vitamin-d-2 and Nephrocalcinosis

Vitamin D, a fat-soluble vitamin, can be associated with significant morbidity when prescribed in large doses. We describe a hypoparathyroid patient with vitamin D intoxication who developed painful periarticular calcinosis, nephrocalcinosis with hypertension and chronic renal failure in addition to band keratopathy and hearing loss. He was treated with combination therapy including prednisone, phosphate-binding antacid, phenytoin and disodium etidronate. After 20 months of follow-up there was a significant reduction of periarticular calcinosis, but no improvement in renal function, band keratopathy or hearing loss and possible calcification of the ossicles. The clinicopathologic features of metastatic calcification and the various treatment modalities are reviewed.

Topics: Adult; Aluminum Hydroxide; Calcinosis; Ergocalciferols; Etidronic Acid; Humans; Joint Diseases; Male; Nephrocalcinosis; Phenytoin; Prednisone

Children with hyperprostaglandin E syndrome, a neonatal variant of Bartter syndrome with enhanced renal and systemic formation of prostaglandin E2, have hypercalciuria, nephrocalcinosis, and osteopenia. Because prostaglandin E2 affects tubular calcium handling, stimulates the formation of calcitriol in vitro, and has osteolytic activity, we studied calcium homeostasis and the influence of prostaglandin E2 formation on hypercalciuria in nine patients with hyperprostaglandin E syndrome during long-term indomethacin treatment and after its withdrawal. Suppression of prostaglandin E2 formation by indomethacin resulted in improvement of biochemical and clinical features of hyperprostaglandin E syndrome. However, hypercalciuria, osteopenia, and nephrocalcinosis did not completely resolve. Despite a low calcium diet, daily urinary calcium excretion was enhanced during and after withdrawal of indomethacin treatment (median 6.3, range 5.3 to 14, and median 9.4, range 4.4 to 38 mg/kg per day, respectively). Daily urinary calcium excretion was greater after withdrawal than during indomethacin treatment. Urinary calcium excretion was not correlated with urinary prostaglandin E2 excretion. Plasma levels of intact parathyroid hormone (median 11, range 6.8 to 12 pmol/L) and calcitriol (median 157, range 108 to 236 pg/ml) were elevated during indomethacin treatment and decreased after withdrawal of indomethacin. These data suggest that hypercalciuria in hyperprostaglandin E syndrome is mainly due to a renal leak of calcium, which is caused by enhanced renal formation of prostaglandin E2 and a tubular defect not related to prostaglandin E2 formation. There is no evidence for prostaglandin-stimulated calcitriol formation. Decreasing plasma levels of parathyroid hormone in the presence of renal calcium losses after withdrawal of indomethacin treatment may be due to a bone resorption process caused by systemic prostaglandin formation; the process may contribute to hypercalciuria in the patient not receiving indomethacin.

Topics: Bone Diseases, Metabolic; Calcitriol; Calcium; Calcium Metabolism Disorders; Calcium, Dietary; Child; Child, Preschool; Dinoprostone; Ergocalciferols; Female; Homeostasis; Humans; Indomethacin; Infant, Newborn; Male; Nephrocalcinosis; Parathyroid Hormone; Phosphates; Renin; Syndrome

Options for chronic treatment of hypoparathyroidism include calcitriol, recombinant human parathyroid hormone, and high-dose vitamin D (D2). D2 is used in a minority of patients because of fear of prolonged hypercalcemia and renal toxicity. There is a paucity of recent data about D2 use in hypoparathyroidism.. Compare renal function, hypercalcemia, and hypocalcemia in patients with hypoparathyroidism treated chronically with either D2 (D2 group) or calcitriol.. A retrospective study of patients with hypoparathyroidism treated at the University of Maryland Hospital. Participants were identified by a billing record search with diagnosis confirmed by chart review. Thirty patients were identified; 16 were treated chronically with D2, 14 with calcitriol. Data were extracted from medical records.. Serum creatinine and calcium, hospitalizations, and emergency department (ED) visits for hypercalcemia and hypocalcemia.. D2 and calcitriol groups were similar in age (58.9 ± 16.7 vs 50.9 ± 22.6 years, P = 0.28), sex, and treatment duration (17.8 ± 14.2 vs 8.5 ± 4.4 years, P = 0.076). Hospitalization or ED visits for hypocalcemia occurred in none of the D2 group vs four of 14 in the calcitriol group (P = 0.03); three in the calcitriol group had multiple ED visits. There were no differences between D2 and calcitriol groups in hospitalizations or ED visits for hypercalcemia, serum creatinine or calcium, or kidney stones.. We found less morbidity from hypocalcemia in hypoparathyroid patients treated chronically with D2 compared with calcitriol and found no difference in renal function or morbidity from hypercalcemia. Treatment with D2 should be considered in patients with hypoparathyroidism, particularly in those who experience recurrent hypocalcemia.

Topics: Adult; Aged; Calcitriol; Calcium; Creatinine; Emergency Service, Hospital; Ergocalciferols; Female; Hospitalization; Humans; Hypercalcemia; Hypocalcemia; Hypoparathyroidism; Kidney Calculi; Male; Middle Aged; Nephrocalcinosis; Renal Insufficiency; Retrospective Studies; Vitamins

Nephrocalcinosis (NC) detected by ultrasound is a recognized abnormality for some patients with X-linked hypophosphatemia (XLH) who received vitamin D2 and inorganic phosphate therapy, but is commonly observed in XLH patients treated with 1,25-dihydroxyvitamin D3 and inorganic phosphate supplementation. Nevertheless, long-term follow-up of kidney function in XLH patients with NC detected ultrasonographically has not been reported. We investigated two women with XLH, ages 31 (patient 1) and 39 (patient 2) years, each of whom had suffered at least one documented episode of vitamin D2-induced hypercalcemia and renal azotemia during childhood. Patient 2 had also been treated with inorganic phosphate. No medications for XLH had been taken during adulthood. Renal ultrasonography at our institution demonstrated marked bilateral medullary NC in both women. No other explanation was found for their NC that apparently occurred several decades earlier from medical therapy for XLH. Detailed studies (including creatinine clearance, beta2-microglobulin excretion, and fasting urinary osmolality and acidification) revealed no impairment of kidney function in either patient. Our findings indicate that subradiographic medullary NC acquired during medical therapy for XLH may persist for decades, but with no adverse renal sequelae. Definitive (long-term) assessment of kidney function in the XLH population with NC, however, will be necessary to fully understand the risk of current medical treatment for this most common heritable form of rickets.

Topics: Adult; Ergocalciferols; Family Health; Female; Humans; Hypophosphatemia, Familial; Kidney; Kidney Diseases; Kidney Medulla; Nephrocalcinosis; Time Factors; Uremia

The treatment of X-linked hypophosphatemia (XLH) consists of phosphate and vitamin D3 derivatives. Transient hypercalciuria and hypercalcemia are well-known signs of vitamin D intoxication. Despite urinary calcium excretion control, the danger of nephrocalcinosis in treated patients has been emphasized. It has recently been suggested that hyperoxaluria might be a causative factor of nephrocalcinosis other than calcium in phosphate-treated XLH patients. We measured urinary oxalate and phosphate excretion in 12 patients with the syndrome of hereditary hypophosphatemic rickets with hypercalciuria (HHRH) receiving only oral phosphates and in 5 XLH patients receiving both oral phosphates and vitamin D. No correlation was found between the dosage of phosphate supplements or urinary phosphate excretion and urinary oxalate excretion, in either group of patients. Nephrocalcinosis, presenting as hyperechogenicity of the medullary pyramids, was found in 2 of the 5 XLH patients and only in 2 HHRH patients who had been treated with excessive doses of vitamin D2 and calcium, prior to the true diagnosis being established. We conclude: (1) hyperoxaluria is not a cause of nephrocalcinosis in phosphate-treated patients with hereditary hypophosphatemic rickets; (2) prolonged phosphate treatment alone does not induce nephrocalcinosis in HHRH patients, and (3) we believe that in XLH patients, nephrocalcinosis is essentially due to vitamin D overdosage at some stage, or noncompliance in phosphate intake, leading to repeated undetected hypercalciuric periods.

Topics: Adolescent; Adult; Calcium; Child; Child, Preschool; Ergocalciferols; Female; Humans; Hyperoxaluria; Hypophosphatemia, Familial; Infant; Male; Nephrocalcinosis; Phosphates

An experimental electron-microscopic study of the kidneys was carried out in experimental oxamide nephrolithiasis in rabbits and hypervitaminosis D in rats. The most pronounced changes were revealed in the proximal and the distal convoluted tubules. It is suggested that cytosomes and lysosome-like bodies possibly participated in stone formation and nephrocalcinosis. It is supposed that they played an important role in the morphogenesis of nephrolithiasis man.

Topics: Animals; Ergocalciferols; Kidney; Kidney Calculi; Male; Nephrocalcinosis; Oxalates; Rabbits; Rats

Topics: Administration, Oral; Animals; Bone Diseases; Cholecalciferol; Diet; Ergocalciferols; Gout; Haplorhini; Hypercalcemia; Kidney; Macaca; Nephrocalcinosis; Uric Acid; Vitamin A Deficiency

Topics: Animals; Calciphylaxis; Cholecalciferol; Dihydrotachysterol; Ergocalciferols; Female; Heart; Hypercalcemia; Kidney; Male; Nephrocalcinosis; Pregnancy; Pregnancy, Animal; Rats; Reserpine

Topics: Animals; Ergocalciferols; Female; Glycosaminoglycans; Hydronephrosis; Hypercalcemia; Kidney; Nephrocalcinosis; Rats; Sulfates; Sulfur Isotopes; Urinary Calculi

Topics: Analysis of Variance; Animals; Aorta; Blood Sedimentation; Body Weight; Calcinosis; Cholesterol; Chondroitin; Coronary Vessels; Ergocalciferols; Female; Flavonoids; Hematocrit; Necrosis; Nephrocalcinosis; Rats; Rutin

Topics: Adrenal Cortex Hormones; Adult; Calcium; Diet Therapy; Ergocalciferols; Female; Goiter; Humans; Hypercalcemia; Hypocalcemia; Inositol; Kidney Failure, Chronic; Male; Middle Aged; Nephrocalcinosis; Thyroidectomy; Time Factors; Vitamin D

Topics: Animals; Calcium Phosphates; Citrates; Depression, Chemical; Ergocalciferols; Estradiol; Estrogens; Hydro-Lyases; Kidney; Male; Nephrocalcinosis; Rats

Topics: Animals; Ergocalciferols; Nephrocalcinosis; Parathyroid Glands; Rabbits; Thyroid Gland

Topics: Animals; Ergocalciferols; In Vitro Techniques; Nephrocalcinosis; Parathyroid Glands; Rabbits; Rats; Thyroid Gland

Topics: Cytoplasm; Electrons; Ergocalciferols; Metabolism; Microscopy; Microscopy, Electron; Microsomes; Mitochondria; Nephrocalcinosis; Oxidative Phosphorylation; Pathology; Pharmacology; Rats; Research; Toxicology

Topics: Alloxan; Calcinosis; Cholecalciferol; Dihydrotachysterol; Ergocalciferols; Islands; Islets of Langerhans; Kidney Diseases; Kidney Tubules; Nephrocalcinosis; Pancreas; Pathology; Rats; Research

Topics: Animals; Cortisone; Ergocalciferols; Kidney Diseases; Nephrocalcinosis; Rats; Vitamin D

Topics: Calcinosis; Drug-Related Side Effects and Adverse Reactions; Ergocalciferols; Nephrocalcinosis; Tetany; Vitamin D