METABOLIC-ACIDOSIS DOES NOT CONTRIBUTE TO CHRONIC RENAL INJURY IN THERAT

1. Metabolic acidosis invariably accompanies chronic renal failure, an d short periods of metabolic acidosis cause renal growth and proteinur ia in normal rats. Rates of ammoniagenesis are increased in chronic re nal failure, and it has been suggested that this contributes to diseas e progression. This study assessed (i) whether prolonged acidosis caus es chronic renal injury in the normal kidney and (ii) whether abrogati on of acidosis slows disease progression in the remnant kidney. 2. Met abolic acidosis was induced in normal rats by dietary hydrochloric aci d. Urinary excretion of total protein, lysozyme and albumin increased, peaking at week 8 but returning to baseline by week 14. At killing af ter 14 weeks, kidney weights, glomerular filtration rates and serum cr eatinine were the same in both groups, but kidney/body weight and kidn ey/heart weight ratios were greater in the acidotic group. All kidneys were normal by light microscopy. 3. Rats subjected to five-sixths nep hrectomy were given sufficient dietary bicarbonate to abolish uraemic acidosis, and their outcome was compared with that of non-alkalinized remnants (controls). Proteinuria, glomerular filtration rates, blood p ressure, histological injury and time to the development of terminal u raemia were no better in bicarbonate-supplemented animals than in cont rols. 4. These data demonstrate that metabolic acidosis neither causes nor exacerbates chronic renal injury. We conclude that the treatment of uraemic acidosis is unlikely to influence disease progression in pa tients with chronic renal failure.