Acid-Base, Electrolytes, and Renal Failure

1 Metabolic acidosis is a wellrecognized component of chronic renal failure (CRF). Metabolic acidosis in renal failure results primarily from the limited ability of failing kidneys to excrete hydrogen ions and regenerate bicarbonate. Normal acid-base balance is maintained by a combination of tubular reabsorption of filtered bicarbonate and excretion of hydrogen ions with ammonia and urinary buffers, primarily HPO4 (termed titratable acidity). Renal excretion of hydrogen ions effectively regenerates bicarbonate lost via the gastrointestinal or urinary tracts or through respiratory buffering of metabolic acids. As the quantity of functioning renal mass declines in CRF, hydrogen ion excretion is maintained largely by increasing the quantity of ammonium excreted by surviving nephrons. However, at some level of renal dysfunction, the capacity to further increase renal ammoniagenesis is lost and metabolic acidosis ensues. It is assumed that the fall in total ammonium excretion that occurs in advanced renal failure results from the limited number of functioning nephrons. Decreased medullary recycling of ammonia due to structural renal damage may also contribute to impaired ammonium excretion. In a retrospective case series of cats with renal failure, approximately 80% had metabolic acidosis based on decreased venous blood pH values and bicarbonate concentrations. In contrast, acidosis appears to occur less consistently in dogs with chronic renal failure. There is some evidence that feline kidneys may respond differently to metabolic acidosis as compared with other mammalian species studied. One investigator has shown that acidosis fails to increase the rate of production of ammonia in cultured feline proximal tubular cells. Whether cats are at increased risk for developing metabolic acidosis because of this limitation is unknown, but the unexpectedly high incidence of acidosis in cats with CRF would be consistent with this suggestion. Although species-related differences in renal acid excretion may contribute to this apparent difference, it is likely that the high incidence of uremic acidosis in cats relates, at least in part, to the acidifying nature of many cat foods. It has been speculated that routine use of acidifying diets may contribute to the relatively high incidence of chronic renal failure observed in cats over the past decade. Further, uremic acidosis may contribute to the chronic wasting typical of renal failure.