Myth: Kidney donation does not jeopardize function in the remaining kidney

Abstract

If results in experiments in rodents were directly translatable to humans, live donor kidney transplantation would have been seriously constrained by the physician’s primary mandate of “first do no harm.” In some rat strains such as the Munic Wistar, reduction in renal mass per se induces a nephroinjurious sequence of increase in intraglomerular pressure, hyper-tension, glomerular hyperfiltration, proteinuria, and ultimately, renal insufficiency. Termed the “Brenner Hypothesis” (1), these pathophysiologic events cast a pall on the long-term integrity of residual nephrons in human kidney donors. Indeed, initial studies of kidney donors indicated a higher rate of proteinuria and hypertension than that of age and gender matched healthy controls. Upon reflection, however, it was appreciated that these donors were family members of individuals who developed kidney disease and thus might themselves be at greater genetic risk for hypertension and proteinuria than the population at large.