blood volume than to the absolute degree of blood volume contraction. 8 These include determination of the relative participation from both intravascular and interstitial compartments to the total ECF loss during hemodialysis as well as the effect of hypovolemia on cardiac filling and possible influence of changed preload on cardiac output.

SUMMARY Blood pressure response to hemodialysis was investigated in IS patients with end-stage kidney disease; mean arterial pressure was unchanged in fire (Group 1) and reduced 10 mm Hg in 10 (Group 2). The two groups did not differ significantly with regard to either biochemical rallies or hemodynamic indices before dialysis, and both sustained comparable reduction in body weight, total blood volume, and cardiac output following dialysis. Heart rate remained unchanged In both. The only significant difference between the two was the response of total peripheral resistance (TPR) to fluid depletion. TPR rose adequately in Group 1 but was unchanged in Group 2 (7.5 ± 2.2 (SE) VS 0.7 ± 1.1 units, p < 0.02S) despite equal fall in cardiac output in both (881 ± 212 vs 890 ± 173 ral/m, p > 0.10). Thus, differences in arterial pressure response to fluid loss by hemodialysis could be due to impaired autonomic control of resistance vessels; this abnormality might not be revealed by tests of baroreceptor activity that depend only on heart rate responses to blood pressure variations. UREMIC patients frequently present difficulties in management during hemodialysis, particularly because of severe hypotension in some patients. This has been related either to the magnitude of fluid loss or to the autonomic neuropathy that has been reported in renal insufficiency.

The management of sickle cell nephropathy (SCN) at an early stage is an important issue to prevent renal and cardiovascular morbidity and mortality. This study aimed to evaluate in this population, whether angiotensin converting enzyme inhibitors (ACEIs) treatment could exert a cardio-renal protection in a SCN cohort. Forty-two SCN patients (urine albumin:creatinine ratio (ACR) > 10 mg/mmol) were treated with ACEIs for 6 months, then evaluated for ACR, measured glomerular filtration rate (mGFR) together with haematological and cardiovascular parameters. A 1-month washout was also performed in order to differentiate short- and long-term ACEIs effects. A decrease in ACR baseline value (>30%) was detected in 62% of cases (mean ACR: 46·4 ± 7·6 and 26·4 ± 3·9 mg/mmol at baseline and 6 months respectively; P = 0·002), whereas mGFR values were unchanged. ACR decrease was detected at 1 month following ACEI initiation (32·9 ± 6·9, P = 0·02) with a persistent trend after withdrawal (P = 0·08). ACEIs also decreased diastolic blood pressure (P = 0·007), pulse wave velocity (P = 0·01), tricuspid regurgitation velocity (TRV; P = 0·04), asymmetric dimethyl arginine (ADMA: P = 0·001) and haemoglobin (P = 0·01) while conventional haemolytic biomarkers were unchanged. Our data suggest that ACEIs are safe and effective at decreasing albuminuria in sickle cell patients with a beneficial effect on specific mortality risk factors, such as TRV and asymmetric dimethyl arginine.