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)

Case records from 21 dogs with hypercalcemia and hyperparathyroidism were evaluated. The dogs were greater than or equal to 7 years old, and 6 were Keeshonds. The most common clinical signs were polydipsia/polyuria, listlessness, and muscle weakness. The serum calcium concentrations were 12.1 to 19.6 mg/dl. Serum phosphorus concentrations were low in 5 dogs, within the reference range in 13 dogs, and high in 3 dogs that also had high concentrations of BUN. Twenty dogs had a parathyroid adenoma, and 1 had a parathyroid carcinoma. Nineteen dogs had their parathyroid tumor surgically removed. Within 5 days of tumor removal, 11 of the 19 dogs became hypocalcemic and the remaining 8, normocalcemic. Nine of the 11 hypocalcemic dogs developed clinical signs. Iatrogenic hypercalcemia was induced in 7 of 16 dogs treated orally with calcium carbonate plus vitamin D. Only 1 of 19 dogs that had their parathyroid tumor excised died in hypocalcemic tetany. Two additional dogs died within 2 weeks of surgery, one because of pancreatitis, the other due to renal failure. Eight dogs died 9 to 37 months after surgery of unrelated problems. Eight dogs were alive for at least 7 to 28 months after surgery.
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PMID:Primary hyperparathyroidism in dogs: 21 cases (1976-1986). 365 3

Orally administered calcium carbonate was evaluated as a phosphate binding agent in 15 children, ages 0.6 to 17.2 years, receiving maintenance dialysis. Changes in plasma aluminum concentration were assessed after discontinuation of treatment with aluminum-containing gels. The mean daily dose of calcium carbonate was 5.1 +/- 2.5 gm (384 +/- 315 mg/kg/day), and correlated inversely with body weight (r = 0.72, P less than 0.01) and age (r = 0.71, P less than 0.01). Mean serum calcium, phosphorus, and bicarbonate values were unchanged throughout the study. Plasma aluminum concentration fell from 90 +/- 51 to 34 +/- 22 micrograms/L (P less than 0.005). Dietary phosphorus intakes were 44 +/- 21 and 42 +/- 19 mg/kg/day during the control period and at the end of the study, respectively. Transitory hypercalcemia was the only side effect in 92% of the patients. In none of the patients did uncontrolled hyperphosphatemia, metabolic alkalosis, diarrhea, or symptoms or signs of hypercalcemia develop. Our data indicate that calcium carbonate is an effective phosphate binding agent in children receiving dialysis, and should be used in lieu of aluminum-containing gels in young children with renal failure.
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PMID:Effects of oral calcium carbonate on control of serum phosphorus and changes in plasma aluminum levels after discontinuation of aluminum-containing gels in children receiving dialysis. 370 25

The serum concentrations of calcium, phosphorus, parathyroid hormone, vitamin D3 metabolites and their transport protein (DBP) were measured in 18 patients with the nephrotic syndrome (mean daily proteinuria 8.8 g). The glomerular filtration rate was normal in 13 patients while the remaining 5 had a mild degree of renal failure. The serum concentrations of total protein, albumin and DBP were significantly decreased in patients with the nephrotic syndrome. The serum calcium concentration was decreased but the calculated ionized calcium concentration remained normal. The serum concentrations of 25-hydroxycholecalciferol (5.3 +/- 3.1 micrograms/l) and 1,25-dihydroxycholecalciferol [1,25-(OH)2D3 (20 +/- 12 ng/l)] were significantly lower in patients with the nephrotic syndrome and normal glomerular filtration rates than in normal controls (14.4 +/- 4 micrograms/l and 42 +/- 13 ng/l, respectively). The free 1,25-(OH)2D3 index was also significantly below normal (0.9 +/- 0.4 vs. 1.8 +/- 0.4). Total and free 1,25-(OH)2D3 were still further reduced in patients with mild renal failure. The nephrotic syndrome thus results in mild vitamin D depletion with decreased free 1,25-(OH)2D3 concentrations but generally without secondary hyperparathyroidism.
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PMID:Decreased free 1,25-dihydroxycholecalciferol index in patients with the nephrotic syndrome. 375 49

The phosphate-binding capacities of 19 liquid and solid aluminum hydroxide gel antacids were determined in vitro under varying pH conditions. The resulting data provide a basis explaining the phosphate-binding characteristics observed when patients are treated with long-term aluminum hydroxide therapy. No antacid, liquid or solid, showed significant binding at pH 1.0. Maximum phosphate binding (expressed as phosphorus; P) was observed at pH 2.0 and 3.0 for most antacids and decreased markedly at alkaline pH. The liquid antacids showed a significantly greater phosphate-binding capacity than did tablets or capsules (p less than 0.01). At pH 2.0, the liquid antacids bound a mean of 22.3 mg P/5 ml. At pH 8.0 binding was reduced to a mean of 7.3 mg P/5 ml. Significant interbrand differences were observed. At pH 2.0, the solid antacids bound a mean of 15.3 mg P/tablet or capsule. At pH 8.0, binding was reduced to a mean of 5.8 mg P/tablet or capsule. Interbrand differences, while substantial, were less than those observed among the liquid antacids. Variations in sodium and potassium content were clinically insignificant for most of the antacids in this study, while the differences in phosphate-binding properties were sufficient to warrant attention in the patient with renal failure.
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PMID:Phosphate-binding properties and electrolyte content of aluminum hydroxide antacids. 380 43

Histologic bone changes of osteitis fibrosa and osteomalacia are commonly present in patients with end-stage renal disease. Although many patients are not symptomatic from these bone changes, some patients are severely disabled. Altered metabolism of vitamin D, calcium, phosphorus, and parathyroid hormone occurs in renal failure and contributes to the development of uremic bone disease. This article reviews the current theories of pathogenesis and treatment of renal osteodystrophy. In addition, the clinical presentation, pathogenesis, and treatment of the various aluminum-associated osteomalacic syndromes in uremia are discussed.
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PMID:Renal osteodystrophy--pathogenesis and treatment. 390 12

It has recently been documented that a small amount of aluminum is absorbed from a variety of different orally administered aluminum compounds. A variety of factors including gastric acidity, fluoride ingestion, parathyroid hormone, vitamin D and the quantity of aluminum ingested could theoretically modulate aluminum absorption from the gastrointestinal tract. However, partially because of the unavailability of an aluminum isotope, knowledge regarding factors which modify aluminum absorption is quite limited. In healthy individuals the absorbed aluminum is largely eliminated from the body by the kidneys. However, with renal failure the absorbed aluminum is retained and can markedly alter the body aluminum burden with resulting toxicity. In view of this finding, it is suggested that uremic patients receive the smallest amount possible of aluminum-containing, phosphate-binding gels consistent with the control of serum phosphorus levels and that alternate methods for the control of the serum phosphorus should be sought.
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PMID:Gastrointestinal absorption of aluminum. 391 61

The rate of progression of early renal failure was evaluated in three groups of adult patients with renal disease of diverse etiology on dietary protein and phosphorus restriction (about 0.6 g/kg of protein, 700 mg of phosphorus) and in a control group of 22 patients with the same renal disease, retrospectively studied, on a free diet. Group 1 had 33 patients with chronic glomerulonephritis (CG), initial serum creatinine (Scr) of 1.4 to 4.3 mg/dl (mean, 2.20), followed for 5 to 94 months (mean, 44). Group 2 had 17 patients with polycystic kidney disease (PKD), Scr 1.3 to 4.7 mg/dl (mean, 2.40), followed for 8 to 81 months (mean, 42). Group 3 had 28 patients with primary chronic pyelonephritis (CP), Scr of 1.5 to 4.5 mg/dl (mean, 2.57), followed for 9 to 92 months (mean, 41). The control group had 22 patients (11 with CG, five with PKD, and six with CP), with Scr 1.7 to 4.1 mg/dl, followed for 6 to 72 months (mean, 24). In the regression analysis between reciprocal creatinine and time, the slopes were -0.0017, -0.0025, and -0.00016 dl/mg/month in the three patient groups on a protein-restricted diet, respectively. The difference between both groups 1 and 2 and group 3 was statistically significant (P less than 0.05). The slopes in patients on a free diet were significantly greater than those found in patients on a protein-restricted diet. The actuarial survival probability at 72 months, assuming as "renal death" a Scr of 10 mg/dl, was 45% in patients with CG, 44% in those with PKD, and 67% in those with CP on a protein-restricted diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Progression of renal failure in patients with renal disease of diverse etiology on protein-restricted diet. 399 43

Parathyroid allotransplantation was performed in a 25-year-old woman with idiopathic hypoparathyroidism that had been diagnosed at age 4 years. Long-term medical management of the primary condition with vitamin D and oral calcium supplementation was complicated by multiorgan calcinosis and renal failure. At the age of 21 years she received a successful cadaver renal allograft. Four years later she developed calcinosis cutis with widespread skin necrosis. Medical control of calcium and phosphate metabolism was unsatisfactory and the skin necrosis became progressive and life threatening. A parathyroid allograft that was performed with tissue from a parathyroid adenoma resulted in normalization of the serum calcium and phosphorus levels with arrest and subsequent healing of the skin necrosis. Later failure of the parathyroid allograft was followed by successful retransplantation of normal parathyroid tissue from a cadaver organ donor.
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PMID:Parathyroid allotransplantation in the treatment of complicated idiopathic primary hypoparathyroidism. 407 84

One hundred cases of hypophosphataemia (</= 2.0 mg/100 ml) and 84 cases of hyperphosphataemia (>/= 5.0 mg/100 ml) occurring in a hospital population were studied in order to determine the cause of the abnormality. Examples of hyperphosphataemia due to renal failure were excluded from the study.A low serum phosphorus concentration was most frequently due to intravenous administration of carbohydrate, usually glucose, which accounted for 40% of cases. The next commonest cause was vomiting (12%). No obvious explanation could be found in 26% of cases, but in most of these factors were present which are known to affect phosphorus metabolism.No one cause of hyperphosphataemia was outstanding in frequency and in over 50% of cases no definite explanation for the abnormality could be found.
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PMID:Hypophosphataemia and hyperphosphataemia in a hospital population. 500 77

Two tests were used to differentiate abnormalities in release of platelet factor 3 (PF3) from quantitative deficiencies of this factor in normal subjects and in patients with renal failure. The first test was an assay which determined availability of PF3 (PF3-A time) and involved the use of a mixture of patient's platelet-rich plasma (PRP) and normal platelet-poor plasma (PPP) in a fixed ratio (1:8). The second test was similar but used "frozen and thawed" platelets to obtain a quantitative estimate of PF3 (PF3-F time). An abnormal PF3-A time was found in approximately three-quarters of 55 patients with renal insufficiency; 43 of these had chronic and 12 had acute renal failure. This abnormality was present both in patients with and without hemorrhagic manifestations, although it was slightly more common in bleeders. The PF3-F test was abnormal in approximately one-third of the bleeding patients and one-quarter of the non-bleeders. The PF3-A time returned to normal or was significantly shortened 24-48 hr after peritoneal or hemodialysis. Studies on patients who were not dialyzed showed no statistically significant correlations between the PF3-A time and either the serum urea nitrogen, creatinine, calcium, or phosphorus. Furthermore, the PF3-A time was not affected by guanidinosuccinic or guanidinoacetic acids. We therefore conclude that the demonstrable platelet abnormality in patients with uremia is produced by an unknown dialyzable material. The mean plasma clot retraction of uremic patients was also significantly different from the mean plasma clot retraction or normal controls. However, unlike the PF3-A time, the abnormality of plasma clot retraction was not immediately affected by dialysis. Correction of plasma clot retraction did occur after repeated dialyses.
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PMID:Platelet factor 3 in normal subjects and patients with renal failure. 564 25


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