The Renal Lesions of Electrolyte Imbalance

Oliver, Jean; MacDowell, Muriel; Welt, Louis G.; Holliday, Malcolm A.; Hollander, William; Winters, Robert W.; Williams, T. Franklin; Segar, William E.

doi:10.1084/jem.106.4.563

Cited by 135 publications

(33 citation statements)

References 8 publications

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“…The functional and morphological similarities between the lesions of potassium deficiency in the rat (23,24) and those observed in the present study are noteworthy. Both are characterized by spotty necrosis and hyperplasia localized chiefly to tubular cells in the outer medulla, although the lesions observed in rats kept on a potassium-free diet for three to six weeks are more numerous than those of the present report (24,25).…”

Section: Discussionsupporting

confidence: 81%

“…Both are characterized by spotty necrosis and hyperplasia localized chiefly to tubular cells in the outer medulla, although the lesions observed in rats kept on a potassium-free diet for three to six weeks are more numerous than those of the present report (24,25). Both are associated with a depression of renal concentrating ability out of proportion to other tests of renal function.…”

Section: Discussioncontrasting

confidence: 68%

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The Effect of Hypercalcemia Induced by Calciferol Upon Renal Concentrating Ability1

Epstein¹,

Rivera²,

Carone³

1958

J. Clin. Invest.

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Polyuria and loss of renal concentrating ability have frequently been observed in patients with hypercalcemia (1-8). It has not been clear whether the capacity of the kidneys to concentrate urine is selectively impaired by hypercalcemia or whether it is depressed together with many other renal functions as a result of substantial injury to and encroachment upon active renal parenchyma (9). In the present experiments the effects of hypercalcemia on renal function and morphology were studied in rats given large doses of calciferol (vitamin D2) for several days. The results suggest that hypercalcemia and renal damage produced in this manner specifically impair renal concentrating ability. This functional defect is associated with alterations in the structure of the collecting tubules of the renal medulla. METHODSEighteen male albino rats of the Sprague-Dawley strain, weighing about 300 Gm., were maintained on a measured diet of Purina Lab Chow and allowed to drink tap water ad libitum. Following initial determinations of blood urea nitrogen, urea clearance, phenolsulfonphthalein (PSP) excretion and maximum urinary osmolality, 200,-000 units or 400,000 units of vitamin D2 in peanut oil was injected subcutaneously daily for four days. At the end of this time, the same tests were repeated. The animals were then sacrificed by exsanguination from the abdominal aorta during pentobarbital anesthesia and the kidneys removed for morphologic examination. Eight rats served as controls, receiving only peanut oil for four days, with food intake limited to that taken by matched animals receiving vitamin D2.For the measurement of urea clearance, 0.2 to 0.3 ml. of heparinized blood was obtained from the tail. Rats

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Section: Discussionsupporting

confidence: 81%

Section: Discussioncontrasting

confidence: 68%

The Effect of Hypercalcemia Induced by Calciferol Upon Renal Concentrating Ability1

Epstein¹,

Rivera²,

Carone³

1958

J. Clin. Invest.

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“…The effect of potassium deficiency per se (1) was found to be principally localized to the collecting tubules and consisted of three separate changes: a general hyperplasia of the tubular epithelial ceils in the outer zone of the medulla, a specific hyperplasia of the intercalated ceils in the same area, and a development of droplets in the cells of the papillary portion of the collecting system which had been previously noted by Spargo (3,4). These changes were associated with a defect in ability to concentrate urine, and further studies of this relation have been described (5,6).…”

mentioning

confidence: 62%

The Renal Lesions of Electrolyte Imbalance

Holliday

Bright

Schulz

et al. 1961

The Journal of Experimental Medicine

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Two previous studies (1, 2) have described the structural changes in the kidneys of rats that occur as a response to the alterations in electrolyte balance which accompany potassium deficiency. The effect of potassium deficiency per se (1) was found to be principally localized to the collecting tubules and consisted of three separate changes: a general hyperplasia of the tubular epithelial ceils in the outer zone of the medulla, a specific hyperplasia of the intercalated ceils in the same area, and a development of droplets in the cells of the papillary portion of the collecting system which had been previously noted by Spargo (3, 4). These changes were associated with a defect in ability to concentrate urine, and further studies of this relation have been described (5, 6). The effect of massive phosphate loading in producing extensive changes in the kidney consisting of necrosis and calcification of the terminal segment of the proximal convolutions was first described by MacKay and Oliver (7). The same lesion was found to develop with a modest phosphate intake which of itself produced no change in normal animals when potassium deficiency was present (2); this added lesion then existed in association with the lesions of potassium deficiency.In the original description of the changes noted in potassium deficiency varying degrees of cellular hyperplasia were noted in some proximal convolutions. In the experimental design of that study a diet had been used that was low in chloride content. Extensive change had been noted previously in the cortex of rats acutely depleted of chloride although the locus of this change was not certain (8).

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“…The model is well suited to the purposes of this investigation except that a striking lowering of carcass potassium may occur (6). The production of potassium nephropathy by a marked deficiency of this ion has been shown by Oliver and co-workers (11). In order to avoid this complicating renal lesion, supplementary potassium was furnished the experimental rats.…”

Section: Discussionmentioning

confidence: 99%

Susceptibility of Rats with Hormonal Hypertension to Experimental Pyelonephritis12

Woods¹

1958

J. Clin. Invest.

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Congenital malformations and urinary tract obstructions are accepted predisposing factors in human pyelonephritis. Ureteral ligation (1, 2), mechanical trauma (3), scar formation in the kidney after recovery from severe staphylococcal infection (4), and localized thermal injury to the renal medulla (5) have been shown to predispose to the development of acute, hematogenous, Escherichia coli pyelonephritis in the experimental animal. It is conceivable that other renal insults such as arteriolar nephrosclerosis and necrotizing arteriolitis might similarly increase susceptibility to infection. There are no experimental data to support this supposition. The postmortem examination of "end stage" kidneys and analysis of clinical charts do not yield evidence which clearly establishes the sequential relationship of hypertension and pyelonephritis. The present investigation was therefore designed to test by experiment the hypothesis that animals which are made hypertensive and which have renal arteriolar disease may have an increased susceptibility to pyelonephritis. Bacteriological techniques. Study of the susceptibility of the kidneys of these animals to infection by E. coli injected intravenously was based on the work of Guze and Beeson (2). Strains of E. coli to be used for intravenous inoculation were isolated from the urine of patients with active pyelonephritis. After identification, the organism was injected intravenously into a rat with a ligated ureter, subsequently recovered from the infected kidney, and inoculated into tubes containing 10 ml. of sterile broth. The tubes were incubated for three hours, sealed with parafilm, frozen, and stored at -200 C.Colony counts were plotted against Klett-Summerson colorimeter readings on a broth culture at frequent intervals in order to simplify the determination and standardization of inoculum size for future experiments. When a group of animals were to be injected with E. coli, a frozen culture was warmed to 370 C., incubated for 12 hours, and a small inoculum placed in 150 ml. of sterile broth. When growth produced marked turbidity, the culture was diluted with sterile broth to the desired colorimeter reading, i.e., equivalent to the number of million bacteria to be injected. Then 20 to 25 ml. was removed, centrifuged and the sediment resuspended in an equivalent volume of sterile saline. One ml. of this saline suspension was then injected into the tail veins of 1686

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The Renal Lesions of Electrolyte Imbalance

Cited by 135 publications

References 8 publications

The Effect of Hypercalcemia Induced by Calciferol Upon Renal Concentrating Ability1

The Effect of Hypercalcemia Induced by Calciferol Upon Renal Concentrating Ability1

The Renal Lesions of Electrolyte Imbalance

Susceptibility of Rats with Hormonal Hypertension to Experimental Pyelonephritis12

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