Hypocalcemia has been observed in conjunction with severe magnesium depletion (1–8). This association is seen mainly in pathological conditions characterized by decreased absorption of magnesium from the gastrointestinal tract. The postulate that the hypocalcemia is the consequence of magnesium deficiency per se, and not calcium deficiency, is supported by studies showing that this syndrome can be reproduced by restricting magnesium in the diet or that hypocalcemia can be corrected by replacing magnesium alone without supplementation of calcium and/or vitamin D. The pathogenesis of hypocalcemia in magnesium depletion is multifactorial; however, recent studies have clarified previous controversial results regarding the role of PTH in this syndrome (2–5).

An insulin-dependent diabetic patient received a renal transplant from a living related donor without evidence of rejection. In the posttransplant period, his serum potassium concentration (3.7 to 6.7 mEq/liter) fluctuated widely with the serum glucose concentration (165 to 470 mg/dl) during the day. Serum glucose and potassium concentrations were directly correlated (r = .734, P less than .001). Other factors controlling the serum potassium concentration were examined. Plasma and urinary aldosterone levels were normal, plasma renin activity and aldosterone levels rose during upright activity, and urinary potassium excretion increased with the administration of exogenous mineralocorticoid. Thus, mineralocorticoid secretion and responsiveness were intact. These observations indicate that hyperkalemia in a diabetic patient can occur in the absence of a defect in potassium excretion and are consistent with the interpretation that insulinopenia, as evidenced by hyperglycemia, can result in hyperkalemia due to diminshed translocation of both potassium and glucose from the extracellular to the intracellular compartment.

ARTICLESEffects of inhibitors of prostaglandin synthesis on renal sodium excretion in normal dogs and dogs with decreased renal massP. Altsheler, S. Klahr, R. Rosenbaum, and E. SlatopolskyP. Altsheler, S. Klahr, R. Rosenbaum, andE. SlatopolskyPublished Online:01 Oct 1978https://doi.org/10.1152/ajprenal.1978.235.4.F338MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByInhibition of prostaglandin and nitric oxide synthesis prevents cortisol-induced renal vasodilatation in sheepR. de Matteo, andC. N. May1 April 1999 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 276, No. 4 More from this issue > Volume 235Issue 4October 1978Pages F338-F344 Copyright & PermissionsCopyright © 1978 the American Physiological Societyhttps://doi.org/10.1152/ajprenal.1978.235.4.F338PubMed696873History Published online 1 October 1978 Published in print 1 October 1978 Metrics

Severe hypocalcemia secondary to magnesium depletion has been described in numerous patients with gastrointestinal disorders. The development of profound hypomagnesemia in chronic renal disease is a rare finding. We studied three patients with advanced renal failure and magnesium depletion. Severe hypocalcemia also was present in these patients. Despite hyperplasia of the parathyroid glands, the levels of immunoreactive parathyroid hormone (PTH) in blood were inappropriately low for the degree of renal insufficiency. After the administration of magnesium there was a significant increase in the levels of circulating i-PTH in serum with a concomitant improvement in the hypocalcemia.

Complications following percutaneous renal biopsy have been infrequent with a 0.7% reported incidence [1][2][3].Recently, an analysis of 1,000 consecutive renal biopsies yielded an overall complication rate of 9.4% [41.Complications considered in-

Serum phosphorus concentrations are maintained within narrow limits in humans. In the extracellular fluid most of the phosphorus is present in the inorganic form and at the level of the glomerulus greater than 90% of PO4 is ultrafilterable. The kidney plays a key role in PO4 homeostasis. Micropuncture experiments have demonstrated that 60 to 70% of the filtered PO4 is reabsorbed in the proximal tubule; however, there is evidence that a significant amount of PO4 is reabsorbed in the distal tubule. Phosphate secretion probably plays a minor role in the overall renal regulation of phosphate. In normal individuals the amount of PO4 ingested plays a key role in the amount that ultimately will be excreted in the urine. The reabsorption of PO4 along the nephron is regulated by a series of factors of which parathyroid hormone is the most important one. Hyperphosphatemia is seen frequently in clinical medicine and by far, the most common cause is a decrease in urinary PO4 excretion secondary to renal failure. From the practical point of view, the most effective way to treat hyperphosphatemia is to decrease PO4 absorption in the GI tract by the use of PO4 binders.

Patients with adult respiratory distress syndrome in association with acute pancreatitis were studied intensively. A rise in pulmonary wedge pressure was seen after elevation of the serum amylase level with concomitant depression of the serum calcium level. Pharmacologic doses of steroids did not seem to be efficacious in reducing QsQt changes. However, inception of positive end expiratory pressure ventilation caused diminution in QsQt ratios.

HAYES, MARTIN F. JR MD; MORELLO, DANIEL C. MD; ROSENBAUM, ROBERT W. MD; MATSUMOTO, TERUO MD, PhD Author Information