A B S T R A C T The concentration of serum albumin in proximal tubule fluid of normal rats and animals with aminonucleoside nephrosis was studied using renal micropuncture techniques. Albumin was quantitated by an ultramicrodisc electrophoresis method capable of measuring 3 X 10'" g of albumin, in 10 nl volumes. With this sensitivity., only small samples of tubule fluid were required for analysis. Collectifn times could be kept short, therefore decreasing the opportunity for sample contamination with extraneous serum albumin. The measured mean concentration of albumin in proximal tubule fluid (1 mg/100 ml in females and 0.7 mg/ 100 ml in males) was somewhat lower than values reported by others, but even these values are apt to have been artifactually high as a result of animal preparation and trace contamination of samples during micropuncture. Rats injected with aminonucleoside of puromycin 4 days earlier, showed a significant increase in tubulefluid albumin concentration coincident with a fall in serum albumin concentration and a 43-fold increase in urine albumin concentration. Tubular absorption of albumin was small relative to that of water. Although albumin filtration was significantly increased over that in normal animals, the glomerular basement membrane still served as a highly efficient barrier to albumin transfer.

Inulin and mannitol clearances, BUN concentrations and renal morphologic alterations were studied in rats 24 h after the injection of low doses of mercuric chloride. Water drinking rats given 4.7 mg/kg body weight of HgCl₂ developed renal failure and severe tubular necrosis. Their clearance of inulin was decreased to the same degree as their simultaneously determined mannitol clearance. Any significant change in tubular permeability should have resulted in a greater loss of mannitol than inulin, and it is suggested that tubular permeability to neither molecule was greatly increased. This is supported by the fact that rats drinking one percent saline in place of tap water for a month prior to receiving the same dose of HgCl₂ showed insignificant changes in inulin clearance and minimal elevations in BUN concentration. Nevertheless, histologic sections of their kidneys showed frank tubular necrosis that was equally severe as, but slightly less extensive than that observed in the water drinking rats whose inulin clearance was 6 % of normal. In view of these findings, it seems unlikely that alterationin tubular permeability per se are responsible for the development of acute renal failure in low dose mercury poisoning. The protective effect of salt loading does not depend on the prevention of tubular injury, and may well reflect inhibition of pre-glomerular vasoconstriction by suppression of the renin-angiotensin axis.

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Enzyme histochemical techniques were utilized to examine the progression and extent of proximal tubular injury during the development of cis-diamminedichloroplatinum (II) (CDDP)-induced acute renal failure. Acute renal failure was induced in male rats by the intraperitoneal administration of 10 mg CDDP/kg body weight. At 6, 24, 48, 72, and 96 hr following treatment, renal function was assessed and tissue was collected for renal morphologic and enzyme histochemical studies. The enzymes examined were gamma-glutamyl transpeptidase, alkaline phosphatase, sodium-potassium ATPase (nitrophenyl phosphatase), acid phosphatase, glucose-6-phosphatase, succinic dehydrogenase, alpha-glycerophosphate dehydrogenase, and lactic dehydrogenase. By 24 hr, the activity of acid phosphatase was reduced throughout the proximal tubule, with the greatest decrease occurring in the P3 segment of the proximal tubule located in the outer stripe of the outer medulla. Changes in the histochemical staining of the remaining enzymes were not consistently observed until 48 or, in some cases, 72 hr. These alterations involved all portions of the proximal tubule with the most severe changes involving P3. The results of the enzyme histochemical studies along with the morphologic findings indicating that the initiation of CDDP-induced acute renal failure, first apparent at 48 hr in this model, is associated with cell injury throughout the proximal tubule. The majority of the histochemical changes did not become apparent until late in the course of tubular injury. This suggests that most of the changes in enzyme activity represent nonspecific effects of CDDP-induced tubular injury, as opposed to direct enzyme inhibition by the drug.

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Despite the availability of modern techniques, mortality continues to be high in acute renal failure (ARF) (Fig 1, top).The acute renal failure resulting from glycerol-induced myohemoglo¬ binuria and methemoglobin adminis¬ tration have been most extensively investigated, primarily because of some similarities to human acute re¬ nal failure. Micropuncture of super¬ ficial renal cortical tubules has been used in many recent studies, since oli-