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Results for “Hyperphosphatemia”

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PubMed1977

Vascular calcifications under maintenance hemodialysis.

In a cross-sectional study X-rays of the forefoot and the pelvis of 101 adult dialysis patients were taken. Vascular calcifications (forefoot) were observed in 20 patients. The incidence was higher in patients who had been started on dialysis several years ago. However, in a longitudinal prospective study de novo appearance of vascular calcificaitons was observed only in 1 out of 50 dialysed patients, although hyperparathyreoidism and moderate hyperphosphatemia persisted. Vascular calcifications were seen only once in 138 uremic children (56 uremic children without dialysis; 82 uremic children on maintenance hemodialysis). However at autopsy visceral calcifications of the lung were found in three (out of 11) children who did not have vascular calcificaitons on X-rays.

Adolescent↗

PubMed1990

[Pseudohypoparathyroidism and adrenal cortex insufficiency. A case of multiple endocrinopathy due to peripheral hormone resistance].

Since his childhood a now 31-year-old male showed typical symptoms of parathyroid hormone deficiency with hypocalcemia and hyperphosphatemia. We found a target organ resistance to parathyroid hormone and diagnosed pseudohypoparathyroidism. In addition adrenal insufficiency with hypocortisolism was seen. Both hormone systems act by stimulating adenylate cyclase. A defective receptor-adenylate cyclase complex may cause this--for the first time described--combination of endocrine insufficiency.

Adrenal Insufficiency↗

PubMed1978

Effects produced by the administration of high doses of 1,25-dihydroxycholecalciferol to the chick embryo.

White Leghorn chick embryos were injected on the 15th day of incubation with 70 to 300 pmoles 1,25-(OH)2D3. All doses produced hypercalcemia; with the highest dose, the concentration of calcium in serum started to rise 4 h after the injection, reached a peak 20 h after, and was still high 48 h after. Twenty hours after the injection of the same dose, the concentration of inorganic phosphorus in the serum was significantly lower than in the corresponding controls. The tibias from 17-day-old chick embryos injected with 300 pmoles on day 15 were shorter, lighter, and had a lower ash content than those from controls. Histological signs of resorption appeared to be reduced with respect to controls, but no precise quantitation was conducted. The fact that hypercalcemia was not accompanied by hyperphosphatemia may suggest that the vitamin stimulates resorption of calcium from the shell, which is mainly formed by calcium carbonate rather than from the bone from which calcium and phosphate are usually resorbed together.

Animals↗

PubMed1990

Role of vitamin D metabolites in the prevention of the osteopenia induced by ovariectomy in the axial and appendicular skeleton of the rat.

Forty Fischer-344 rats (10 weeks old, 130 g BW) were either bilaterally ovariectomized (OVX) or sham-operated (SHAM). The rats were allocated to the following groups: SHAM; OVX; OVX + 15 ng 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3]/rat/d; OVX + 30 ng 1 alpha,24R,25-trihydroxyvitamin D3 [1,24,25(OH)3D3]/rat/d; OVX + 15 ng 1,25(OH)2D3/rat/d + 30 ng 1,24,25(OH)3D3/rat/d. The vitamin D metabolites were fed orally starting 4 weeks after surgery. Urine and blood samples were taken at several time points during the experiment. Twenty-one weeks after surgery all rats were sacrificed, and the proximal tibiae and the first lumbar vertebrae were processed undecalcified for static bone histomorphometry. Ovariectomy induced a 40% reduction in vertebral cancellous bone area, and a 69% reduction in tibial cancellous bone area. This bone loss in OVX rats was associated with moderately increased biochemical and histomorphometric indices of bone formation and resorption as compared to values in sham-operated animals. Through inhibition of bone resorption, treatment of OVX rats with 1,25(OH)2D3, 1,24,25(OH)3D3, and the metabolite combination prevented the ovariectomy-induced osteopenia in the lumbar vertebra, and partially prevented cancellous bone osteopenia in the tibial metaphysis. However, OVX rats receiving 1,25(OH)2D3 alone or in combination with 1,24,25(OH)3D3 exhibited hypercalcemia, hyperphosphatemia, hypercalciuria, and impaired bone mineralization. Treatment of OVX rats with 1,24,25(OH)3D3 alone, on the other hand, only slightly increased serum calcium levels and did not impair bone mineralization. Furthermore, the inclusion of 1,24,25(OH)3D3 with 1,25(OH)2D3 partially antagonized the untoward effects of 1,25(OH)2D3 on bone mineralization. These data suggest that the actions of 1,24,25(OH)3D3 on bone metabolism might differ from that of 1,25(OH)2D3, and that 1,25(OH)2D3 and, particularly, 1,24,25(OH)3D3 may be potentially effective agents for the prophylaxis of postmenopausal osteoporosis.

24,25-Dihydroxyvitamin D 3↗

PubMed1996

Biochemical effects of oral sodium phosphate.

Our objective was to monitor serum and urine biochemical changes after oral sodium phosphate cleansing in a prospectively designed study. The study subjects were seven healthy, asymptomatic adults. Sodium phosphate 45 ml diluted in 45 ml water was given orally at baseline and 12 hr later. Calcium, ionized calcium, phosphorus, sodium, potassium, creatinine, and PTH were analyzed at 2, 4, 6, 9, 12, 14, 16, 18, 21 and 24 hr after the first challenge. Urinary calcium, phosphorus, sodium, potassium, and cyclic AMP were analyzed at baseline and every 2 hr after oral sodium phosphate. Blood pressure, pulse, and respiratory rate were recorded every 2 hr and symptom questionnaires using visual analog scales were completed. A marked rise in phosphorus (peak range 3.6-12.4 mg/dl, P < 0.001) and falls in calcium (P < 0.001) and ionized calcium (P < 0.001) were seen. Rises seen in PTH and urinary cAMP confirmed the physiologic significance of the biochemical effect. There were no significant changes in other serum and urine laboratory or clinical assessments. Reported significant symptoms included bloating, cramps, abdominal pain, and nausea. Significant hypocalcemia and hyperphosphatemia after oral sodium phosphate raises concern about its use in normal individuals. Oral sodium phosphate should not be administered in patients with cardiopulmonary, renal, or hepatic disease.

Abdominal Pain↗

PubMed1996

Hypocalcaemia and chronic alcohol intoxication: transient hypoparathyroidism secondary to magnesium deficiency.

The authors report the observation of an alcoholic patient admitted for tetanic manifestations, in whom severe hypocalcaemia associated with hyperphosphatemia were suggestive of hypoparathyroidism. Administration of magnesium supplementation alone improved the clinical features and led to the correction of the calcium abnormalities. The mechanisms of hypomagnesemia in alcohol intoxication are reviewed as well as the links with hypocalcaemia.

Aged↗

PubMed1980

Tumoral calcinosis: evidence for concurrent defects in renal tubular phosphorus transport and in 1 alpha,25-dihydroxycholecalciferol synthesis.

A 50-year-old Latin American man with tumoral calcinosis presented with hyperphosphatemia (6.62 +/- 1.04 SD mg/dl), elevated renal threshold phosphorus concentration (TmP) (7.3 mg/GFR), and 1,25-dihydroxyvitamin D [1,25-(OH)2D] (69 pg/ml) hypercalciuria (239 mg/day), and a high fractional intestinal calcium (Ca) absorption (0.74). Sodium cellulose phosphate therapy (20 g/day) lowered urinary Ca, and partially reduced serum phosphorus (P) and TmP to 5.91 +/- 0.63 mg/dl and 6.2 mg/GFR, respectively. Serum 1,25-(OH)2D remained elevated at 58-64 pg/ml. Amphojel therapy (4 oz/day) decreased urinary P to 23 +/- 21 mg/day and lowered serum P to 5.75 +/- 0.36 mg/dl (P < 0.05). TmP increased to a value of 8.0 mg/GFR while serum 1,25-(OH)2D continued to remain elevated at 53 pg/ml. This case illustrates the probable operation of dual abnormalities in tumoral calcinosis represented by augmented renal conservation of P and an elevation in the circulating concentration of 1,25-(OH)2D.

Calcinosis↗

PubMed1987

The effect of intravenous sodium fluoride and synthetic salmon calcitonin on plasma total calcium, inorganic phosphate, and ionic fluoride.

Various doses of sodium fluoride (NaF), salmon calcitonin (CT) and NaF combined with CT were given intravenously to rats (236 +/- 2 g). Blood plasma samples were collected at various times up to 24 hours and measured for total calcium (adjusted for variation in plasma albumin), inorganic phosphate, ionic fluoride, urea, and creatinine. Following injection of NaF alone, significant hypocalcemia and hyperphosphatemia was observed. In contrast, CT injections resulted in hypocalcemia and hypophosphatemia. NaF and CT given in combination generally resulted in the hypocalcemia being equal to or greater than that calculated from the simple addition of their individual effects. Significant increases in both plasma creatinine and plasma urea were observed following treatment with NaF alone or with CT and NaF together, whereas CT alone had negligible effect. These results suggest that NaF does not mimic the effects of CT; rather that NaF and CT interact to modify their individual effects. The influence of NaF probably occurs via an effect on kidney function.

Analysis of Variance↗

PubMed1987

Effects of vitamin D deficiency in the chicken embryo.

Vitamin D-deficient chicken embryos were obtained by feeding laying hens a diet in which 5 micrograms 1,25(OH)2D3/kg feed were substituted for the vitamin D3 supplement in the control diet. Hatchability, total Ca and inorganic P concentration in blood, and tibial ash/dry weight ratio were determined in the vitamin D-deficient embryos and in embryos obtained from hens fed the control diet supplemented with 1100 IU vitamin D3/kg feed. After 5 weeks on the substituted diet the hens laid eggs that showed decreased hatchability in spite of excellent shell quality. All determinations in blood and bones were made on embryos of eggs laid after 6-12 weeks on the diets. On the 17th day of incubation the embryos derived from hens fed the substituted diet showed significant hypocalcemia and hyperphosphatemia and a low tibial ash/dry weight ratio. Injection of 1,25(OH)2D3 3 days before killing corrected the hypocalcemia of the deficient embryos. Those chicks that managed to hatch had normal levels of calcium and inorganic phosphate 1 day after hatching. These findings support previous suggestions by us and other authors that vitamin D metabolites are required by the embryo in order to mobilize calcium from the shell, and decreased hatchability in vitamin D-deficient embryos is related to a defect in calcium mobilization from the shell. While in previous studies a decrease in hatchability was the only parameter used to judge D deficiency of the embryos in our present studies, the deficiency is confirmed by demonstrating a deficit in mineral metabolism which is a more specific sign of D deficiency.

24,25-Dihydroxyvitamin D 3↗

PubMed2004

Pseudohypoparathyroidism presenting with bony deformities resembling rickets.

Pseudohypoparathyroidism (PHP), characterized by hypocalcemia, hyperphosphatemia and elevated parathormone level, may rarely be associated with bony deformities resembling rickets. The authors report two siblings with clinical and radiological features suggestive of rickets unresponsive to treatment with vitamin D. Low serum calcium, elevated serum phosphate, normal renal functions, raised tubular maximum of phosphate and high serum parathormone were suggestive of PHP. Treatment with 1-hydroxyvitamin D and calcium carbonate led to decrease in bone pain, increase in height and weight and resolution of radiological features. PHP should be suspected in patients with bony deformities, hypocalcemia, elevated blood phosphate levels and normal renal functions.

Bone Diseases↗

PubMedDate not supplied

Effect of birth asphyxia on serum calcium levels in neonates.

Serum calcium and phosphorus levels were measured at birth, 6 hours, 24 hours, and on 5th day of life in 35 neonates with birth asphyxia (one-minute Apgar score of 6 or less), and in 37 neonates without asphyxia (one-minute Apgar score of 7 or more). Infants were divided into three groups: FT-AGA (n = 30, asphyxia = 15), FT-IUGR (n = 20, asphyxia = 10) and PT-AGA (n = 22, asphyxia = 10). Asphyxiated infants--FT-AGA as well as FT-IUGR--had significantly lower serum calcium levels than control infants during each of the time period studied. In PT-AGA infants with asphyxia, the serum calcium was significantly low only on 5th day of life. Lack of calcium intake, and hyperphosphatemia were identified as possible risk factors for low serum calcium in asphyxiated infants. No change in serum calcium levels was found in bicarbonate-treated asphyxiated infants in comparison to those who did not receive sodium bicarbonate. In view of the high incidence of low serum calcium in asphyxiated infants, serial monitoring of serum calcium levels is recommended in these infants.

Apgar Score↗

PubMed2006

Neonatal pseudohypoparathyroidism.

The case of a neonate is presented who had early onset seizure associated with hypocalcemia, hyperphosphatemia, and raised parathyroid hormone. The infant did not have any stigmata of pseudohypoparathyroidism. The hypocalcemia was initially resistant to calcium therapy, but responded to vitamin D analog therapy. The diagnosis of 'neonatal pseudohypoparathyroidism' was entertained; the infant remained stable and seizure-free with normal serum biochemistry during 3 months of follow-up.

Calcitriol↗

PubMed2003

[Atherosclerosis and uremia: signifance of non-traditional risk factors].

Arteriosclerosis, atherosclerosis and vascular calcification are causally related to the high morbidity and mortality of patients with chronic renal failure. Oxidative stress and carbonyl stress of uremia, dialysis procedure and/or intravenous iron therapy result in AGE (advanced glycation end-product), ALE (advanced lipoxidation end-product) and AOPP (advanced oxidation protein product) formation, favouring together with elevated CRP (C-reactive protein) levels the development of cardiovascular and cerebrovascular complications. Enhanced plasma levels of homocysteine and ADMA (asymmetric dimethylarginine) contribute to this process. In addition, in chronic renal insufficiency hyperphosphatemia and an enhanced calcium x phosphorus ion product are associated with the morbidity and mortality of the patients, particularly in the presence of fetuin deficiency. Phosphorus, AGEs and AOPPs, beside other factors, catalyze the conversion of vascular smooth muscle cells to osteoblast--like cells (particularly in the presence of monocytes/macrophages), resulting in bone matrix protein formation. Other risk factors, such as age, male sex, smoking, hypertension, diabetes, chronic inflammation, insulin resistance or dyslipidemia (enhanced non-HDL-cholesterol) also contribute to the atherosclerotic risk profile of the patient with chronic renal insufficiency. While there is growing understanding of the mechanisms involved in arteriosclerosis, atherosclerosis and vascular calcification in uremia, we are still missing effective therapeutic maneuvers for reduction of excess mortality in uremic patients.

Arginine↗

PubMed2003

Recurrent calcinosis in consecutively transplanted kidney grafts.

Repeated renal transplant calcinosis is a rare event. We report a young woman in whom repeated calcinosis was observed in two consecutive renal transplants. Persistent secondary hyperparathyoidism and hyperphosphatemia due to impaired renal function were assumed as the pathogenic factors for calcinosis. Sub-total parathyroidectomy performed shortly after the third transplantation and good function of the renal graft have prevented calcinosis in the third graft for more than five years.

Adult↗

PubMedDate not supplied

Metastatic calcifications and severe hypercalcemia in a patient with parathyroid carcinoma.

Primary hyperparathyroidism is rarely produced by parathyroid carcinoma. We present the case of a 63-yr-old man who was admitted due to recent onset of constipation, weakness and progressive lethargy. At physical examination, a left cervical mass was palpated. Marked hypercalcemia (serum calcium 25 mg/dl) (6.22 mmol/l) complicated by renal insuficiency (serum creatinine 4.4 mg/dl) (388 micromol/l) was found, but both were unresponsive to conventional therapy and hemofiltration. Autopsy examination showed a carcinoma of the upper left parathyroid gland, multiple foci of metastatic calficications in the vessel walls and parenchyma of both lungs and kidneys, and the myocardium, which contributed to multi-organ failure and death. In addition to describing the clinical presentation, we review the mechanism of metastatic calcifications as well as the role of renal function and hyperphosphatemia, and the basis for therapy of hypercalcemic crisis.

Autopsy↗

PubMed2005

[Acute renal failure].

The acute renal failure is characterized by a rapid deterioration of the renal function. In addition to the usual prerenal, intrinsic and postrenal causes of an acute renal failure distinct causes have to be considered for oncological patients. Factors imminent to the malignant disease, e. g. paraneoplastic syndromes or retroperitoneal bulks can account for an acute renal failure. Paraproteins as produced by a multiple myeloma are other possible causes for renal dysfunction. For some anticancer drugs nephrotoxicity is a potential side effect, in particular for cisplatin, methotrexate, ifosfamide and melphalan. A hemolytic uremic syndrome may be induced by mitomycin and gemcitabine. Extensive surgery can be associated with rhabdomyolysis and myoglobinuria and results in renal impairment. Treatment of a chemosensitive neoplasia with a highly effective regimen may result in a tumor lysis syndrome with hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia.

Acute Disease↗

PubMed1996

[Acute reversible encephalopathy with brain edema and serial seizures in pseudohypoparathyroidism].

A 16 year old patient with the typical clinical signs of Albright's hereditary dystrophia developed series of epileptic seizures with loss of consciousness, tonic muscle contractions and bite of the tongue. After termination of the seizures there was coma without focal neurological signs. CT scan revealed diffuse brain edema. Electroencephalographic studies showed generalized slowing. In laboratory tests the only abnormalities were marked hypocalcemia (1.15 mmol/l) and hyperphosphatemia. Blood parathyroid hormone (PTH) was elevated. PTH-Test confirmed the diagnosis of pseudohypoparathyroidism. The patient was treated with calcium and 1,25-dihydroxy-cholecalciferol. After few days the severe encephalopathy, CT and electroencephalographic changes were completely reversible. Hereditary disturbances of the parathyroid hormone metabolism are rare diseases. Hypocalcemia must be included into the differential diagnosis of seizures and brain edema to avoid invasive diagnostic and irrational treatment.

Adolescent↗

PubMed2004

Acute renal failure due to tumor lysis syndrome in a patient with non-Hodgkin's lymphoma.

Tumor lysis syndrome is characterized by multiple metabolic derangements resulting from the release of intracellular components into the bloodstream due to abrupt malignant cell death, spontaneously or following antineoplastic therapy. The syndrome is characterized by hyperkalemia, hyperuricemia, hyperphosphatemia, and hypocalcemia, while deposition of uric acid and calcium phosphate crystals may result in acute renal failure, which is often exacerbated by concomitant intravascular volume depletion. A case of tumor lysis syndrome complicated by acute renal failure in a patient with non-Hodgkin's lymphoma is reported and the pathophysiology, the clinical features, and the treatment options are discussed.

Acute Kidney Injury↗