Llach F, Felsenfeld A J, Haussler M R
N Engl J Med. 1981 Jul 16;305(3):117-23. doi: 10.1056/NEJM198107163050301.
We studied six oliguric patients with rhabdomyolysis-induced acute renal failure. On admission, all had marked hyperphosphatemia and hypocalcemia associated with low levels of 1,25-dihydroxycholecalciferol [1,25(OH)2D]. During the early polyuric phase, moderate hypercalcemia was accompanied by marked elevations in plasma 1,25(OH)2D and persistent elevations in parathyroid hormone (both amino and carboxy terminals). During the late polyuric phase, the levels of serum calcium and 1,25(OH)2D reverted to normal. Thus, in rhabdomyolysis-induced acute renal failure, the hypocalcemia of the oliguric phase may be secondary to decreased synthesis of 1,25(OH)2D; severe hyperphosphatemia may also have a major role. The hypercalcemia of the polyuric phase may be partly due to increased synthesis of 1,25(OH)2D, resulting from the high parathyroid hormone levels and recovery of renal function.
我们研究了6例因横纹肌溶解症导致急性肾衰竭的少尿患者。入院时，所有患者均有明显的高磷血症和低钙血症，并伴有低水平的1,25 - 二羟胆钙化醇[1,25(OH)₂D]。在早期多尿期，中度高钙血症伴随着血浆1,25(OH)₂D的显著升高以及甲状旁腺激素（氨基端和羧基端）的持续升高。在晚期多尿期，血清钙和1,25(OH)₂D水平恢复正常。因此，在横纹肌溶解症导致的急性肾衰竭中，少尿期的低钙血症可能继发于1,25(OH)₂D合成减少；严重的高磷血症可能也起主要作用。多尿期的高钙血症可能部分归因于1,25(OH)₂D合成增加，这是由于甲状旁腺激素水平升高和肾功能恢复所致。
