THE INFLUENCE OF GLOMERULAR FILTRATION RATE, SOLUTE EXCRETION AND HYDRATION ON THE CONCENTRATING MECHANISM OF THE EXPERIMENTALLY DISEASED KIDNEY IN THE DOG *

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Abstract
The present observations, in concert with studies previously reported provide evidence that the concentrating ability of the experimentally diseased kidney in the dog is not markedly impaired when the contralateral kidney is intact and the internal environment remains essentially normal. Comparison of the concentrating ability of the diseased kidney with that of the normal kidney, however, did reveal certain differences. In the hydropenic state this was reflected by a lower value for maximal urinary osmolality; and during hign rates of urine flow induced by mannitol infusion, values for solute -free water abstracted/100 ml of glomerular filtrate (TCH2O/GFR) were less for the diseased kidney. The slightly lower values for TCH2O/GFR character-istically were associated with excretion of a greater fraction of filtered solute and Na, lower urinary osmolalities and higher urinary Na concentrations. These same differences have been noted between hemiinfarcted kidneys (in which the residual nephrons are free of a progressive renal disease) and the contralateral normal kidneys. Moreover, the differences could be diminished substantially by decreasing the filtration rate to the diseased kidney through experimental constriction of the renal artery and also by constriction of the aorta. The data indicate that the structural abnormalities of the 3 forms of experimental renal disease did not render the concentrating mechanism impotent. It had also been suggested that the modest diminution in concentrating ability (and the associated changes in solute excretion) in the diseased kidneys may have been related, at least in part, to functional adaptations in intact residual nephrons.