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. When the patients recovered renal function and muscle injuries healed, calcium deposits disappeared. The results show that calcium deposits in damaged muscle occur during the oliguric phase of acute renal failure due to rhabdomyolysis and the calcification disappears with recovery of renal failure; and TcDP scans are the most sensitive method of detecting calcium deposits in these patients.

Acute Kidney Injury Facilitates Hypocalcemia by Exacerbating the Hyperphosphatemic Effect of Muscle Damage in Rhabdomyolysis

“…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].…”

Reversible Myocardial Calcification Following Severe Leptospirosis Complicated With Rhabdomyolysis-Induced Acute Kidney Injury and Magnesium-Wasting Nephropathy

“…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.…”

“…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.…”

Drug-Induced Rhabdomyolysis

“…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.…”

“…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.…”