Bone Modulating Factors in Nephrotic Children with Normal Glomerular Filtration Rate

PEDIATRICS ◽  
1985 ◽  
Vol 76 (2) ◽  
pp. 280-285
Author(s):  
Michael Freundlich ◽  
Jacques J. Bourgoignie ◽  
Gaston Zilleruelo ◽  
Allan I. Jacob ◽  
Janet M. Canterbury ◽  
...  

Factors influencing bone and mineral metabolism were evaluated in 16 children with active nephrotic syndrome and normal glomerular filtration rate. All patients were proteinuric and/or hypoalbuminemic and had elevated serum triglyceride and cholesterol levels. Seven patients had never received or had discontinued glucocorticoid treatment at least 6 months before the study; six patients were receiving prednisone at the time of study. Although all patients were hypocalcemic (serum total or ionized calcium), none was hypomagnesemic. Despite the low serum calcium levels, circulating immunoreactive parathyroid hormone was elevated in only nine of 16. Plasma 25-hydroxyvitamin D was low in all 16 patients, averaging 7.6 ± 1.2 ng/mL for the group. In contrast, levels of 1,25-dihydroxyvitamin D were normal in 12 of 14 patients. Bone mineral content measured by photon absorptiometry averaged 83% and was less than 90% of normal in six of nine patients tested. The findings were not influenced by the recent or concurrent administration of glucocorticoid. The data demonstrate abnormalities of mineral and bone modulation in nephrotic children even in the absence of impaired glomerular filtration rate and irrespective of glucocorticoid therapy. The decrease in serum ionized calcium may be related to an absolute deficiency in 25-hydroxyvitamin D and/or a relative deficiency in 1,25-dihydroxyvitamin D. Undermineralization of bone may result from the low levels of vitamin D metabolites and, in some patients, from an increase in immunoreactive parathyroid hormone. Whether treatment with vitamin D metabolites and/or calcium supplementation will prevent the abnormalities remains to be demonstrated.

2011 ◽  
Vol 6 (9) ◽  
pp. 2141-2149 ◽  
Author(s):  
Ian H. de Boer ◽  
Ronit Katz ◽  
Michel Chonchol ◽  
Joachim H. Ix ◽  
Mark J. Sarnak ◽  
...  

Author(s):  
Alberto Maria Saibene ◽  
Cecilia Rosso ◽  
Giovanni Felisati ◽  
Carlotta Pipolo ◽  
Simone De Leo ◽  
...  

AbstractTransient postoperative hypocalcemia is a common complication after total thyroidectomy. Evidence on contributing metabolic factors is contradictory. Our work aims to define the role of preoperative 25-hydroxyvitaminD levels in developing transient postoperative hypocalcemia. 183 consecutive patients who underwent total thyroidectomy at our institution (May 2017–December 2019) were included in the retrospective study. We reported gender, age, estimated glomerular filtration rate, creatinine, preoperative 25-hydroxyvitaminD, serum pre- and postoperative calcium, pre- and postoperative PTH levels and transient postoperative hypocalcemia occurrences. We compared variables both among patients with and without transient postoperative hypocalcemia and between patients with different 25-hydroxyvitaminD levels (< 10 ng/ml deficitary; 11–30 ng/ml insufficient; > 30 ng/ml, normal). A binomial logistic regression model evaluating the risk for transient postoperative hypocalcemia was elaborated. Patients with transient postoperative hypocalcemia had lower levels of postoperative PTH (p < 0.001) and more frequently normal or deficitary 25-hydroxyvitaminD levels (p = 0.05). When comparing patients according to their 25-hydroxyvitaminD levels, insufficiency was associated with a lower rate of transient postoperative hypocalcemia (p = 0.05); deficiency was associated with higher preoperative PTH (p = 0.021), postoperative PTH (p = 0.043) and estimated glomerular filtration rate (p = 0.031) and lower serum creatinine (p = 0.014). In the regression model higher preoperative PTH (OR = 1.011, p = 0.041) and 25-hydroxyvitaminD deficiency (OR = 0.343, p = 0.011) significantly predicted transient postoperative hypocalcemia. Data analysis revealed a correlation between transient postoperative hypocalcemia and 25-hydroxyvitaminD levels: our work points towards the possibility to stratify the risk of transient postoperative hypocalcemia according to patients’ preoperative 25-hydroxyvitaminD status.


2016 ◽  
Vol 37 (5) ◽  
pp. 521-547 ◽  
Author(s):  
Peter J. Tebben ◽  
Ravinder J. Singh ◽  
Rajiv Kumar

AbstractHypercalcemia occurs in up to 4% of the population in association with malignancy, primary hyperparathyroidism, ingestion of excessive calcium and/or vitamin D, ectopic production of 1,25-dihydroxyvitamin D [1,25(OH)2D], and impaired degradation of 1,25(OH)2D. The ingestion of excessive amounts of vitamin D3 (or vitamin D2) results in hypercalcemia and hypercalciuria due to the formation of supraphysiological amounts of 25-hydroxyvitamin D [25(OH)D] that bind to the vitamin D receptor, albeit with lower affinity than the active form of the vitamin, 1,25(OH)2D, and the formation of 5,6-trans 25(OH)D, which binds to the vitamin D receptor more tightly than 25(OH)D. In patients with granulomatous disease such as sarcoidosis or tuberculosis and tumors such as lymphomas, hypercalcemia occurs as a result of the activity of ectopic 25(OH)D-1-hydroxylase (CYP27B1) expressed in macrophages or tumor cells and the formation of excessive amounts of 1,25(OH)2D. Recent work has identified a novel cause of non-PTH-mediated hypercalcemia that occurs when the degradation of 1,25(OH)2D is impaired as a result of mutations of the 1,25(OH)2D-24-hydroxylase cytochrome P450 (CYP24A1). Patients with biallelic and, in some instances, monoallelic mutations of the CYP24A1 gene have elevated serum calcium concentrations associated with elevated serum 1,25(OH)2D, suppressed PTH concentrations, hypercalciuria, nephrocalcinosis, nephrolithiasis, and on occasion, reduced bone density. Of interest, first-time calcium renal stone formers have elevated 1,25(OH)2D and evidence of impaired 24-hydroxylase-mediated 1,25(OH)2D degradation. We will describe the biochemical processes associated with the synthesis and degradation of various vitamin D metabolites, the clinical features of the vitamin D-mediated hypercalcemia, their biochemical diagnosis, and treatment.


Sign in / Sign up

Export Citation Format

Share Document