A Physiological and Cytochemical Study of the Kidney and the Adrenal Cortex During Acute Choline Deficiency in Weanling Rats

Abstract

The effects of acute choline deficiency in weanling male rats on the cytochemistry of the adrenal cortex and the cytology and function of the kidney have been studied. The renal lesion of acute choline deficiency is characterized by fatty infiltration of the tubular epithelium, congestion and hemorrhage of the cortex, fragmentation and disappearance of mitochondria in the tubular epithelium, and a decrease in the respiration of slices of kidney cortex in vitro. At the time of maximum kidney damage (9 days), casts of material resembling hemoglobin appear in the lumens of the tubules. Concomitant with the renal congestion there is nitrogen and electrolyte retention. The excretion of glycocyamine is depressed more than is the excretion of creatinine. The renal damage is accompanied by an enlargement of the adrenal cortex and atrophy of the thymus. The zona fasciculata appears only moderately stimulated, apparently as a result of the “alarming” stimulus of inanition. The zona glomerulosa is much more markedly stimulated, possibly as a result of altered electrolyte balance during renal failure. With kidney repair, which occurs without added choline, the adrenal cortex returns to normal, the zona fasciculata recovering more rapidly than the zona glomerulosa. Both zones appear normal by the 42nd day of deficiency, despite the continued fatty liver.