Hypercalcaemia in Association With Renal Failure: The Role of Immobilisation

Prince, Richard; Eisman, JA; R, Simpson

doi:10.1111/j.1445-5994.1983.tb04537.x

Cited by 16 publications

(2 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is in accordance with other authors' findings, demonstrating that in previously healthy subjects immobilization-induced hypercalcemia is not a common event [15], as opposed to the observations in critically ill subjects [24,25]. Hypercalcemia may ensue also when renal excretion of calcium is impaired by renal dysfunction [4,26], which was not the case in the present study.…”

Section: Discussionsupporting

confidence: 88%

Immobilization and hypercalciuria in children

et al. 2006

View full text Add to dashboard Cite

Intermediate-term immobilization may lead to an increase in serum and urinary calcium. In order to test this hypothesis, we evaluated 46 children, 21 with Legg-Calvé-Perthes disease (LCP; 7.2+/-1.8 years old) and 25 with developmental dysplasia of the hip joint (DDH; 10+/-5 months of age), submitted to immobilization for up to 16 weeks. These two conditions require intermediate-term immobilization as treatment modality, and no studies evaluating calcium metabolism in these groups of patients have been conducted. In LCP patients, blood and 24-h urine samples were obtained before the beginning of treatment and after 1, 6, 8, 14 and 16 weeks of immobilization, while in DDH patients, blood and spot urine samples were collected before treatment and after 6 and 14 weeks of treatment. Urinary calcium, creatinine, potassium and sodium as well as serum calcium, phosphorus, parathyroid hormone, creatinine and alkaline phosphatase were determined in those samples. Renal ultrasound was performed before and after treatment. A mean increase of 2.3 times baseline values of urinary calcium was observed in 40% of previously normocalciuric LCP patients after only 1 week of immobilization. Among the DDH children, who had never previously ambulated, there was no significant variation in the urinary calcium excretion. None of the serum parameters changed in either group throughout the study. Urinary stones were not evidenced by renal ultrasound. Therefore, the present data suggested that intermediate-term immobilization led to a transient increase in urinary calcium in 40% of LCP patients. Complications such as urinary stones were not observed. In conclusion, this modality of treatment does not impose an increased risk of urinary stone formation in LCP and DDH patients.

show abstract

Section: Discussionsupporting

confidence: 88%

Immobilization and hypercalciuria in children

et al. 2006

View full text Add to dashboard Cite

show abstract

“…There has been histological evidence of active calcium phosphate deposits dissolution on muscle biopsy (11). Hypercalcemia occurring after immobilization with normal to low PTH levels and low 1,25(OH)2D levels in patients with renal failure (12) has been demonstrated. So far the exact mechanism of statin induced rhabdomyolysis is not clear.…”

Section: O N I I N T E R N a Z I O N A L Imentioning

confidence: 99%

Bone scintigraphy of severe hypercalcemia following simvastatin induced rhabdomyolysis

Mirza

Amorosa

2016

ccmbm

View full text Add to dashboard Cite

SummarySimvastatin induced rhabdomyolysis with renal failure is a well reported clinical entity with hyperkalemia recognized as a life threatening risk. The risk of delayed hypercalcemia during the recovery of renal function is not well appreciated as this varies in severity and can be caused by multiple mechanisms. We present a patient with high dose simvastatin induced rhabdomyolysis leading to late onset of severe hypercalcemia due to calcium phosphate deposition in muscles diagnosed by distinctive bone scintigraphy. A 60-year-old Asian male was admitted to the hospital for profound weakness one week following the initiation of simvastatin 80 mg daily post myocardial infarction. His clinical course was complicated by contrast nephropathy. One week later, he developed progressive weakness in all his extremities and inability to raise his head and eat. Simvastatin was discontinued at this point. CPK elevation to greater than 425,000 U was found, consistent with rhabdomyolysis. He became oliguric requiring hemodialysis. Muscle biopsy showed severe muscle necrosis and type 2 fiber atrophy. One month later, he developed hypercalcemia with suppressed intact PTH and 1, 25(OH) D levels. Whole body bone scintigraphy showed calcium phosphate deposition throughout his musculature. His calcium levels normalized in 1 week on hemodialysis. This patient's experience illustrates the marked risk of delayed severe hypercalcemia from rhabdomyolysis due to dissolution of myocellular calcium phosphate deposits. It also provides an opportunity to review the different mechanisms of hypercalcemia especially in statin induced rhabdomyolysis. Recognition of this phenomenon is critical for appropriate follow up and treatment of such patients.

show abstract

Hypercalcemia. A complication of advanced chronic liver disease

Gerhardt¹

1987

Archives of Internal Medicine

View full text Add to dashboard Cite

Hypercalcaemia in Association With Renal Failure: The Role of Immobilisation

Cited by 16 publications

References 17 publications

Immobilization and hypercalciuria in children

Immobilization and hypercalciuria in children

Bone scintigraphy of severe hypercalcemia following simvastatin induced rhabdomyolysis

Hypercalcemia. A complication of advanced chronic liver disease

Contact Info

Product

Resources

About