No abstract

Angiotensin-converting enzyme inhibitors can decrease proteinuria and preserve glomerular filtration rate in patients with diabetes. These effects occur independent of changes in systemic blood pressure.

Background There have been few prospective controlled studies of kidney donors. Understanding the pathophysiological effects of kidney donation is important for judging donor safety and for improving our understanding of the consequences of reduced kidney function in chronic kidney disease. Study Design Prospective, controlled, observational cohort study. Setting & Participants Three-year follow-up of kidney donors and paired controls suitable for donation at their donor’s center. Predictor Kidney donation. Outcomes Medical history, vital signs, glomerular filtration rate and other measurements at 6, 12, 24 and 36 months after donation. Results At 36 months, 182 of 203 (89.7%) original donors and 173 of 201 (86.1%) original controls continue to participate in follow-up visits. The linear slope of the glomerular filtration rate measured by plasma iohexol clearance declined 0.36±7.55 mL/min per year in 194 controls, but increased 1.47±5.02 mL/min per year in 198 donors (P = 0.005) between 6 and 36 months. Blood pressure was not different between donors and controls at any visit, and at 36 months all 24-hour ambulatory blood pressure parameters were similar in 126 controls and 135 donors (mean systolic: 120.0±11.2 [SD] v. 120.7±9.7 mmHg [P=0.6]; mean diastolic: 73.4±7.0 v. 74.5±6.5 mmHg [P=0.2]). Mean arterial pressure nocturnal dipping was manifest in 11.2%±6.6% of controls and 11.3%±6.1% donors (P=0.9). Urinary protein-creatinine and albumin-creatinine ratios were not increased in donors compared to controls. From 6 to 36 months post-donation, serum parathyroid hormone, uric acid, homocysteine and potassium levels were higher, whereas hemoglobin was lower in donors compared to controls. Limitations Possible bias resulting from an inability to select controls screened to be as healthy as donors, short follow-up duration, and drop-outs. Conclusions Kidney donors manifest several of the findings of mild chronic kidney disease. However, at 36 months after donation, kidney function continues to improve in donors while controls have expected age-related declines in function.

With the exception of calcium antagonists, nearly all antihypertensive agents affect serum lipids. These effects differ among patient populations.

No abstract

Background Most previous studies of living kidney donors have been retrospective and have lacked suitable healthy controls. Needed are prospective controlled studies to better understand the effects of a mild reduction in kidney function from kidney donation in otherwise normal individuals. Study Design Prospective, controlled, observational cohort study. Setting & Participants Consecutive patients approved for donation at 8 transplant centers in the US were asked to participate. For every donor enrolled, an equally healthy control with 2 kidneys who theoretically would have been suitable to donate a kidney was also enrolled. Predictor Kidney donation. Measurements At baseline pre-donation and at 6 months after donation, a medical history, vital signs, measured (iohexol) glomerular filtration rate and other measurements were collected. There were 201 donors and 198 controls that completed both baseline and 6 month visits and form the basis of this report. Results Compared to controls, donors had 28% lower glomerular filtration rate at 6 months (94.6±15.1 [SD] v. 67.6±10.1 mL/min/1.73m2; P<0.001), associated with a 23% greater parathyroid hormone (42.8±15.6 v. 52.7±20.9 pg/mL; P<0.001), 5.4% lower serum phosphate (3.5±0.5 v. 3.3±0.5 mg/dL; P<0.001), 3.7% lower hemoglobin (13.6±1.4 v. 13.1±1.2 g/dL; P<0.001), 8.2% greater uric acid (4.9±1.2 v. 5.3±1.1 mg/dL; P<0.001), 24% greater homocysteine (1.20±0.34 v. 1.49±0.43 mg/L; P<0.001), and 1.5% lower high density lipoprotein cholesterol (54.9±16.4 v. 54.1±13.9 mg/dL; P=0.03) level. There were no differences in albumin-creatinine ratios (5.0 [IQR, 4.0-6.6] v. 5.0 [IQR, 3.3-5.4] mg/g; P=0.5), office blood pressure, or glucose homeostasis. Limitations Short duration of follow-up and possible bias resulting from an inability to screen controls with kidney and vascular imaging performed in donors. Conclusions Kidney donors have some, but not all, abnormalities typically associated with mild chronic kidney disease 6 months after donation. Additional follow up is warranted.

No abstract

The relationship between specific histopathologic findings of chronic rejection (CR) and the clinical course of renal transplant recipients with a chronic progressive decline in allograft function (CPDAF) is unknown. We used one or two hinged regression lines, fitted by least-squares to serial creatinine clearances, to define the onset and clinical course of CPDAF. Biopsies (N = 100) from patients transplanted from 1978 to 1982 were studied retrospectively. Interstitial fibrosis, tubular atrophy, and fibrointimal arterial narrowing were more pronounced in biopsies obtained after, but not before the onset of CPDAF. Interstitial hemorrhage, an infrequent finding in acute vascular rejection, preceded the onset of CPDAF, but the more common histologic findings of acute cellular rejection did not. The severity of histologic features of CR (as reflected by a score combining fibrointimal arterial narrowing, interstitial fibrosis, tubular atrophy, glomerular sclerosis, glomerular mesangial expansion, and glomerular basement membrane reduplication) correlated with the duration of subsequent allograft survival (r = -0.65, P less than 0.001). Glomerular size increased after transplantation, but was not different in patients with or without CPDAF, suggesting that mechanisms related to compensatory hypertrophy did not play a major role in the pathogenesis of CR. In summary, the histologic findings of CR did not predict the onset of CPDAF, did not distinguish whether the pathogenesis was mediated by immune or nonimmune events, but did correlate with the duration of subsequent allograft survival.