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The most prominent abnormality in renal function in potassium depletion in man and in experimental animals is a defect in concentrating power. Although it has been suggested that in rats this may be due to lesions in the collecting tubules, the virtual absence of these histological abnormalities in human material and in dogs is paradoxical. In the experiments reported here, mild potassium depletion has been induced in rats by dietary restriction and the kidneys of these animals examined by the electron microscope. The most obvious early and constant abnormality was found in the basement membrane of the thin segment of the loop of Henle. The width of this membrane is increased to 3–5 times normal and it becomes fibrillar in appearance. This thickening and fibrillation involves also the pars recta of the proximal tubule, but does not extend into the thick ascending segment of the loop of Henle, the convoluted tubules or the collecting tubules. In the later stages of potassium depletion electron microscopy confirmed the abnormalities already reported in light microscopic studies— i.e. granulation, hyperplasia and degeneration of the cells of the collecting tubules. The relationship between the basement membrane abnormality and the known effect of potassium depletion on renal concentrating power is discussed in the light of the counter‐current hypothesis. It is suggested that the physical state of the ground substance of the basement membrane may have an important influence on the movement of water and electrolytes within the medullary region of the kidney and may be responsible for the renal defect in water conservation which occurs in potassium depletion.

Thirty rats were divided into three equal groups; the control group C and the two experimental groups were fed on diets identical in all respects other than the magnesium content. Group A were kept on a magnesium deficient diet for 13 days, and group B for 3 days. At the end of the experimental period, muscle, kidney and plasma were analyzed for their Mg and Ca contents and the kidneys were examined by the light and electron microscopes. No significant change was noted in the magnesium content of the kidneys of the deficient rats. In skeletal muscles, there was progressive depletion of magnesium, and the plasma magnesium also fell. The only highly significant result in the calcium content was a marked increase in the kidneys of the deficient groups. After as early as 3 days on the deficient diet, foci of dilated proximal tubules were seen in the cortico‐medullary zone even by the light microscope, but after 13 days they were observed all over the cortex and outer zone of the medulla. The lining cells of the slightly dilated tubules were swollen and vacuolated. As the dilatation increased, the tubular lining cells appeared to lose their brush border and to become flattened. The cells contained structureless cytoplasmic granules. Important negative findings are the normal appearance of the mitochondria, the normal thickness of the basement membrane, and the absence of any demonstrable obstruction in the dilated tubules or in more distal sites. It seems possible that in magnesium deficiency the proximal tubule cells, which normally reabsorb Ca++ and Mg++ by a common transport mechanism, reabsorb an excess of Ca++ from the glomerular filtrate which is deficient in Mg++. The excess of absorbed calcium ions is largely deposited locally in these cells, appearing as the dense granules. This would explain the high calcium content in the kidneys and the nephrocalcinosis in late stages.