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)

Control of phosphorus accumulation in chronic renal insufficiency is crucial to the prevention of secondary hyperparathyroidism and metastatic calcification. In early renal failure, calcitriol levels are normal and parathyroid hormone levels are elevated. The phosphorus levels are maintained in the normal range by the phosphaturia induced by hyperparathyroidism. In this situation, dietary phosphorus restriction increases calcitriol levels and suppresses parathyroid hormone secretion. As renal failure progresses into late stages, hyperphosphatemia is evident along with low levels of calcitriol and worsening hyperparathyroidism. Phosphorus restriction will not affect calcitriol concentrations, yet parathyroid levels may decline. During long-term dialysis, urinary excretion of phosphorus is usually minimal. Therefore, phosphorus balance is determined primarily by the net amount absorbed by the bowel and the quantity removed during dialytic therapy. Given an adequate diet, no form of conventional dialysis is able to fully compensate for the gastrointestinal absorption of phosphorus. Hence, compounds that bind phosphorus in the bowel are often necessary. With the realization that the use of phosphorus binders containing aluminum leads to aluminum accumulation and its sequelae: osteomalacia, dementia, myopathy, and anemia, other phosphorus binders have been evaluated. Calcium carbonate has been investigated the most thoroughly and is in wide use. It is inexpensive and contains a high percent of elemental calcium. However, it is only modestly potent in the binding of phosphorus, and large doses are often necessary to attain satisfactory control of phosphorus. This may lead to hypercalcemia. One approach to this problem is to decrease the concentration of calcium in the dialysate. Alternatively, a more effective phosphorus binder may be used. Calcium acetate has been shown in acute studies to have twice the binding capacity of phosphorus per calcium absorbed than calcium carbonate. Whether use of this compound decreases the incidence of hypercalcemia is unproven. Calcium citrate increases the gastrointestinal absorption of aluminum and offers no advantage over calcium carbonate. Other compounds, such as calcium ketoacids and calcium alginate, have not been extensively studied and are not generally available. The use of phosphorus binders containing magnesium in conjunction with a dialysate low in magnesium may be efficacious. Large doses of magnesium will cause diarrhea and thus limit its use as a single agent. Reasons for failure to control hyperphosphatemia include poor compliance, improper prescription of binders, poor dissolution rates seen with some generic brands of calcium carbonate, and the presence of severe hyperparathyroidism. Optimal control of serum phosphorus in dialysis patients should always be viewed in the context of adequate nutrition and protein intake.
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PMID:Hyperphosphatemia: its consequences and treatment in patients with chronic renal disease. 156 18

Alterations in renal calcitriol synthesis are important in the pathogenesis of secondary hyperparathyroidism in patients with progressive renal failure. Many of the manifestations of secondary hyperparathyroidism can be reversed by treatment with 1 alpha-hydroxylated vitamin D sterols, such as calcitriol and 1 alpha-hydroxyvitamin D3, but some studies suggest that such treatment accelerates the rate of progression of renal disease in patients with mild to moderate renal failure. Thus, calcitriol and 1 alpha-hydroxyvitamin D3 have been used infrequently in this group of patients. A review of more than 20 clinical reports indicates that the use of calcitriol or 1 alpha-hydroxyvitamin D3, in daily doses of 0.25-0.5 microgram, is rarely associated with hypercalcemia, hyperphosphatemia, or impairment in renal function. If such complications arise, they are usually reversible when treatment with vitamin D sterols is withdrawn and serum calcium levels return to pretreatment values. There is evidence that calcitriol impairs creatinine secretion by the renal tubule; thus, serum creatinine levels may increase and measurements of creatinine clearance may fall during calcitriol therapy in patients with mild to moderate renal failure without any change in true glomerular filtration rate. Daily oral doses of 0.25-0.50 microgram of calcitriol or 1 alpha-hydroxyvitamin D3 are well tolerated, and they can reverse the biochemical and histologic features of secondary hyperparathyroidism. Calcitriol therapy may be particularly valuable in patients recognized to be at higher risk of developing progressive secondary hyperparathyroidism as their renal failure slowly advances.
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PMID:The use of 1,25-dihydroxyvitamin D3 in early renal failure. 158 May 87

Hyperphosphatemia is an electrolyte abnormality that most frequently results from renal insufficiency and the attendant inability to excrete phosphorus (PO4) efficiently. A case is presented in which a young man with hemorrhagic shock developed severe hyperphosphatemia in the absence of renal failure. This is the first such case documented to the authors' knowledge. The prompt correction of the primary cause (ie, hypoperfusion and acidosis) resulted in a rapid return of PO4 levels to normal. This was probably related to the intracellular shift of PO4. Physicians should be aware of this electrolyte disturbance because it is not a well-recognized complication and because, in most cases, proper treatment of shock will also correct the elevated PO4.
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PMID:Severe hyperphosphatemia associated with hemorrhagic shock. 161 21

A patient with hypophosphatemic vitamin D-resistant rickets developed secondary erythrocytosis during treatment with large doses of vitamin D2 and phosphate. Erythrocytosis was accompanied by a fall in circulating plasma volume and appeared to have developed as a consequence of nephrocalcinosis because it occurred after the appearance of nephrocalcinosis following several episodes of hypercalcemia and hyperphosphatemia. Nephrocalcinosis and erythrocytosis did not disappear even after recovery of renal function. Thus, the present observations point to the importance of preventing these irreversible complications that could cause renal failure, erythrocytosis, and thrombotic events during the management of hypophosphatemic vitamin D-resistant rickets.
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PMID:Erythrocytosis in hypophosphatemic rickets: irreversible complication due to nephrocalcinosis after vitamin D and phosphate therapy. 166 79

The calcemic response to parathyroid hormone (PTH) is decreased in renal failure. The reduction of hyperphosphatemia improves the calcemic response to PTH in animals with advanced renal failure. However, since low calcitriol levels in renal failure may also contribute to the decreased calcemic response to PTH, the improved calcemic response observed during the reduction of serum phosphorus may be partially mediated by an increase in serum calcitriol levels. The present study evaluated the calcemic response to PTH in rats with moderate and advanced renal failure and how this response was modified by a high and a low phosphorus diet. In addition, the effect of a change in dietary phosphorus on calcitriol levels was also evaluated. A 48-hour continuous infusion of 1-34 rat PTH increased the serum calcium level to 18.2 +/- 0.4 mg/dl in normal rats, versus 13.7 +/- 0.9 and 12.1 +/- 0.2 mg/dl in rats with moderate and advanced renal failure, respectively. During the PTH infusion, a high phosphorus diet increased the serum phosphorus and resulted in a reduced calcemic response to PTH at each level of renal function; respective serum calcium levels were 13.8 +/- 0.6 mg/dl in normals, 11.2 +/- 0.2 mg/dl in moderate renal failure and 9.6 +/- 0.5 mg/dl in advanced renal failure. In normal rats and in rats with moderate renal failure, dietary phosphorus restriction during the PTH infusion increased serum calcitriol levels. In rats with advanced renal failure, serum calcitriol levels were lower than in the other two groups and were not affected by changes in dietary phosphorus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcemic response to parathyroid hormone in renal failure: role of phosphorus and its effect on calcitriol. 176 6

Hyperparathyroidism due to renal failure begins in the early stages of renal insufficiency and is in part secondary to skeletal resistance to the calcemic action of parathyroid hormone (PTH). Factors which have been reported to reduce the calcemic response to PTH include: decreased calcitriol levels, hyperphosphatemia and down regulation of PTH receptors in bone. While hyperphosphatemia may directly decrease the calcemic response to PTH, it may also act indirectly by a suppression of calcitriol synthesis. In this study, the effect of calcitriol on the calcemic response to PTH was evaluated in normal rats and in rats with moderate and advanced renal failure. To determine the combined effect of calcitriol and phosphorus on the calcemic response to PTH, rats receiving calcitriol were fed either a high (1.0%) or low (0.2%) phosphorus diet during a 48-hour PTH infusion. In advanced renal failure, calcitriol administration increased the calcemic response to PTH independent of the dietary phosphorus intake. During ingestion of a low phosphorus diet, a 48 hour PTH infusion resulted in a serum calcium level of 13.7 +/- 0.5 and 12.1 +/- 0.2 mg/dl (P less than 0.02) with and without calcitriol administration, respectively. In normal rats and in rats with moderate renal failure, calcitriol administration improved the calcemic response only during a high phosphorus intake. After a 48-hour PTH infusion in normal rats, the serum calcium levels with and without calcitriol were 16.1 +/- 0.9 and 14.8 +/- 0.6 mg/dl, P less than 0.01 respectively; in rats with moderate renal failure, calcitriol administration increased serum calcium, 13.2 +/- 0.5 versus 11.2 +/- 0.4 mg/dl, P less than 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcemic response to parathyroid hormone in renal failure: role of calcitriol and the effect of parathyroidectomy. 176 7

Hyperphosphatemia (HP) is usually seen in patients with hypoparathyroidism, renal failure, and tumor lysis. The authors described a patient with HP due to a phosphate-binding immunoglobulin (Ig). An 86-year-old woman had serum phosphate levels as high as 4.75 mmol/l, (normal, 0.77 to 1.45 mmol/l). Serum ionized calcium, blood urea nitrogen (BUN), creatinine, and N-terminal parathyroid hormone (PTH) levels were normal, but serum 1,25-dihydroxyvitamin D level was subnormal at less than 12 pmol/l (normal, 36 to 146 pmol/l). Serum total protein was elevated at 105 g/l (normal, 60 to 80 g/l), and additional studies confirmed a diagnosis of immunoglobulin G (IgG) multiple myeloma. Results of in vitro studies using anti-human IgG antibodies showed that the IgG of the patient bound inorganic phosphate. Several isolated case reports have documented spurious HP due to interference of the paraprotein in the routine serum phosphate assay. In only one patient, however, has actual binding of phosphate to a myeloma protein been documented. The studies of the authors document phosphate binding by an IgG paraprotein and suggest that in this setting HP may be of physiologic significance as evidenced by depressed serum levels of 1,25-dihydroxyvitamin D.
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PMID:Hyperphosphatemia in multiple myeloma due to a phosphate-binding immunoglobulin. 191 79

The present study was designed to clarify the characteristics of metabolic acidosis in aged patients with chronic renal failure. The subjects consisted of ambulatory cooperative patients (19 males and 18 females). Their values of creatinine clearance (Ccr) varied from 6.8 to 107.5 ml/min/1.73 m2. The relationship of Ccr to acid-base and electrolyte disturbances was investigated. The estimations of normal values in acid-base and electrolyte composition were based on the method of Hoffmann. The results are summarized as follows: 1. A high incidence of metabolic acidosis was demonstrated in patients whose Ccr values were below 20 ml/min/1.73 m2. 2. A significant positive correlation of Ccr values and plasma levels of bicarbonate (p less than 0.001) and a significant inverse correlation of Ccr values and serum levels of chloride (p less than 0.01) were observed. 3. The values of the anion gap did not change, irrespective of Ccr values. 4. Serum concentrations of potassium were inversely correlated with plasma levels of bicarbonate (p less than 0.01). Hyperchloremic normal anion gap acidosis with hyperpotassemia was the characteristic feature of metabolic acidosis in aged patients with chronic renal failure. The normal anion gap could be explained by normophosphatemia or mild hyperphosphatemia, even in the patients with advanced renal failure.
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PMID:[The characteristics of metabolic acidosis in aged patients with chronic renal failure]. 194 34

Signs of depression, hyperphosphatemia, azotemia, high anion gap metabolic acidosis, and renal failure developed in an adult cat following administration of an excessive dose of a phosphate-containing urinary acidifier. After extracellular fluid volume expansion, diuresis, and administration of a phosphate binder, serum phosphorus concentration returned to normal in 12 hours; the cat recovered fully. The urinary acidifier had been given as part of treatment for a urinary tract infection. Findings suggest that phosphate-containing urinary acidifiers should be administered cautiously because, like other sources of phosphate, they are capable of causing life-threatening metabolic disturbances.
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PMID:Poisoning induced by administration of a phosphate-containing urinary acidifier in a cat. 202 46

Many renal structural and functional abnormalities have been associated with sickle cell disease. The patients have an impaired urinary concentrating ability but an intact diluting capacity. There are defects in both urinary acidification and potassium excretion, although overt metabolic acidosis and hyperkalemia occur infrequently. Proximal tubular function is supranormal, as manifested by increased reabsorption of phosphate and increased secretion of creatinine. The former results in mild hyperphosphatemia, while the latter causes substantial overestimation of the glomerular filtration rate (GFR) by creatinine clearance. Both GFR and renal plasma flow are increased in young patients with sickle cell disease, but prostaglandin inhibitors decrease the GFR. The GFR progressively decreases with increasing age. Proteinuria, and even nephrotic syndrome, are relatively frequent; the most common renal lesion in children is focal glomerular sclerosis, which may be associated with progressive deterioration in renal function. Glomerular hyperfiltration has been implicated in the pathogenesis of the glomerular lesions, as well as in the development of renal failure. In patients with end-stage renal disease, both hemodialysis and kidney transplantation have been successful. Recurrent hematuria is a relatively common problem in patients with sickle cell disease. The bleeding usually remits spontaneously, but occasionally requires therapy with aminocaproic acid. Papillary necrosis may occur, and is thought to result from medullary ischemia.
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PMID:Renal abnormalities in sickle cell disease. 217 77


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