Serum Calcium and Parathyroid Hormone Derangements in Rhabdomyolysis
Author(s) -
Soledad García de Vinuesa,
Francisco Ahijado,
José Luño
Publication year - 1989
Publication title -
the nephron journals/nephron journals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000185600
Subject(s) - medicine , icon , citation , hypercalciuria , library science , humanities , calcium , computer science , art , programming language
Soledad García de Vinuesa, Servicio de Nefrología, Hospital General ‘Gregorio Marañón’, Dr. Esquerdo 46, E-28007 Madrid (Spain) 15 10 5 u0 15 10 ¦3⁄8 5 Dear Sir, Abnormalities in calcium metabolism are frequent in rhabdomyolysis-induced acute renal failure. Marked hy-pocalcemia, which occurred during the oliguric phase, is a well-recognized biochemical feature of this disorder, and those patients who are initially hypocalcemic, may become hypercalcemic during the diuretic phase of acute renal failure [1–3]. Early studies suggest that the severity of hypocalcemia varies directly with hyperphospha-temia, is related with the intensity of muscle injury and may be due to the rapid deposition of calcium salts in traumatized skeletal muscle and cytoplasmic sequestration [1, 2]. Possible explanations for hypercalcemia include mobilizations of calcium already sequestered in muscle [4, 5], volume depletion and autonomous secretion of parathyroid hormone (PTH) [6, 7]. Llach et al. [7] consider that the hypocalcemia of the oliguric phase may be secondary to decreased synthesis of l,25(OH)2-D associated to hyperphosphatemia and skeletal resistance to the calcemic action of PTH and describe high levels of l,25(OH)2-D during the recovery phase in addition to elevated PTH, suggesting that repair of the vitamin D abnormality restores bone responsiveness to PTH: For these authors, the most likely cause of the hypercalcemia of the diuretic phase is the increased production of l,25(OH2-D associated to persistent secretion of PTH. We had the opportunity to study one alcoholic patient with nontraumatic rhabdomyolysis (CPK = 190,000 UI/ 1) who went into acute renal failure. During the oliguric phase (diuresis < 300 cmVday), which persisted for more than 30 days, he developed hypercalcemia. Peritoneal dialysis was started (calcium concentration of the peritoneal fluid: 3.5 mEq/1). As shown in figure 1, the lowest level of serum calcium appeared on the 5th day: total calcium 4.4 mg/dl; ionized calcium 1.68 mg/dl; phosphate 14 mg/dl and PTH (1,84-
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