A case report is presented which illustrates the massive urinary loss of sodium, chloride and water which occasionally develops after relief of urinary tract obstruction. Astonishingly high rates of solute and water excretion occurred in this particular patient, apparently, at least partly, the result of an unexpectedly high (normal) glomerular filtration rate and almost certainly augmented unnecessarily by the intravenous administration of glucose-containing fluids with consequent glycosuria. The data collected support the conclusion of Bricker et al.  that the proximal portion of the nephrons is the principal site of defective sodium reabsorption. During at least one phase of the diuresis, 24 to 36 hours after its onset, renal excretion of sodium and chloride decreased during an intravenous infusion of 9-alpha-fluorohydrocortisone; however, it is not certain that this was a cause and effect relationship. During the same period evidence was obtained which is interpreted as indicating that the renal tubules were responsive to vasopressin but that the usual renal medullary hypertonicity had been eliminated by the massive solute flow through the loops of Henle.
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