The morphology and pathogenesis of magnesium deficiency-induced nephrocalcinosis

Bunce, G. E.; Saacke, R. G.; Mullins, John J.

doi:10.1016/0014-4800(80)90019-2

Cited by 29 publications

(12 citation statements)

References 18 publications

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“…The crystals subsequently move down the nephron, enlarging by further mineralization and collection of cellular debris. Eventually they block the tubule, forming characteristic deposits around the corticomedullary junction of the kidney (Oliver, MacDowell, Whang & Welt, 1966; Bunce, Saacke & Mullins, 1980). As a consequence of tubular obstruction, there may be atrophy of nephron segments distal to the deposit.…”

Section: Introductionmentioning

confidence: 99%

Kidney function in rats with corticomedullary nephrocalcinosis: effects of alterations in dietary calcium and magnesium.

Al-Modhefer¹,

Atherton²,

Garland³

et al. 1986

The Journal of Physiology

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SUMMARY1. Single-nephron and whole-kidney function were studied in female rats with corticomedullary nephrocalcinosis, and in animals where the lesion had been prevented either by a dietary magnesium supplement or by using a diet with a calcium: phosphorus ratio in excess of 1.2. At the single-nephron level, rats with nephrocalcinosis had prolonged tubular fluid transit times. Proximal transit time was 19-42 + 1-98 (mean+ S.E. of mean) vs. 1 1-58 + 0-19 s for controls; distal transit time was 62-64 + 9-16 vs. 31-50 + 1-03 s for controls.3. Although single-nephron function is altered in nephrocalcinosis, data obtained from rats in metabolism cages indicate that whole-kidney function is largely unaffected by the lesion.

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Section: Introductionmentioning

confidence: 99%

Kidney function in rats with corticomedullary nephrocalcinosis: effects of alterations in dietary calcium and magnesium.

Al-Modhefer¹,

Atherton²,

Garland³

et al. 1986

The Journal of Physiology

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“…With regard to the onset time of renal tubular injury by the Mg-deˆcient diet, within 12 h after the start of feeding of the Mgdeˆcient diet, electron-dense granules were found in the brush border of the proximal tubules in cortex and corticomedullary junction. 8) Kidney calciˆcation appears in the inner stripe of the outer zone of the medulla in rats fed the low Mg diet within 4 to 6 d. 6) After the Mg-deˆcient diet feeding, mitochondrial swelling was found in the distal segment of the proximal convolution in inner cortex at 3 d, and necrosis of epithelia in the distal segment of the proximal convolutions were encountered, and calcium deposits were observed in necrotic cells at 9 d. 16) Indeed, our nding supports the results of previous studies. 6,8,16) Namely, the results in our study of biochemical indicators demonstrated that intake of a Mg-deˆcient diet rapidly induces renal tubular injury.…”

Section: Kidney Function In Magnesium Deˆcient Ratsmentioning

confidence: 99%

“…Rats fed a Mg-deˆcient diet develop an increase in calcium (Ca) and phosphorus (P) concentrations in the kidney by chemical analysis, and kidney calciˆcation by histological examination. [6][7][8][9] It might be inferred from theseˆndings in previous studies [6][7][8][9] that Mg deˆciency not only induces kidney calciˆcation but also diminishes kidney function. With regard to the eŠects of Mg deˆciency on kidney function, the previous studies 10,11) suggest that rats fed the Mg-deˆcient diet may have depressed kidney function.…”

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confidence: 99%

Changes inN-Acetyl-β-D-Glucosaminidase Activity in the Urine and Urinary Albumin Excretion in Magnesium Deficient Rats

Matsuzaki

Ohdachi

Fuchigami

et al. 2002

Bioscience, Biotechnology, and Biochemistry

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“…Summarizing the morphological changes, the intracellular accumulation of crystal-forming ions might have been due to an impairment in membrane integrity and subsequently enhanced ion influx, ultimately leading to the impressive calcium phosphate precipitation seen on routine histology. If this view is true, the sequence of events and the degree of calcium phosphate deposits may depend on the severity and duration of the Mg deficiency, the effects being only mild after 10-12 days [44,45], but pronounced after several weeks [42] or months (this work).…”

Section: Renal Calcificationsmentioning

confidence: 99%

Reappraisal of the Quantity and Nature of Renal Calcifications and Mineral Metabolism in the Magnesium-Deficient Rat

Schmiedl¹,

Schwille²,

Berge³

et al. 1998

Urol Int

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There is an urgent need for drugs capable of inhibiting renal calcifications, nephrocalcinosis and stones included, in humans. Current anticalcification medication is based mainly on alkalinization of the metabolism using potassium-containing citrate alone, despite the fact that calcium stone patients suffer marginally from both magnesium and potassium deficiency. We investigated the anticalcification efficacy of oral potassium citrate versus the combined administration of this drug and magnesium citrate in the magnesium-deficient rat developing corticomedullary nephrocalcinosis and luminal microliths in the long term. Among other things we employed specific stains for calcium and oxalate, light microscopy and element analysis for renal tissue and calcifications, respectively. In addition, minerals in renal tissue, urine and plasma were determined, as well as the state of extracellular calcium homeostasis. Magnesium deficiency caused pure calcium phosphate tissue deposits, containing no magnesium, but no deposition of calcium oxalate in the tubular lumen; tissue magnesium, calcium and phosphorus were increased, and there was marked potassium wastage via urine; despite mild hypercalcemia other signs of hyperparathyroidism were not found. Alkalinization with the two kinds of medication evoked an increase in urinary pH, citrate, and potassium; however, potassium citrate alone tended to aggravate renal concretions, whereas the combination of this drug with magnesium citrate completely prevented concretions. It was concluded that: (1) magnesium deficiency-induced calcifications are oxalate-free and are not sensitive to mobilization by alkalinization with potassium citrate, which might explain the failure of the drug to prevent stone recurrence in clinical stone patients, and (2) the combination of potassium citrate and magnesium citrate, which shows enormous anticalcification efficacy, deserves high priority in clinical trials aimed at evaluating strategies for the prevention of stones.

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The morphology and pathogenesis of magnesium deficiency-induced nephrocalcinosis

Cited by 29 publications

References 18 publications

Kidney function in rats with corticomedullary nephrocalcinosis: effects of alterations in dietary calcium and magnesium.

Kidney function in rats with corticomedullary nephrocalcinosis: effects of alterations in dietary calcium and magnesium.

Changes inN-Acetyl-β-D-Glucosaminidase Activity in the Urine and Urinary Albumin Excretion in Magnesium Deficient Rats

Reappraisal of the Quantity and Nature of Renal Calcifications and Mineral Metabolism in the Magnesium-Deficient Rat

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