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PubMedDate not supplied

Aluminum-related osteomalacia in renal-failure patients.

The pathophysiology, clinical presentation, prevention, and treatment of aluminum-related osteomalacia in renal-failure patients are reviewed. Aluminum-related osteomalacia can develop in patients exposed to high concentrations of aluminum either in dialysis solutions or through gastrointestinal aluminum absorption from aluminum-containing antacids used to treat hyperphosphatemia. Although the exact etiology of aluminum-related osteomalacia is unknown, aluminum is believed to inhibit bone mineralization by forming an inhibitory complex with citric acid at physiologic concentrations. The complex is deposited along bone mineralization fronts and in bone marrow. The major symptoms of aluminum-related osteomalacia include skeletal pain, fractures, and vertebral collapse. The disease is difficult to diagnose because patients may have normal or slightly elevated serum concentrations of calcium, phosphate, alkaline phosphatase, and parathyroid hormone. Direct measurement of bone aluminum content (using biopsy) is often needed to confirm diagnosis. The aluminum-chelating agent deferoxamine mesylate can be used to measure bone aluminum content indirectly. Aluminum intoxication can be managed either by preventing exposure to aluminum or by removing deposited aluminum from bone. New standards restrict aluminum content in dialysis solutions, and prevention now focuses on the use of aluminum-free phosphate binders for treatment of hyperphosphatemia. Calcium carbonate may be as effective as aluminum-containing antacids in controlling serum phosphate concentrations, but it should be used cautiously in patients who are hypercalcemic or at risk of developing metastatic calcification. Chelation therapy with deferoxamine has improved the symptoms and bone histology in a small number of patients. Clinical improvements have been seen in patients receiving intravenous deferoxamine 2-6 g per week for 20 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗

PubMed1969

Metabolic bone disease secondary to renal and intestinal disorders.

Metabolic bone disease occurring in renal or intestinal disorders has been reviewed with particular reference to etiological factors. Hyperparathyroidism is seen as a recurring cycle of renal damage-hyperphosphatemia-hypocalcemia-parathyroid stimulation-mobilization of bone calcium and phosphate-renal tubular phosphate rejection. In intestinal cases, the initial stimulus is presumably hypocalcemia. Osteomalacia is seen as resulting from phosphate depletion for the following reasons:1. Experimentally, rickets results from dietary phosphate restriction in rats.2. Such rickets is not prevented by the presence of normally adequate amounts of dietary vitamin D, and may therefore be termed "resistant" in the clinical sense.3. Osteomalacia or rickets in intestinal malabsorption and renal tubular disorders is associated with hypophosphatemia due to excessive fecal or urinary loss.4. Renal tubular rickets has been healed by oral phosphate loading in some studies.5. Acidosis may induce osteomalacic changes, experimentally and clinically (for example, in uretero-sigmoidostomy). Reversal of systemic acidosis with oral bicarbonate has resulted in phosphate retention and a rising serum phosphate in one such case.6. Preliminary data from analysis of full-thickness bone biopsy in two osteomalacic patients shows a significant reduction in calcium and phosphate content.7. Despite the hyperphosphatemia of azotemic renal failure, over-all phosphate depletion may be present in this situation also due to: * Diminished dietary phosphate in low protein diets * Nausea and vomiting * Occasional diarrhea * The use of oral phosphatebinding antacids * Perpetuation of urinary phosphate losses by reduction in proportion of tubular reabsorbed phosphate (secondary hyperparathyroidism) and possibly high filtered load per nephron * Repeated losses of phosphate to bath fluid during dialysis.

Bone Diseases↗

PubMedDate not supplied

[Effect of 24,25-dioxycholecalciferol on calcium-phosphorus metabolism and bone tissue in rats with experimental renal failure].

Experimental chronic renal failure (CRF) in rats gave rise to azotemia, hyperphosphatemia, reduction in the proportion of the diaphyses, decrease in them of calcium, phosphorus and hydroxyproline, and to the lowering of the calcium content in the epiphyses. Administration to the animals of 0.025 microgram of 1,25-dioxycholecalciferol (1,25(OH)2D3) a day did not make the indicators under consideration return to normal. At the same time 1,25(OH)2D3 enhanced the degree of hyperphosphatemia and demineralization of the epiphyses, provoked moderate hypercalcemia and dramatically enhanced calcinosis in the aorta and in the remainder of the kidney. Administration of 24,25-dioxycholecalciferol (24,25(OH)2D3) in a dose of 0.25 microgram made the majority of the indicators return to normal, increasing the proportion of the diaphyses and the content in them of calcium and phosphorus, reducing the blood phosphorus content and the degree of azotemia. Furthermore, 24,25(OH)2D3 raised the collagen content in the diaphyses and epiphyses. A higher dose of 24,25(OH)2D3 (1.25 microgram) did not appear more effective. In none the doses applied, 24,25(OH)2D3 produced hypercalcemia or calcinosis. Combination of 1,25(OH)2D3 in a dose of 0,025 microgram and 24,25(OH)2D3 in a dose of 1,25 microgram slightly reduced the hypercalcemic, hyperphosphatemic and calcinosis-inducing effects of 1,25(OH)2D3, completely prevented osteoporotic alterations in the diaphyses, but enhanced the demineralization in the epiphyses, which may point to the advisability of reducing the doses of these metabolites on combined use. The data obtained indicate that 24,25(OH)2D3 is a more effective and safer agent for correcting the disturbances of the phosphorus-calcium metabolism and osseous lesions in CRF than 1,25(OH)2D3.

24,25-Dihydroxyvitamin D 3↗

PubMed1980

Clinical relationships between serum phosphorus and other blood chemistry values in alcoholics.

Hypophosphatemia was found in 11 of 434 (2.5%) male patients admitted to an alcohol treatment program and 21 of 69 (30.4%) male alcoholic patients admitted to the medical wards. In contrast, hyperphosphatemia was found in 43 of 434 (9.9%) treatment program alcoholics, and only one of 69 (1.4%) medical-ward alcoholics. Analysis of a sample of 57 nonalcoholic inpatients from the same hospital revealed one (1.8%) patient with hypophosphatemia and one (1.8%) patient with hyperphosphatemia. No relationship was found between phosphorus levels and magnesium, creatinine phosphokinase, RBCs, or hematocrit. A transient by significant (P less than .05) hypophosphatemia was found between the second and fifth days after admission in a subsample of 26 medical-ward alcoholics who had had a normal serum phosphate level on admission. It is suggested that phosphate levels of less than 1.1 mg/dL may predict impending hemolysis or rhabdomyolysis in the alcoholic.

Adult↗

PubMed1995

[Pseudohypoparathyroidism].

A 5 year old boy with normal phenotype and normal renal function presented tetany. Hypocalcemia and hyperphosphatemia, with increased serum levels of parathyroid hormone (PTH) were detected in serial measurements. Pseudohypoparathyroidism was diagnosed. This disease presents the biochemical abnormalities of hypoparathyroidism (hypocalcemia, hyperphosphatemia) with peripheral resistance to PTH activity. The patient was treated effectively with calcium and vitamin D supplements. The causes of hypocalcemia related to parathyroid gland activity are reviewed and the physiopathology of pseudohypoparathyroidism is described.

Alkaline Phosphatase↗

PubMed1995

[Vitamin D treatment and renal osteodystrophy: indications and modalities].

1. 1 alpha (OH) vitamin D3 derivatives have an inconstant long term inhibitory effect on PTH secretion. As a matter of fact they act by three mechanisms, one of these being antagonistic: 1) a direct inhibitory action on the prepro-PTH gene; 2) an indirect inhibitory action by increasing plasma calcium; 3) an indirect stimulatory action by increasing plasma phosphate. These two latter phenomena are due to the stimulation of the intestinal absorption of these ions as well as to an intrinsic osteolytic action which may override the inhibition of the bone release of these ions in relation with the decrease of the PTH plasma levels. 2. The use of 1 alpha (OH)D3 derivatives in patients on chronic dialysis is justified in about 30% of the patients on dialysis when in spite of native vitamin D repletion and adequate predialysis control of plasma calcium (2.5 +/- 2 mmol/l) and of plasma phosphate (1.4 - 1.7 mmol/l), the PTH plasma levels are 3 or 5 fold the upper limit of normal whether the patient is on hemodialysis or on CAPD. When hyperphosphatemia is > 1.7 mmol/l it is first necessary to correct it by the use of higher doses of alkaline calcium salts given with the meals as phosphate binder together with a negative perdialytic calcium balance induced by a lower dialysate calcium in order to avoid hypercalcemia. Control of hyperphosphatemia is indeed a necessary prerequisite for the long term PTH suppressive efficacy of 1 alpha OH vitamin D derivatives. 3. The use of 1 alpha(OH)D3 derivatives in the treatment of the predialysis uremic patients is even more limited because there is no additional mean to decrease the risk of hypercalcemia when oral calcium is used as phosphate binder because of the danger of aluminum and magnesium phosphate binders. Fortunately in the adult, oral calcium used as phosphate binder in association with phosphate restriction and correction of possible vitamin D depletion and acidosis is usually efficace to control hyperparathyroïdism without 1 alpha OH vitamin D3. This is not the case in the child to whom protein and phosphate restriction should not be prescribed because of its incompatibility with the Recommended Diet Allowance. Fortunately the high remodeling rate of his growing bones, decreases the risk of hypercalcemia due to the combination of CaCO3 and 1 alpha OH vitamin D3.

Chronic Kidney Disease-Mineral and Bone Disorder↗

PubMedDate not supplied

[The characteristics of histocompatibility antigen distribution in urolithiasis patients with a phosphorus metabolic disorder].

Phosphorus metabolic disturbances play a great role in the occurrence of urolithiasis. This study covered 150 patients with urolithiasis to establish correlations between the frequency of histocompatibility antigens and the increase in blood and urinary phosphorus levels. The HLA antigens were identified by the routine microlymphocytotoxic method involving a histotyping serum panel. The ABO antigens and rhesus were determined by the agglutination method by using reference sera. The study revealed specific distribution of histocompatibility antigens in urolithiasis patients with disturbed phosphorus metabolism. Hyperphosphatemia correlated with the higher frequency of HLA-B35 (chi 2 = 9.89) and E/E system rhesus (chi 2 = 8.63); hyperphosphaturia showed a negative association with the HLA-A28 antigens (chi 2 = 9.7), as well as with E/e (chi 2 = 14.69) and e/e (chi 2 = 39.36) and a positive association with HLA-B13 (chi 2 = 5.98) and B35 (chi 2 = 36.58). The highest relative risk for hyperphosphatemia associated with the B27 and B35 antigens was observed with genetic predisposition, being 3.63 and 7.13, respectively. B12- and B35-positive individuals were at higher risk for hyperphosphaturia up to 11.25. There were significant differences in antigen frequency, and sex, genetic predisposition to urolithiasis, association of phosphorus metabolic disturbances with other metabolic disorders, and their effects of parathyroid lesions, etc. The findings reveal the immunogenetically induced risk for the occurrence and development of urolithiasis with disturbed phosphorus metabolism to make goal-oriented prophylactic measures.

ABO Blood-Group System↗

PubMed1977

Hypocalcemic coma following two pediatric phosphate enemas.

Coma, tetany, dehydration, hypotension, tachycardia, and hyperpyrexia developed in a 2 1/2-year-old girl following two hypertonic phosphate pediatric enemas. She had marked hyperphosphatemia, hypocalcemia, hypernatremia, and acidosis. Hypocalcemia due to hyperphosphatemia can explain all of these findings. Calculations indicate that about one third of the phosphorus and sodium contents of the enema were absorbed. Physicians should be aware of the potentially lethal complication of this treatment, which is part of everyday practice.

Child, Preschool↗

PubMed1997

Hypomagnesemic hypokalemia and hypocalcemia: clinical and laboratory characteristics.

Clinically important electrolyte disturbances such as hypokalemia and hypocalcemia have been well described in patients with hypomagnesemia of various causes. We undertook the present study to describe in detail the clinical characteristics as well as the acid base and electrolyte abnormalities in an effort to better understand the conditions that favor the appearance of this syndrome of hypomagnesemic hypokalemia and hypocalcemia, and the underlying pathogenetic mechanisms. A total of 35 adult patients (23 male, 12 female), aged 21-79 years, who exhibited profound hypomagnesemia, hypokalemia, and hypocalcemia on their admission were studied. The most common causes of the syndrome were alcoholism and cisplatin administration. All but 2 patients with diarrhea had inappropriate magnesiuria. Despite hypokalemia and hypocalcemia all patients exhibited renal potassium and calcium wasting. Eight alcoholic patients with alcohol withdrawal syndrome or acute intoxication had pure respiratory alkalosis, while 6 patients with severe hypokalemia presented with metabolic alkalosis. Three chronic alcoholic patients exhibited metabolic alkalosis coexisting with respiratory alkalosis, while 1 alcoholic patient had the syndrome of alcoholic ketoacidosis. Hyponatremia was evident in only 2 patients with clinical and laboratory evidence of extracellular volume depletion. Hypophosphatemia was observed in 12 patients mainly due to inappropriate phosphaturia. Finally, hyperphosphatemia was found in 2 alcoholic patients with severe respiratory alkalosis. In conclusion, patients with hypomagnesemic hypokalemia and hypocalcemia exhibit multiple interrelated acid base and electrolyte abnormalities and mainly hypokalemia due to inappropriate kaliuresis, hypophosphatemia or rarely hyperphosphatemia, respiratory and metabolic alkalosis, as well as mixed acid base disorders.

Acid-Base Imbalance↗

PubMedDate not supplied

Bone fractures in children with chronic cholestasis.

The clinical features, biochemical data, roentgenographical bone changes and liver histological studies of four children with fractures related to chronic cholestasis are described. Two of them had Alagille syndrome and the other two, biliary atresia. Only one patient presented with forearm fracture associated with typical radiographic evidence of rickets. The others revealed generalized osteopenia together with fractures in arms, forearms, and wrists respectively. Of these, one with rickets had hypocalcemia and hypophosphatemia; one had decreased parathyroid hormone with mild hypocalcemia and hyperphosphatemia; one had hyperphosphatemia solely. Eucalcemia and euphosphatemia were noted in the remaining patient. Their bone lesions deteriorated in spite of treatment, except for the one with clinical rickets. All the patients succumbed eventually. It was concluded that the real pathogenesis of bone lesions in end-stage liver disease of chronic cholestatic children remains unclear. However, because rickets may intervene, continuing efforts to supply vitamin D and calcium since diagnosis of chronic cholestasis on a long-term basis, to prevent fracture, is still mandatory.

Child, Preschool↗

PubMedDate not supplied

Vitamin D retains an important role in the pathogenesis and management of secondary hyperparathyroidism in chronic renal failure.

Chronic kidney disease (CKD) causes alterations in mineral metabolism inducing the development of secondary hyperparathyroidism (HPT) and renal osteodystrophy. Recently, it has been suggested that these alterations play an important role in determining extraskeletal calcification and thus cardiovascular morbidity and mortality among CKD patients. An impaired 1 alfa -hydroxylation of 25-hydroxycholecalciferol (25(OH)D3) to 1,25-dihydroxycholecalciferol (1,25(OH)2 D3) with decreased circulating 1,25(OH)2 D3 levels is commonly observed in patients with creatinine clearance below 70 ml/min. The reduction in 1,25(OH)2 D3 production triggers the up-regulation of parathyroid hormone (PTH) synthesis, through a decreased suppression on PTH gene transcription and a decreased intestinal calcium absorption. A reduced expression of vitamin D receptor (VDR) and a less efficient binding of the complex 1,25(OH)2 D3 -VDR to specific DNA segments account for the resistance to 1,25(OH)2 D3 in target cells. Thus, absolute and relative 1,25(OH)2 D3 deficiency is one of the causes of secondary HPT in patients with CKD, together with phosphate retention and skeletal resistance to PTH. Consistently with these pathophysiological mechanisms, the therapeutic use of 1,25(OH)2 D3 still represents a milestone for the treatment of secondary HPT and renal osteodystrophy, even though hypercalcemia and hyperphosphatemia are common adverse events and may increase the risk of cardiovascular calcifications. To reduce the impact of such adverse effects while retaining anti-PTH activity, 1,25(OH)2 D3 analogues with lower calcemic effects have been synthesized and are now available for clinical use.

Calcinosis↗

PubMed1976

Calciphylaxis in man. A syndrome of tissue necrosis and vascular calcification in 11 patients with chronic renal failure.

Eleven patients with chronic renal failure and presumed secondary hyperparathyroidism developed a syndrome of medial calcinosis of the arteries and painful ischemic ulcers of the fingers, legs, or thighs, or any combination of the three. Five patients required maintenance hemodialysis; six had functioning renal homografts. Severe hyperphosphatemia had existed in each; seven showed roentgenographic evidence of subperiosteal resorption. Similarities are evident between the lesions and experimentally produced calciphylaxix. The lesions demonstrated a relentless, progressive course, with serious morbidity and mortality. Hyperplastic or adenomatours parathyroid tissue was removed from ten of 11 patients unergoing surgical procedures; healing followed in seven patients. Treatment with phosphate-binding antacids to lower serum phosphorus levels may prevent this syndrome. Total or subtotal parathyroidectomy should be considered when ischemic skin lesions appear in uremic patients or in renal transplant recipients.

Adolescent↗

PubMed2003

Electrolyte disorders following oral sodium phosphate administration for bowel cleansing in elderly patients.

BACKGROUND: Oral sodium phosphate is currently used for colon preparation prior to colonoscopy or barium enema. Sodium phosphate induces hyperphosphatemia, hypocalcemia, and hypokalemia. Elderly patients are at an increased risk for phosphate intoxication due to decreased glomerular filtration rate, medication use, and systemic and gastrointestinal diseases. We investigated these electrolyte disorders and their correlation with creatinine clearance, coexistent diseases, medications, and functional status. METHODS: Thirty-six hospitalized patients were included in the study. On day 1, patients were administered 2 doses of oral sodium phosphate. Venous blood samples for electrolyte determination were obtained at 7 AM on days 1, 2 (the procedure day), and 3. Urine samples were obtained from 10 patients. RESULTS: An increase in serum phosphorus level was correlated with a decreased creatinine clearance (R = -0.52; P =.001). Hypocalcemia and hypokalemia were present in 21 (58%) and 20 (56%) patients, respectively. Patients with a serum potassium concentration of 3.5 mEq/L or less on day 2 had a lower serum potassium concentration on day 1 vs those with a serum potassium concentration greater than 3.5 mEq/L on day 2 (P =.03). Five (dependent patients) had a serum potassium concentration of 3 mEq/L or less and 2 had severe diarrhea, necessitating treatment. There were more demented patients with hypokalemia compared with normokalemic patients (P<.05). Urinary fractional excretion of phosphorus tripled on day 2 (P =.01). Potassium and sodium fractional excretion remained unchanged. CONCLUSIONS: Sodium phosphate induces serious electrolyte abnormalities in the elderly. The frequency and severity of hypokalemia is due to intestinal potassium loss associated with inadequate renal potassium conservation and is apparently more prevalent in frail patients. Assessment of serum electrolytes, phosphorus, and calcium prior to sodium phosphate preparation is advised, and in selected patients, postprocedural assessment and correction may be required.

Administration, Oral↗

PubMed1996

Ocular tumoral calcinosis. A clinicopathologic study.

Tumoral calcinosis is a rare systemic disorder characterized by para-articular ectopic soft-tissue calcification. This case report describes the ophthalmic features (palpebral conjunctival calcific nodules, the white limbal girdle of Vogt, disc drusen, and angioid streaks) in a 38-year-old Asian woman who had tumoral calcinosis associated with hyperphosphatemia. A morphologic study of the calcified nodules on the palpebral conjunctiva disclosed deposition of hydroxyapatite crystals in an extracellular matrix (deposit) containing alcianophilic mucopolysaccharides. Excision of the eyelid nodules was not followed by recurrence.

Adult↗

PubMed1980

Phosphate poisoning complicating treatment for iron ingestion.

A 15-month-old child was treated for iron intoxication with a hypertonic sodium phosphate mixture. Clinical deterioration manifested by fever, obtundation, abdominal distention, dehydration, and hypotension followed soon after the administration of this mixture. Such symptoms may occur with either iron overdosage or with phosphate poisoning. At this time, the patient's serum chemistry values included: iron, 49 micrograms/dL; phosphorus, 24.6 mg/dL; and calcium, 4.5 mg/dL. The hypocalcemia, hyperphosphatemia, and dehydration were treated with parenteral gluconate calcium, intravenous fluids, and general supportive measures. Although the child had an uneventful recovery despite severe phosphate poisoning, therapeutic alternatives, such as sodium bicarbonate, should be used as adjuncts in the treatment of acute iron ingestion.

Adolescent↗

PubMed1981

Tumoral calcinosis in an infant.

Tumoral calcinosis is a disease characterized by large, calcified, painless masses, usually near joints, in otherwise healthy children and young adults. Biochemical findings are normal except for an association with hyperphosphatemia. A familial and racial predisposition is seen, with most cases affecting blacks. This disease is believed to represent an unknown inherited abnormality in phosphate metabolism. Because of the tendency of the masses to recur after incomplete excision, the recommended treatment is early and complete excision. Phosphate binders may be useful in certain cases.

Adolescent↗

PubMed1984

Continuous nasogastric phosphorus infusion in hypophosphatemic rickets of prematurity.

Radiologic and biochemical abnormalities associated with nutritional hypophosphatemic rickets were discovered in a 945-g preterm infant despite daily supplementation with 800 to 1,600 IU of ergocalciferol (vitamin D2) and an elevated serum 25-hydroxyvitamin D concentration. Vitamin D supplementation was stopped, and the rickets was corrected by phosphorus supplement alone with the use of a unique technique of long-term, continuous nasogastric phosphorus infusion. Normophosphatemia was rapidly achieved and effectively maintained. Hypocalcemia did not occur at rates of infusion of 100 mg of elemental phosphorus per day. The data are consistent with specific phosphorus deficiency as the cause of rickets in this infant, rather than insufficient vitamin D intake or disturbed vitamin D metabolism. We speculated that continuous phosphorus infusion prevents the intermittent hyperphosphatemia of bolus phosphorus supplement and that continuous phosphorus infusion may be useful in the treatment of other hypophosphatemic states of infancy.

Female↗

PubMed1991

Calciphylaxis in secondary hyperparathyroidism. Diagnosis and parathyroidectomy.

Calciphylaxis is a rare, severe complication of secondary hyperparathyroidism. Patients present with painful, violaceous, mottled skin lesions of the upper and lower extremities, which become necrotic and produce nonhealing ulcers. Gangrene of fingers and toes frequently requires amputation, produces nonhealing wounds, and can lead to sepsis and death. We reviewed the clinical course of five patients with calciphylaxis treated in our institution. The three men and two women (aged 47 to 72 years) had secondary hyperparathyroidism from chronic renal failure. All patients had severe pruritus, painful ulcers, and severe hyperphosphatemia with elevated serum calcium-phosphate product (greater than 12 mmol2/L2), but the serum parathyroid hormone levels were only moderately elevated. Most patients had medical calcification of medium and small blood vessels, and some had soft-tissue calcification visible on roentgenography. Treatment consisted of local wound care, antibiotics, phosphate-binding agents, and parathyroidectomy. Two patients died of uncontrollable sepsis. The three survivors had dramatic improvement of pain and ulcers after parathyroidectomy. Calciphylaxis is a limb- and life-threatening complication of secondary hyperparathyroidism. Diagnosis can be made by recognizing the characteristic painful skin lesions, ulcers, and gangrene of the digits, and patients should be treated with subtotal parathyroidectomy.

Aged↗