https://www.amjmed.com/article/0002-9343(82)90826-9/pdf

Arachidonic Acid Metabolism, Prostaglandins and the Kidney

The renal excretion of hydrogen ion in renal tubular acidosis:I. Quantitative assessment of the response to ammonium chloride as an acid load

2 – Water Metabolism of Mammals1

Renal tubular lesions during the early phases of progressive potassium depletion in rats were found in nephrons isolated by microdissection in two locations, the collecting tubules and the proximal convolutions. All other portions of the nephron, in particular the "distal tubule," i.e. ascending limbs of Henle's loop and distal convolutions, showed no structural alterations except the passive effects of dilatation and cellular compression which developed as a result of primary disturbances lower in the tubular system. The alterations affected all the collecting tubules uniformly and took two forms; the more severe, a swelling and hyperplasia of the tubular epithelium and the lesser, an intracellular accumulation of granule droplets. The former was limited to the outer zone of the medulla, the latter to its inner zone. In the proximal convolution the structural alteration began in its middle third and extended downward towards the medulla; only occasional nephrons were affected. The essential nature of the more severe epithelial lesion was similar in both collecting tubule and proximal convolution, beginning as a swelling of cell bodies, increasing to protoplasmic disturbances with disintegration of the mitochondrial pattern, followed by rupture of cells and nuclear disappearance. These retrogressive alterations were followed by prolific regenerative hyperplasia. In the collecting tubules of the outer zone these epithelial alterations were present in both the clear and the intercalcated cells; in the latter the swelling of the cells was not prominent, but the hyperplastic proliferative increase in their number was the predominating feature of the lesion when the dissected tubules were viewed intact in the continuity of their topographical relations. The cellular alterations in the tubules are associated with an inability to concentrate the urine; reasons are given for considering this functional disturbance a correlate of the structural lesion in the collecting tubules.

https://rupress.org/jem/article-pdf/106/4/563/1391133/563.pdf

The renal lesions of electrolyte imbalance i. the structural alterations in potassium-depleted rats

A decrease in the ability of the kidneys to excrete a highly concentrated urine is one of the earliest hallmarks of potassium depletion in animals and in humans (1). According to present views of the mechanism of the renal concentrating process (2), this might be the result of a) impairment of the countercurrent multiplier system by which a high concentration of sodium (and urea) is created and maintained in the interstitial space of the renal papilla, and/or b) decreased permeability of the walls of the collecting ducts and distal tubules to the back-diffusion of water. If the first alternative were correct, analysis of the renal papilla from potassium-deficient animals excreting a maximally concentrated urine should reveal a lower concentration of sodium than that present in the papilla of normal animals. Should the second mechanism be operative, the fall in maximum urinary osmolality observed in potassium deficiency might be entirely unassociated with a decrease in papillary sodium, or else would be out of proportion to it. In the present experiments samples of maximally concentrated urine and renal papilla, medulla and cortex from potassium-depleted rats and dogs were analyzed. By placing all animals on a sodium-free diet prior to sacrifice, difficulties in the interpretation of tissue analyses consequent to high concentrations of sodium in the urine were avoided. The results indicate that the

/pdf/on-the-mechanism-of-impairment-of-renal-concentrating-g3apfpd3ig.pdf

On the mechanism of impairment of renal concentrating ability in potassium deficiency

The effect of graded degrees of K depletion on the ability to produce a concentrated urine was studied in Sprague-Dawley rats. With increasing degrees of K depletion, as measured by the concentration of K in fat-free skeletal muscle, there was a progrossive decrease in the maximum urinary concentration. This defect of the renal concentrating mechanism appeared to be better correlated with the degree than with the duration of potassium depletion and could be demonstrated either by the use of exogenous vasopressin or by water deprivation. The potassium-deficient rats in at least one experiment developed a significant polydipsia. The data do not allow any conclusions with respect to the relationship of the polydipsia to the renal concentrating defect except that the latter at least was not severe at the onset of the increased water intake.

Defect in the renal tubular reabsorption of water associated with potassium depletion in rats.

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Defect in the renal tubular reabsorption of water associated with potassium depletion in rats.