CARBON TETRACHLORIDE POISONING IN MAN. I. THE MECHANISMS OF RENAL FAILURE AND RECOVERY 1

Open Access
Publisher Website
Google Scholar
Abstract
Studies of renal function were performed in 4 adult male subjects with acute renal insufficiency caused by inhalation of CCl4 vapors. The renal plasma flow, as measured by means of the Fick principle with p-aminohippuric acid (PAH) as the test substance, was markedly depressed during the late oliguria and early recovery phases, as was the renal extraction of PAH. During these latter phases the renal clearances of PAH, inulin, endogenous creatinine and urea, the maximum tubular secretory capacity for PAH (Tm PAH), the selective reabsorption of water, the ability to secrete phenol red and to elaborate a concd. urine were all markedly impaired. With the onset of diuresis the renal clearance values for inulin, endogenous creatinine and urea revealed little change. For this reason rising plasma concns. of nitrogenous substances occurred in spite of adequate urine output for 1-3 days. Following this there was a rapid rise in the clearance values and a concomitant fall in the plasma creatinine and urea concns. By about the 40th day from the onset of oliguria the renal clearances of endogenous creatinine, inulin and PAH had returned to between 40 and 70% of the expected normal values. During this period the relative increments of the endogenous creatinine clearances were greater than the PAH clearances which in turn were greater than the inulin clearances. 80% of the expected normal clearance values for these 3 substances were reached between the 100th and 200th day. Tm PAH returned to the expected normal values for 3 subjects soon after the 40th day. Proteinuria disappeared between the 29th and 37th days and abnormal urinary sediment between the 20th and 26th days. The ability to elaborate a urine with a specific gravity of at least 1.025 returned between 96 and 220 days. It is believed that early anuria is the result of severe tubular damage, due to either specific nephrotoxic action or prolonged anoxia, the glomerular filtrate thus being lost through passive back-diffusion into the renal interstitium, and that in late anuria or oliguria, in addition to back-diffusion, there is a marked depression of renal blood flow and glomerular filtration. Diuresis may start without a discernable increase in glomerular filtration, the rising urine output being primarily a result of decreased tubular back-diffusion.