OBSERVATIONS ON THE ACIDIFYING CAPACITY OF THE EXPERIMENTALLY DISEASED KIDNEY IN THE DOG*

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Abstract
The patterns of ammonium and titratable acid excretion were investigated in dogs with experimental renal disease. In the majority of experiments, one kidney in the experimental model was maintained free of disease so as to permit comparison of the acidifying capacity of a diseased kidney with that of an intact kidney subsisting in the same environment. In addition, several experiments were performed on an animal with bilateral disease of different severity in the two kidneys. Exogenous metabolic acidosis was produced by administering ammonium chloride for 1 to 5 days preceding clearance measurements. Excretion of both ammonium and titratable acid per unit of glomerular filtrate was closely comparable in experimental and control kidneys and bicarbonate reabsorption was virtually complete bilaterally. Thus, both total hydrogen ion secretion and net hydrogen ion excretion per unit of glomerular filtrate remained equal in experimental and control organs. These results indicate that under conditions evoking high rates of acid excretion, there is an organized pattern of proton transfer in the functioning nephrons of the experimentally diseased kidney of the dog. The relevance of these data to the interpretation of acidifying capacity in the human with chronic uremic acidosis is considered in the discussion.