Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adynamic (or aplastic) bone disease is a bone histologic pattern characterized by decreased bone formation rate, low cellularity, and normal or decreased osteoid thickness. It was first described in symptomatic patients undergoing dialysis who were overloaded with aluminum because of contaminated dialysate or chronic ingestion of aluminic phosphate binders; the evidence of the overload was extensive coloration (more than 25%) with aurin tricarboxylic acid, whereas the Perls stain coloration for iron was negative. We have, however, reported these histologic changes in asymptomatic patients with uremia who were never exposed to aluminum, in two patients before end-stage renal failure and in six patients undergoing dialysis. The main step in the prevention of adynamic bone disease is the absolute exclusion of aluminum exposition even by so-called "safe doses" of aluminum phosphate binders because in the long term they are never actually safe. Because idiopathic adynamic bone disease may nevertheless occur, parathyroid hormone suppressive treatment by oral calcium taken with meals as phosphate binders (+/- 1 alpha-hydroxyvitamin D3 derivatives) should be carefully monitored by measurements of plasma concentrations of not only calcium and phosphate but also of intact parathyroid hormone levels. In order to have normal bone formation rate levels, patient intact parathyroid hormone levels should be between one and three times the upper limit of the normal level. Although adynamic bone disease may not be a true bone disease when not due to aluminum, it is a risk factor for increased incidence of hypercalcemia and hyperphosphatemia and therefore for metastatic calcifications. Therefore, when hypercalcemia occurs with hyperphosphatemia and normal intact parathyroid hormone in patients treated with 1 alpha-hydroxyvitamin D3, it is proposed that the latter drug should be discontinued first, whereas oral calcium is increased to correct hyperphosphatemia, and calcium concentration is decreased in the dialysate to prevent hypercalcemia, even though plasma parathyroid hormone may increase up to three times the upper limit of the normal level. In patients previously exposed to aluminum, a deferoxamine test should be performed and a deferoxamine treatment started if the test is positive.
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PMID:Adynamic bone disease in patients with uremia. 807 43

Neuromuscular complications, including tetany and laryngeal spasm, are recognized complications of hypocalcemia and hypomagnesemia. We present a continuous ambulatory peritoneal dialysis patient with hypomagnesemia who developed hyperphosphatemia and profound hypocalcemia after oral phosphate replacement for severe hypophosphatemia. The combination of hypocalcemia and hypomagnesemia resulted in life-threatening bilateral vocal cord paralysis. Phosphate replacement should be determined and given cautiously, particularly in patients with renal failure and concomitant electrolyte disturbances.
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PMID:Bilateral vocal cord paralysis secondary to treatment of severe hypophosphatemia in a continuous ambulatory peritoneal dialysis patient. 828 87

Tumor lysis syndrome is a critical illness characterized by massive tumor cell death leading to severe hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia, and acute renal failure in patients with rapidly growing cancers (especially Burkitt's lymphomas with extensive abdominal bulk). It may be preventable with allopurinol therapy combined with aggressive intravenous fluid therapy aimed at establishing an ongoing alkaline diuresis. In most cases renal failure is completely reversible; however, fatal hyperkalemia and volume overload may develop. Therefore, aggressive management with hemodialysis often is necessary to maintain life support while tumor burden is controlled with cytoreductive therapy. Early recognition and management by a team approach in the intensive care unit where careful monitoring is available serves to forestall severe renal failure, thereby improving short-term prognosis in susceptible patients.
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PMID:Tumor lysis syndrome. 832 27

The incidence of acute renal failure in children is higher due to the prevalence of diarrheal dehydration, use of nephrotoxic substances and sepsis. The occurrence in the newborn has increased, probably due to the large number of seriously sick infants maintained in neonatal intensive care units. Various laboratory examinations have been proposed as diagnostic indices of acute renal failure in children. Among these are the urine-to-plasma concentrations of urea and creatinine and the urine-to-plasma osmolality ratio. The fractional excretion of sodium and the so-called renal failure index are the most reliable of the diagnostic tests. The functional abnormalities and complications of acute renal failure include reduced glomerular filtration rate, retention of nitrogenous wastes, hyponatremia, hyperkalemia, metabolic acidosis, hypocalcemia, hyperphosphatemia and hypermagnesemia. The principles of management and treatment of complications are discussed.
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PMID:[Acute renal insufficiency]. 837 51

The use of 1 alpha-hydroxyvitamin D3 [1 alpha(OH)D3] derivatives in a uremic patient is justified only in the treatment of hyperparathyroidism (i.e. when plasma intact parathyroid hormone - PTH - levels are above five or three times the upper limit of normal according to whether the patient is on continuous ambulatory peritoneal dialysis or on hemodialysis and between 0.5-1.5, 1-2 and 2-3 times the upper limit of normal for a creatinine clearance of, respectively, 30, between 30 and 10, or below 10 ml/min/1.73 m2). The following prerequisites have however to be satisfied: (1) a good vitamin D3 repletion should be secured by plasma 25(OH(D) levels of 20-30 ng/ml (if necessary by administration of native vitamin D or 25(OH)D3), and (2) phosphate retention (which is aggravated by the increased phosphate intestinal absorption induced by the 1 alpha (OH)D derivatives) and the consequent possible hyperphosphatemia should be prevented or corrected by the oral administration of alkaline salts of calcium given before the meals as phosphate binders without inducing hypercalcemia. These prerequisites explain the narrow therapeutical margin of 1 alpha (OH)D3 derivatives in uremic patients before dialysis (more so in the adult than in the child) and the possible broadening of this margin in the patients on dialysis by the use of low dialysate calcium concentrations (1.25-1.00 mmol/l) in order to prevent hypercalcemia by inducing a negative perdialytic calcium balance. Once hyperphosphatemia is prevented by oral calcium, 1 alpha (OH)D3 derivatives have the advantage to suppress the transcription of the prepro PTH gene by a mechanism independent of an increase in plasma calcium. Controlled randomized trials have not confirmed the claimed advantage in efficacy and safety of the parenteral versus the oral route nor of the intermittent versus the daily mode of their administration. The advantages of using the so called 'nonhypercalcemic hyperphosphatemic' vitamin D3 derivatives in combination with oral calcium over 1 alpha(OH)D3 derivatives in the treatment of uremic hyperparathyroidism are still waiting for clinical demonstration. Vitamin D derivatives have no place in the treatment of aluminic bone diseases which necessitate long term deferoxamine treatment and prevention of aluminum exposure by the dialysate and the phosphate binders. They are not indicated in the treatment of 'idiopathic' adynamic bone disease which is due to uremia per se combined with an excessive PTH suppression for the degree of renal failure. This low bone turnover pattern is associated with an increased risk of hypercalcemia and hyperphosphatemia and necessitates only a stimulation of PTH secretion by inducing a negative calcium balance with a lower dialysate calcium concentration or simply by discontinuing the oral calcium supplement in the uremic patient not yet dialyzed. In rare cases this pattern is due to a granulomatosis and is corrected by prednisone.
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PMID:1-alpha-Hydroxyvitamin D3 derivatives in the treatment of renal bone diseases: justification and optimal modalities of administration. 856 75

The aim of this study was to highlight a possible new non-aluminum phosphate-binder to limit hyperphosphatemia in patients with renal failure. Lanthanum chloride hydrate was evaluated as a dietary phosphate binder in rats. Aluminum chloride hexahydrate was evaluated as a reference. Animals were divided in five groups (6 animals per group): 1 control group (C), 2 aluminum groups (Al1 and Al2), receiving different doses of aluminum chloride hexahydrate and 2 lanthanum groups (La1 and La2), receiving different doses of lanthanum chloride hydrate. During the treatment, urine and stools were collected. At the end of the treatment animals were sacrificed and plasma and different organs were collected (liver, spleen, kidneys, brain and femur). To highlight the possible transfer of lanthanum in rat tissues, a long-term (100 days) study was carried with a high dose. At the end of the treatment, lanthanum determinations were carried out on several tissues (liver, spleen, kidneys, brain, femur and lungs). Determinations of phosphorus and calcium levels in plasma indicated that lanthanum chloride hydrate showed as good results as aluminum chloride hexahydrate. Lanthanum chloride hydrate significantly (p < 0.01) reduced the bone phosphorus burden. Decreases of urinary excretion and increases in fecal excretion of phosphorus indicated a severe phosphorus depletion in all treatments (Al and La). Unfortunately, in the long-term study, lanthanum traces could only be determined in the different tissues but not in plasma. However, in comparison with the equivalent aluminum treatment, the transfer of lanthanum was less important than aluminum transfer. Consequently, lanthanum could provide a possible alternative to aluminum.
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PMID:A possible non-aluminum oral phosphate binder? A comparative study on dietary phosphorus absorption. 868 Aug 6

The aim of this study was to study a possible new non-aluminum phosphate-binder to limit hyperphosphatemia in patients with renal failure. Zirconyl chloride octahydrate was evaluated as a dietary phosphate binder in rats. Aluminum chloride hexahydrate was used as a reference. Animals were divided into six groups (6 animals per group): One - control group (C), two - aluminum groups (Al1 and Al2) and three - zirconium groups (Zr1, Zr2 and Zr3) receiving different doses of zirconyl chloride octahydrate. Urines were collected during the experimental period. At the end of the treatment, the animals were sacrified and plasma and different organs were collected (liver, spleen, kidneys, brain and femur). Determination of phosphorus and calcium levels in plasma indicated that zirconyl chloride octahydrate yielded as good results as aluminum chloride hexahydrate did. Zirconyl chloride octahydrate significantly (p<0.01) reduced bone phosphorus burden. Urinary excretion of phosphorus indicated a severe phosphorus depletion in all treatments. Not even traces of zirconium could be determined in the different tissues, in urines or in plasma. Consequently, it is important to carry out experiments with zirconium compounds in order to develop non-aluminum-containing phosphate binders.
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PMID:Reduction of dietary phosphorus absorption by oral phoshorus binders. 874 85

1,25-Dihydroxyvitamin D deficiency plays an important role in the pathogenesis of secondary hyperparathyroidism, and adequate replacement of this hormone is considered essential to normalize parathyroid gland function and restore bone homeostasis in patients with advanced renal failure. Although initial uncontrolled clinical trials suggested the superiority of intravenous calcitriol treatment, more recent controlled investigations show that different routes (oral versus intravenous), frequency (daily versus intermittent), and dosing (physiological versus pharmacological) of calcitriol administration are clinically equivalent. Overall, the response to calcitriol treatment depends more on the severity of secondary hyperparathyroidism and the presence of confounding variables, such as hyperphosphatemia and acquired abnormalities of parathyroid cell function, than the method of calcitriol administration.
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PMID:Calcitriol administration in end-stage renal disease: intravenous or oral? 879 99

The risk for renal insufficiency by uric acid precipitation in medulla of kidney correlates with the degree of uric acid supersaturation in the urine, depending on uric acid concentration and urinary pH. The patients with gout or hyperuricemia have sometimes acidic urine and increased uric acid excretion. Accordingly, these patients frequently accompany by renal insufficiency. Improvement of hyperuricosuria, increasing of urine volume, and alkalinization of urine to pH6 6.5, are effective for the prevention from renal insufficiency. Acute renal failure related to hyperuricemia, can also occured secondary to cell lysis. Tumor lysis syndrome is a critical illness characterized by massive tumor cell death leading to severe hyperuricemia, hyperphosphatemia, hypocalcemia, and acute renal failure after starting chemotherapy to cancers, especially lymphoproliferative malignancies. Administration of allopurinol 500-600 mg and adequate hydration and alkalinization of urine are advocated to prevent acute renal failure. Intensive care with hemodialysis is often required to treat renal failure, because renal failure is reversible in most cases.
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PMID:[Hyperuricemia and the kidney]. 897 5

Hypoparathyroidism is a clinical disorder characterized by hypocalcemia and hyperphosphatemia in the absence of renal failure and hypomagnesemia. The causes of hypoparathyroidism can be classified as two groups: (i) insufficient parathyroid hormone (PTH) secretion in relation to the serum calcium level (hypoparathyroidism); and (ii) impaired PTH action (pseudohypoparathyroidism). The main emphasis in this report is to distinguish subgroups based on the etiology and pathophysiology of the various aspects of the disease.
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PMID:Hypoparathyroidism and pseudohypoparathyroidism. 931 98


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