GFR Loss Research Articles

Long‐Term Consequences of Live Kidney Donation Follow‐Up in 93% of Living Kidney Donors in a Single Transplant Center

Live kidney donation is increasing rapidly. Increases of blood pressure and proteinuria but no accelerated loss of renal function in kidney donors have been described. The credibility of this research is hampered by retrieval rates of only 50-70% of donors. We studied renal function, blood pressure, proteinuria, parathyroid hormone, 1,25(OH)2 cholecalciferol and calcium and phosphate excretion in a live kidney donor cohort with a 93% retrieval rate. A comprehensive physical and laboratory examination including 24-h urine collection was conducted. None of the 152 donors had renal failure. Mean time after uninephrectomy was 11 +/- 7 (range: 1-28) years. GFR had declined by 25%. Blood pressure had increased from 125 +/- 15/79 +/- 11 to 134 +/- 19/81 +/- 9 mmHg (p < 0.01) but remained significantly below normal. Fifty six percent of donors developed proteinuria (>150 mg/day), but only 10% had albuminuria. Nineteen percent had increased PTH, 30% had a decreased tubular reabsorption rate of phosphate. Regarding risk factors for a higher loss of GFR, greater increases in blood pressure or proteinuria no consistent picture emerged. Because of the high incidence of proteinuria and possible changes in bone metabolism inclusion of kidney donors in registries appears worthwhile.

The Influence of Demographic Factors and Modality on Loss of Residual Renal Function in Incident Peritoneal Dialysis Patients

To determine whether gender, race, diabetes, peritoneal dialysis (PD) modality, and comorbid conditions influence loss of residual renal function (RRF). Retrospective study of incident PD patients, using database of prospectively collected demographic, laboratory, and clearance data. Peritoneal Dialysis Registry of the University of Pittsburgh Medical Center. The study included 184 continuous ambulatory PD and automated PD patients who had at least two 24-hour urine collections for glomerular filtration rate (GRF) between April 1991 and March 2000. 836 urine collections were analyzed. Loss of RRF was defined as the slope of the decline in GFR as measured by the average of creatinine and urea clearances in 24-hour urine collections. Stepwise forward regression was used to identify demographic and laboratory factors associated with loss of GFR. Spearman correlations were used to assess the significance of associations. The median rate of decline of renal function was -0.17 mL/minute/month. Gender, race, diabetes, automated PD, peritoneal equilibration test, protein equivalent of nonprotein nitrogen appearance normalized to body surface area, and serum albumin did not predict loss of RRF. Cardiac disease was the only variable affecting decline of RRF (p = 0.045). Modality of PD and patient demographic factors do not contribute to the rate at which RRF is lost in incident PD patients. Additional study of the factors contributing to the decline and maintenance of RRF is needed.

Children who participated in school extracurricular activities were less likely to drop out or to have been arrested

Late antibody-mediated rejection (ABMR) is a leading cause of kidney allograft failure. Uncontrolled studies have suggested efficacy of the proteasome inhibitor bortezomib, but no systematic trial has been undertaken to...

Effect of nitric oxide inhibition on blood pressure and renal function in TGR(mRen2)27 rats.

We examined the effect of acute systemic blockade of nitric oxide synthesis on blood pressure and renal function in the monogenetically hypertensive TGR(mRen2)27 rat strain. Untreated conscious transgenic rats had significantly (p < 0.01) higher systolic blood pressures (185 +/- 9 versus 130 +/- 5 mm Hg) and urinary albumin excretion (32 +/- 5 versus 6 +/- 2 mg/day) than did control animals without evidence of renal insufficiency. Plasma and urinary nitric oxide metabolite levels did not differ between transgenic and control rats. i.v. administration of NG-nitro-L-arginine methyl ester (10 mg/kg) to both groups caused similar elevations in systemic blood pressure (transgenic 25 +/- 3 versus control 24 +/- 3 mm Hg). NG-Nitro-L-arginine methyl ester induced reductions in whole kidney (1.4 +/- 0.2 versus 0.7 +/- 0.1 mL/min), and single nephron (23 +/- 3 versus 11 +/- 2 nL/min) glomerular filtration rates were significantly (p < 0.05) larger in transgenic than in control rats. This greater loss of GFR in transgenic animals was caused by a larger reduction in glomerular ultrafiltration coefficient (1.8 +/- 0.2 versus 1.1 +/- 0.1 nL x min[-1] x mmHg[-1], p < 0.05), a larger increase in afferent arteriole resistance (3.4 +/- 0.2 versus 1.4 +/- 0.1 dyne x s x cm[-5], p < 0.05), and a subsequently smaller rise in glomerular transcapillary pressure (10 +/- 1 versus 5 +/- 1 mmHg, p < 0.05). These results indicate that the renal microvasculature and glomerular hydraulic conductivity or surface area of transgenic rats are more sensitive to nitric oxide inhibition and are consistent with an important role for nitric oxide in TGR(mRen2)27 kidney function.