Hypercalcæmia After Oral Calcium-Carbonate Therapy in Patients on Chronic Hæmodialysis

Ginsburg, DavidS.; Kaplan, EdwinL.; Katz, A I

doi:10.1016/s0140-6736(73)91292-0

Cited by 22 publications

(4 citation statements)

References 19 publications

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“…The worsened atherogenesis seen in HPT is possibly due to the effects of iPTH on calcium channels in endothelial and subendothelial cells. HPT, hyperphosphataemia and elevation of the calcium–phosphate product predispose to soft tissue calcification 28,29 and worsen valvular and advanced plaque calcification. Several echocardiographic studies have found associations between HPT and left ventricular dilatation, systolic dysfunction and an inadequate response to left ventricular hypertrophy 30–33 .…”

Section: Physiologymentioning

confidence: 99%

Pathogenesis and management of hyperparathyroidism in end‐stage renal disease and after renal transplantation

Elder

2001

Nephrology

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SUMMARY: Secondary hyperparathyroidism is an adaptive response to progressive loss of renal function so as to maintain calcium and phosphate homeostasis, 1,25‐dihydroxyvitamin D3 levels and normal bone turnover, despite skeletal resistance to parathyroid hormone. As feedback regulation fails, complications of parathyroid overactivity develop, and by the commencement of dialysis abnormal bone histology is present in almost all patients, with hyperparathyroid changes most commonly found. Post transplantation, persisting hyperparathyroidism predisposes to osteoporosis. The risk of bone disease is reduced by early, carefully targeted dietary measures and suppressive therapy with calcitriol and calcium‐based phosphate binders, while newer therapies include bisphosphonates and calcimimetics. Timely surgical intervention is necessary in some patients.

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Section: Physiologymentioning

confidence: 99%

Pathogenesis and management of hyperparathyroidism in end‐stage renal disease and after renal transplantation

Elder

2001

Nephrology

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“…Pediatric patients on maintenance hemodialysis usually have to ingest large amounts of oral phosphate-binding agents such as calcium carbonate to control hyperphosphatemia [7][8][9][10][11]. About 30% of the calcium ingested is absorbed [12,13], often leading to hypercalcemia, especially under concomitant therapy with 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] [7][8][9][14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Calcium acetate versus calcium carbonate as oral phosphate binder in pediatric and adolescent hemodialysis patients

Wallot¹,

Bonzel²,

Winter³

et al. 1996

Pediatr Nephrol

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Calcium carbonate is widely used as an oral phosphorus binder to control hyperphosphatemia in children on maintenance hemodialysis. Intestinal calcium absorption may induce hypercalcemia, particularly if calcitriol is given simultaneously. In adults, calcium acetate binds phosphorus more effectively than calcium carbonate, while reducing the frequency of hypercalcemic events. We therefore compared calcium acetate with calcium carbonate in nine pediatric patients on long-term maintenance hemodialysis. Following a 1-week withdrawal of phosphorus binders, calcium carbonate was administered for 7 weeks; after a second withdrawal, calcium acetate was given for another 7 weeks. All patients received calcitriol regularly. Both agents lowered the serum phosphorus concentration significantly (calcium carbonate 5.7 +/- 1.4 vs. 7.7 +/- 2.1 mg/ dl, P < 0.005; calcium acetate 5.8 +/- 1.4 vs. 7.8 +/- 2.0 mg/dl, P < 0.005). Significantly less elementary calcium was ingested with calcium acetate than with calcium carbonate: 750 (375-1,500) vs. 1,200 (0-3,000) mg calcium/day, P < 0.0001. Wit calcium carbonate serum calcium increased significantly. The number of episodes of hyperphosphatemia or hypercalcemia did not differ between treatments. Intact plasma parathyroid hormone (PTH) decreased significantly with both phosphate binders, and serum 25-hydroxyvitamin D3 increased. There was a close relationship between serum phosphorus and PTH in prepubertal but not in pubertal patients. We conclude that hyperphosphatemia can be controlled effectively by both calcium acetate and calcium carbonate in pediatric hemodialysis patients. The oral load of elementary calcium is reduced significantly by binding phosphorus with calcium acetate instead of calcium carbonate; nevertheless, hypercalcemic episodes remain equally frequent with both phosphate binders.

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“…As hypercalcemia induces calcification of blood vessels (25,26), the elevated serum BUN and creatinine levels in calcium carbonate-treated rats may indicate that hypercalcemia induced kidney malfunction in these animals. The elevated Ca!…”

Section: Discussionmentioning

confidence: 99%

Utilization of titanium oxide-like compound as an inorganic phosphate adsorbent for the control of serum phosphate level in chronic renal failure

et al. 2010

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Hypercalcæmia After Oral Calcium-Carbonate Therapy in Patients on Chronic Hæmodialysis

Cited by 22 publications

References 19 publications

Pathogenesis and management of hyperparathyroidism in end‐stage renal disease and after renal transplantation

Pathogenesis and management of hyperparathyroidism in end‐stage renal disease and after renal transplantation

Calcium acetate versus calcium carbonate as oral phosphate binder in pediatric and adolescent hemodialysis patients

Utilization of titanium oxide-like compound as an inorganic phosphate adsorbent for the control of serum phosphate level in chronic renal failure

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