Effect of 1,25-Vitamin D and Parathyroidectomy on the Uptake of Aluminum in Bone of Rats with Renal Insufficiency

1988 ◽  
Vol 8 (5) ◽  
pp. 426-430 ◽  
Author(s):  
Kenneth Abreo ◽  
Hartmut H. Malluche
PEDIATRICS ◽  
1983 ◽  
Vol 71 (1) ◽  
pp. 56-58
Author(s):  
W. R. Griswold ◽  
V. Reznik ◽  
S. A. Mendoza ◽  
D. Trauner ◽  
A. C. Alfrey

A child with renal insufficiency was treated with the oral phosphate binder aluminum hydroxide from age 6 to 31 months. The prescribed dose of elemental aluminum varied from 31 to 108 mg/kg/d. Concurrently the patient developed vitamin D-resistant osteomalacia which failed to improve with parathyroidectomy. Encephalopathy with myoclonic seizures, loss of speech, and motor impairment also occurred. Serum and bone aluminum levels were elevated at 334 µg/L (normal 7 ± 3 µg/L) and 156 mg/kg (normal 3.3 ± 2.9 mg/kg), respectively. This case demonstrates that aluminum may accumulate in tissue of children receiving oral aluminum hydroxide. The accumulation of aluminum may have contributed to the vitamin D-resistant osteomalacia and the encephaiopathy in this patient. Children receiving aluminum-containing antacids as phosphate binders should be monitored for aluminum accumulation and signs of aluminum intoxication.


PEDIATRICS ◽  
1960 ◽  
Vol 26 (1) ◽  
pp. 75-85
Author(s):  
Gunnar B. Stickler ◽  
Alvin B. Hayles ◽  
Marschelle H. Power ◽  
John A. Ulrich

Observations on two girls in whom an unusual type of chronic renal insufficiency developed many months after the onset of nephrotic syndrome are reported. Each patient became free of edema in spite of persistent massive proteinuria. Growth was retarded and rickets and attacks of tetany developed. The chemical disturbances of the blood were characterized by hypocalcemia, hypokalemia, azotemia and metabolic acidosis. Hyposthenuria, proteinuria, amino-aciduria, and minimal erythrocyturia, cylindruria and glycosuria were present. Healing of the rickets and cessation of attacks of tetany followed the administration of vitamin D and calcium salts. Prednisone was administered to one patient and thereafter proteinuria decreased and renal tubular function improved. Both girls are relatively asymptomatic 11 and 9 years after the onset of nephrotic syndrome, although they are rather small and still have evidence of renal disease. It is possible that cells of the renal tubules have been damaged as a result of prolonged massive proteinuria.


2014 ◽  
Vol 24 (3) ◽  
pp. 186-193 ◽  
Author(s):  
Laura H. Mariani ◽  
Matthew T. White ◽  
Justine Shults ◽  
Cheryl A.M. Anderson ◽  
Harold I. Feldman ◽  
...  

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. 8520-8520
Author(s):  
Elizabeth O'Donnell ◽  
Andrew Jenho Yee ◽  
Omar Nadeem ◽  
Brea Lipe ◽  
Jacob Laubach ◽  
...  

8520 Background: Bone destruction is a devastating consequence of multiple myeloma (MM). An unmet medical need exists for the management of skeletal complications in MM patients with renal insufficiency. Despite the effectiveness of intravenous bisphosphonates, their use is limited in situations where renal dysfunction is present. Denosumab is a fully human monoclonal IgG2 antibody to RANKL that has been shown to be non-inferior to zoledronic acid for SRE rates in MM (Raje, et al. Lancet Oncol). More importantly, it does not have the same renal toxicity as the bisphosphonates. We hypothesize that denosumab can be safely and effectively administered in MM patients with renal insufficiency to improve bone health. This may fill a gap in clinical care for bone-directed therapy in this patient population. Methods: This multi-center study will include forty adult patients with newly diagnosed or relapsed MM with a creatinine clearance of less than 30 mL/min (NCT02833610). All patients will receive a subcutaneous injection of denosumab 120 mg Q4W for a total of 12 cycles. In addition, it is required that all subjects receive daily vitamin D and calcium supplementation at standard doses (at least 2000 mg calcium citrate and1000 IU of vitamin D), unless documented hypercalcemia develops on study. The primary objective is to assess the effect of denosumab 120 mg Q4W on serum c-terminal telopeptide (sCTX). Secondary objectives include evaluation of safety and tolerability of denosumab in patients with renal insufficiency, incidence of hypocalcemia, effect on bone mineral density, effect on urinary n-terminal telopeptide, and proportion of patients who have a documented skeletal-related event. Results: At the time of this analysis, a total of 20 out of a planned 40 patients have been enrolled, including 9 women, 11 men. Of those treated, 8 patients have completed the planned 12 cycles of therapy. Hypocalcemia was observed in 7 (35%) patients. Four patients (20%) experienced grade 3 hypocalcemia, 3 (15%) grade 2 or less. Two patients developed osteonecrosis of the jaw, one (5%) grade 1 and one (5%) grade 4 event. Data for the analysis of the primary endpoint of sCTX levels will be presented. Conclusions: Investigation of denosumab in MM patients with renal insufficiency defined as a creatinine clearance less than 30 mL/min is ongoing. Early data support that denosumab can be safely administered in this population. However, incidence of hypocalcemia despite aggressive prophylactic calcium dosing underscores the importance of the trial to inform safe practice in this more fragile population. Clinical trial information: NCT02833610 .


1965 ◽  
Vol 209 (1) ◽  
pp. 141-145 ◽  
Author(s):  
David M. Kessner ◽  
Franklin H. Epstein

Chronic experimental renal insufficiency induced by subtotal nephrectomy decreased the ability of the isolated rat duodenal gut sac to transport calcium against a chemical gradient. The defect in intestinal transport was not reproduced by metabolic acidosis, uremia of short duration, or addition of urea to the ambient solution bathing the gut sac. The transport of calcium by the intestine of uremic rats was increased by pretreatment with high doses of vitamin D and, at the dose level employed, there was no evidence of "resistance" to vitamin D. Dietary restriction depressed the gastrointestinal transport of calcium and may play a role in producing the defect in calcium transport of chronic uremia.


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