ter Wee P M
Department of Nephrology, Free University Hospital, Amsterdam, The Netherlands.
Semin Nephrol. 1995 Sep;15(5):426-32.
In the early 1980s, renewed interest was focused on the possible protective effect of protein-restricted diets on the progression of human renal insufficiency. This resulted from observations in several models of experimental renal failure in which protein-restricted diets attenuated the progression of renal insufficiency. Micropuncture studies in subtotally nephrectomized rats and rats with other causes of renal insufficiency had shown that glomerular hyperfiltration occurred in remnant glomeruli to compensate for the loss of renal function. However, such rats developed progressive glomerular sclerosis. In rats fed a protein-restricted diet, such glomerular hyperfiltration did not occur and the development of renal insufficiency was postponed. Thus, it was hypothesized that the compensatory hyperfiltration of remnant glomeruli was ultimately harmful to the kidneys. At the same time, concomitant research was started to establish methods to show the presence of glomerular hyperfiltration in humans, in an attempt to trace patients who could benefit from protein-restricted diets. Thus, the effects of an acute protein load, given as a meat meal or intravenous administration of amino acids, on renal hemodynamics were investigated resulting in the introduction of the concept of renal reserve capacity. In the present report, the effects of intravenously administered amino acids on renal hemodynamics of subjects with and without renal disease will be discussed. Special interest will be focused on the amino acid-induced hormonal changes and their involvement in the renal hemodynamic changes observed during amino acid infusion.
