{"title":"急性肾功能衰竭时低磷血症引起的高钙血症。","authors":"R F Gagnon, P Pajel, M Kaye","doi":"10.3109/08860228309076050","DOIUrl":null,"url":null,"abstract":"<p><p>A case of hypophosphatemia-induced hypercalcemia during post-traumatic acute renal failure is described. Proposed causes for the hypophosphatemia include changes in tissue distribution of phosphate associated with hyperalimentation and phosphate losses during hemodialysis. In the absence of hyperparathyroidism the hypercalcemia as well as changes in osteoclast morphology found on bone biopsy are ascribed to a direct effect of hypophosphatemia on bone.</p>","PeriodicalId":79208,"journal":{"name":"Clinical and experimental dialysis and apheresis","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/08860228309076050","citationCount":"3","resultStr":"{\"title\":\"Hypophosphatemia-induced hypercalcemia during acute renal failure.\",\"authors\":\"R F Gagnon, P Pajel, M Kaye\",\"doi\":\"10.3109/08860228309076050\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>A case of hypophosphatemia-induced hypercalcemia during post-traumatic acute renal failure is described. Proposed causes for the hypophosphatemia include changes in tissue distribution of phosphate associated with hyperalimentation and phosphate losses during hemodialysis. In the absence of hyperparathyroidism the hypercalcemia as well as changes in osteoclast morphology found on bone biopsy are ascribed to a direct effect of hypophosphatemia on bone.</p>\",\"PeriodicalId\":79208,\"journal\":{\"name\":\"Clinical and experimental dialysis and apheresis\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1983-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.3109/08860228309076050\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical and experimental dialysis and apheresis\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3109/08860228309076050\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical and experimental dialysis and apheresis","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3109/08860228309076050","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Hypophosphatemia-induced hypercalcemia during acute renal failure.
A case of hypophosphatemia-induced hypercalcemia during post-traumatic acute renal failure is described. Proposed causes for the hypophosphatemia include changes in tissue distribution of phosphate associated with hyperalimentation and phosphate losses during hemodialysis. In the absence of hyperparathyroidism the hypercalcemia as well as changes in osteoclast morphology found on bone biopsy are ascribed to a direct effect of hypophosphatemia on bone.