The acidosis of chronic renal failure.
The acidosis of chronic renal failure is not due to bicarbonate wastage per se; rather, bicarbonate reabsorption per nephron is markedly enhanced. The ability to lower the urine pH is preserved. While overall ammonium production may be decreased in chronic renal failure, both ammonium production and excretion are markedly increased when expressed per remaining nephron. Titratable acid excretion in chronic renal failure is essentially maximal, owing to the effect of parathyroid hormone on phosphate excretion by the kidney. Thus, it appears that the acidosis of chronic renal failure is solely the consequence of the reduction in functional renal mass. Extrarenal buffering may contribute substantially to the maintenance of a near normal acid-base status in patients with marked reduction in glomerular filtration rate. That homeostasis is so well preserved until glomerular filtration rate falls to approximately 10 per cent of normal is remarkable; the price, however, may be considerable. Prolonged acidosis may magnify the tendency of renal failure to cause osteodystrophy. An obvious treatment for the acidosis of renal failure is exogenous alkali therapy. Most clinicians withhold alkali therapy until the bicarbonate concentration falls below 20 mEq per L. If the acidosis cannot be safely corrected with exogenous therapy, dialysis should be initiated.
D000138:Acidosis / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D000641:Ammonia / Q000652:urine; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D002021:Buffers; D002712:Chlorides / Q000378:metabolism; D006801:Humans; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*
D001639:Bicarbonates; D002021:Buffers; D002712:Chlorides; D000641:Ammonia