1978
DOI: 10.7326/0003-4819-89-6-928
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Resolution of Muscle Calcification in Rhabdomyolysis and Acute Renal Failure

Abstract: We studied four patients with acute renal failure associated with nontraumatic rhabdomyolysis to evaluate the presence and progression of calcium deposits in damaged muscle tissue. Conventional and electron radiography and technetium-99m diphosphonate (TcDP) scans were done during the oliguric phase of acute renal failure and repeated after renal function returned to normal. Three patients showed deposits of calcium by conventional radiography and all by electron radiography and TcDP during the oliguric period… Show more

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Cited by 71 publications
(18 citation statements)
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“…Several factors have been proposed to underlie the pathogenesis of hypocalcemia in rhabdomyolysis [3,4,5,8,9,10,16]. Among them, evidence supports calcium deposition in damaged muscle as a dominant factor, and the volume of damaged muscle is expected to affect the amount of calcium deposited [5,16].…”
Section: Discussionmentioning
confidence: 99%
“…Several factors have been proposed to underlie the pathogenesis of hypocalcemia in rhabdomyolysis [3,4,5,8,9,10,16]. Among them, evidence supports calcium deposition in damaged muscle as a dominant factor, and the volume of damaged muscle is expected to affect the amount of calcium deposited [5,16].…”
Section: Discussionmentioning
confidence: 99%
“…Metastatic calcification is seen in patients on chronic hemodialysis for chronic renal failure, whereas causes of dystrophic calcification include, for example, myocardial calcification after myocardial infarction or myocarditis. In rhabdomyolysis-induced AKI, temporary ectopic calcification in affected skeletal muscles is common and it can decrease or even disappear within few months [1][2][3]. Biphasic calcemic pattern observed here, with hypocalcemia in the oliguric phase followed by hypercalcemia during the recovery diuretic phase is characteristic for rhabdomyolysis-associated AKI.…”
Section: Discussionmentioning
confidence: 54%
“…Biphasic calcemic pattern observed here, with hypocalcemia in the oliguric phase followed by hypercalcemia during the recovery diuretic phase is characteristic for rhabdomyolysis-associated AKI. This sequence reflects widespread deposition of calcium in damaged muscle and subsequent mobilization of the calcium out from the recovering muscle as phosphorous and creatinine values return to normal [1]. The combination of increased release of phosphate from injured muscle and impaired ability to excrete phosphorous because of renal failure causes hyperphosphatemia, the latter causing hypocalcemia due to calcium phosphate precipitation.…”
Section: Discussionmentioning
confidence: 99%
“…The release of organic and inorganic phosphates from the injured muscles causes an increase in serum phosphate levels, which may elevate calcium phosphate product resulting in deposition of calcium salts in muscle and other tissues. 29 Hypocalcemia then ensues. However, in late stages of the disease, mobilization of calcium from damaged muscle results in hypercalcemia.…”
Section: Biochemical Features and Basis For Diagnosismentioning
confidence: 99%
“…The classical triad of symptoms are muscle pain, weakness and dark urine. 4,6,29,[33][34][35] The muscles can be tender and swollen, and there can be skin changes indicating pressure necrosis. However, these classical features are seen in less than 10% of patients.…”
Section: Clinical Manifestationsmentioning
confidence: 99%