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)

A 2-site immunochemiluminometric assay (ICMA) for intact parathyroid hormone (PTH) has been developed to overcome the problems of limited sensitivity and specificity associated with conventional PTH immunoassays. The present investigation assesses the relative merits of the 2-site intact PTH (ICMA) and a midmolecule PTH radioimmunoassay (RIA). Immunoassay profiles of dispersed hyperparathyroid cell supernatants and hyperparathyroid sera obtained during parathyroidectomy and from renal failure patients, fractionated by gel filtration chromatography, facilitated a direct comparison of the specificity of PTH immunoassays. Using gel filtration matrices which permitted the separation of intact hormone, large C-terminal fragment(s), and a small midmolecule fragment in adenomatous cell supernatant and peripheral sera, the intact PTH (ICMA) assay consistently yielded a single peak of immunoreactivity. In contrast, the midmolecule RIA yielded 2 and 3 broad peaks of immunoreactivity after fractionation of serum and adenomatous cell supernatant, respectively. There was no evidence for the secretion of a small midregion fragment in vitro or its peripheral derivation in vivo. These studies demonstrate the superior specificity of the 2-site intact PTH assay compared with a midmolecule RIA and, thus, confirm the potential diagnostic superiority of the ICMA.
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PMID:Laboratory comparison of diagnostic specificity of intact hormone and region-specific immunoassays of parathyroid hormone. 236 46

Phosphorus is a well-known modulator of renal 1 alpha-hydroxylase activity. In early and moderate renal failure it is proposed that dietary Pi reduction ameliorates secondary hyperparathyroidism through increased circulating levels of calcitriol (i.e, 1 alpha, 25-dihydroxycholecalciferol). To gain further insight into the mechanisms by which a low-Pi diet ameliorates secondary hyperparathyroidism in advanced renal insufficiency, studies were performed in five dogs before and 6 mo after the induction of uremia by 5/6 nephrectomy. Glomerular filtration rate decreased from 69.0 +/- 2.3 to 10.5 +/- 0.5 ml/min, immunoreactive parathyroid hormone (irPTH) increased from 66.0 +/- 8.8 to 321.0 +/- 46 pg/ml, and calcitriol decreased from 39.0 +/- 10.4 to 27.0 +/- 6.2 pg/ml. Thereafter, dietary Pi was decreased gradually every 2 wk from 0.95% to 0.6, 0.45, and 0.3%, respectively. Dietary Ca was reduced from 1.6 to 0.6% to prevent development of hypercalcemia. Ionized Ca (ICa) decreased from 5.4 +/- 0.04 to 5.2 +/- 0.05 mg/dl (P less than 0.02), and plasma Pi decreased from 6.3 +/- 0.7 to 4.7 +/- 0.2 mg/dl (P less than 0.05). Calcitriol remained low (23.3 +/- 4.7 pg/ml). However, irPTH gradually decreased from 321.0 +/- 46.0 to 94.7 +/- 22.9 pg/ml (P less than 0.005). These studies indicate that a decrease in dietary Pi from 0.95 to 0.3% suppressed irPTH by approximately 70%. Reduction of irPTH was observed in the absence of a concomitant increase in levels of ICa or calcitriol. These studies suggest that reduction in dietary Pi in advanced renal insufficiency improves secondary hyperparathyroidism by a mechanism that is independent of the levels of calcitriol or plasma ICa.
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PMID:Phosphorus restriction reverses hyperparathyroidism in uremia independent of changes in calcium and calcitriol. 239 69

Four sequential Tc-99m pyrophosphate (PYP) imaging studies were performed in a 28-year-old man with high fever and exudate pharyngitis associated with renal failure. Radiotracer localization in the left ventricle (LV), lungs, kidneys, and skeletal muscles were seen in two, initial imaging studies. In the second and third imaging studies, area of increase in activity was seen in the left-sided bowel. In studies done two months later (in the third study), the radioactivity in the skeletal muscles was no longer seen. Studies obtained nine months (in the fourth study) after the first imaging showed less radiotracer localization in the LV, lungs, and kidneys as compared to that seen in the initial study. Myocardial necrosis and microcalcification were proved by LV biopsy. The exact mechanism of extraosseous bone-imaging agent localization is unknown. However, this phenomenon may be related to renal failure, rhabdomyolysis, hypercalcemia, hyperphosphatemia, or elevated parathyroid hormone. The Tc-99m PYP imaging study is useful and sensitive in the detection of extraosseous tissue calcification and monitoring of the disease process.
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PMID:Extensive extraosseous localization of bone imaging agent in a patient with renal failure and rhabdomyolysis accompanied by combined hypercalcemia and hyperphosphatemia. 254 39

Gentamicin nephrotoxicity increases renal cortex calcium and sodium and decreases renal cortex Na-K-ATPase activity. Human acute renal failure is accompanied by an increase in parathyroid hormone (PTH), a hormone that stimulates calcium uptake by tissues, and by a decrease in thyroid hormone, a hormone that increases renal cortex Na-K-ATPase activity. This study evaluated the role of extracellular calcium, PTH, and thyroxine in the pathogenesis of gentamicin nephrotoxicity. Chronically parathyroidectomized hypocalcemic rats (PTXG) given gentamicin (30 mg/kg s.c. twice daily for 8 days) were not protected from renal failure when compared with intact rats given gentamicin (NG), serum creatinine being 4.4 +/- 1.0 and 3.7 +/- 0.7 mg/dl, respectively, compared with normals (N), 1.2 +/- 0.1 mg/dl. Rats given thyroxine (10 micrograms/100 g body wt for 10 days) before and during gentamicin (PTXT4G) had a serum creatinine not significantly different from normals, 2.1 +/- 0.4 mg/dl. Plasma T4 was reduced in PTXG, NG, and PTXT4G compared with N, but the value for PTXT4G was significantly higher than for either PTXG or NG. Renal cortex Na-K-ATPase activity (mumol Pi X mg prot-1 X h-1) was lower in PTXG (2.3 +/- 0.2) and NG (2.4 +/- 0.5) compared with N (3.7 +/- 0.1), but activity was not reduced in PTXT4G (3.2 +/- 0.2) Thyroxine was protective also against gentamicin nephrotoxicity in intact rats. Clearance and excretion studies indicated that this protection did not result from an increase in glomerular filtration rate, filtered load of calcium, or urinary calcium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of thyroxine but not parathyroidectomy on gentamicin nephrotoxicity. 257 82

Uremic myopathy is relatively unknown, despite the fact that it can be quite a severe handicap. It is a non-specific proximal myopathy which must be distinguished from uremic polyneuropathy. Several disorders linked to renal insufficiency have been implicated, but these only play an adjuvant role with regard to renal osteodystrophy. Indeed the presence of myopathy in cases of severe osteodystrophy, its similarity to the myopathies associated with different types of osteomalacia and hyperparathyroidism without renal failure, suggest that the most important pathogenic factor is related to disorders of the calcium phosphate metabolism: excessive parathyroid hormone, vitamin D deficiency and/or impaired calcium transport. Treatment will depend on the predominant bone lesions: secondary hyperparathyroidism or osteomalacia. However prevention remains the best course.
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PMID:[Myopathy in the uremic patient: apropos of a case]. 263 67

This study represents the first randomized prospective, double-blind, placebo-controlled trial of the efficacy of 1,25(OH)2D3 on bone histology and serum biochemistry in patients with mild to moderate renal failure. Sixteen patients with chronic renal impairment (creatinine clearance 20 to 59 ml per min) received either 1,25(OH)2D3, at a dose of 0.25 to 0.5 microgram daily (eight patients), or placebo. Transiliac crest bone biopsies were performed before entrance into the study and after 12 months of experimental observation. None of the patients were symptomatic or had radiological evidence of bone disease. Of the thirteen patients who completed the study, initial serum 1,25(OH)2D levels were low in seven patients and parathyroid hormone levels were elevated in seven patients. Bone histology was abnormal in all patients. 1,25(OH)2D3 treatment was associated with a significant fall in serum phosphorus and alkaline phosphatase concentrations as well as with histological evidence of an amelioration of hyperparathyroid changes. In contrast to previous reports, no deterioration of renal function attributable to the treatment occurred, perhaps because a modest dose of 1,25(OH)2D3 was employed combined with meticulous monitoring. Further investigation is required to determine whether alternative therapeutic strategies (smaller doses or intermittent therapy) may avoid the potential for suppressing bone turnover to abnormally low levels in the long term.
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PMID:1,25(OH)2D3 administration in moderate renal failure: a prospective double-blind trial. 265 58

We investigated the growth of hyperplastic parathyroid glands removed at operation from 16 patients with chronic renal failure complicated by hypercalcemia, by incubating fresh tissue with tritiated thymidine. In each gland the proportion of cells synthesizing DNA was determined directly by counting labeled nuclei after autoradiography and indirectly from incorporation of label into DNA, and the mean diameter of chief cell nuclei was measured. Both DNA synthesis and mean nuclear diameter were positively correlated with plasma calcium level. Assuming the mean duration of S phase to be 12 hours, the birthrate of new cells (mean +/- SD) was 18.5% +/- 23.6% per year, significantly (p less than 0.05) greater than the 11.5% +/- 7.4% per year found in 63 parathyroid adenomas previously studied. On the basis of estimated disease duration, the minimum birthrate needed to grow glands of the observed weight was 23.4% +/- 16.5% per year. The similarity between observed and needed birthrates indicates that the glands were growing almost as fast as when renal failure began, and that parathyroid growth was no longer regulated in accordance with normal plasma calcium homeostasis. To account for this, we propose that the disordered growth is a consequence of an increase in secretory set point, which in turn is a consequence of calcitriol deficiency. Because the effectiveness of parathyroid hormone is impaired in renal failure, a large increase in total hormone secretion is needed to raise the plasma calcium level to the new set point, and the necessary increase in gland size can be achieved only by a sustained increase in the rate of cell division.
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PMID:The parathyroid glands in chronic renal failure: a study of their growth and other properties made on the basis of findings in patients with hypercalcemia. 267 97

Serum magnesium concentration (sMg) increases in advanced renal failure, and in patients on regular dialysis treatment Mg status mainly depends upon the dialysate Mg concentration (dMg). In fact in uraemia, whereas the intracellular (muscle and blood cell) Mg content seems similar to that of normals and not to be influenced by dMg, the extracellular fluid Mg level as well as Mg content in some organs (skin, bone, etc) parallel the dMg. In the present paper, Mg status and its clinical implications in patients on regular dialysis treatment were therefore reviewed in an attempt to define an optimal dMg. Up to now, dialysis patients have been kept hypermagnesaemic on the assumption that a high sMg suppresses parathyroid hormone secretion (PTH), although this hypothesis has not been confirmed in later papers. On the other hand, more recent clinical studies suggest the possibility of noxious effects of Mg overload on various organs. Therefore, future trends should be towards reducing dMg to such values as will allow sMg to fluctuate across the normal range both in the interdialytic and intradialytic period. The more widespread use of Mg-containing phosphate binders implies the need of a further reduction of dMg which, however, carries the risk of symptomatic postdialytic hypomagnesaemia. Thus, since Mg is retained in uraemia and should be removed by dialysis, it is difficult to associate the use of Mg-containing drugs with an optimal dMg while avoiding severe hypermagnesaemia and hypomagnesaemia.
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PMID:Magnesium status in chronically haemodialyzed patients: the role of dialysate magnesium concentration. 270 62

Statural growth and its relation to growth potential, renal function, blood urea nitrogen (BUN), mineral metabolism hormones and dietary intake were studied in 17 prepubertal children (aged 1.6-9.3 years) on conservative treatment for chronic renal failure due to tubulo-interstitial nephropathy. Statural growth (height SDS) was related to the degree of renal failure, was more retarded than ossification, and was independent of the chronological age of the patients. We observed that the lower the glomerular filtration rate (GFR), the lower was the growth potential (increased bone age/statural age ratio). Growth velocity may be normal regardless of statural and bone maturation delay and the degree of renal insufficiency. Impaired growth rate correlated with parathyroid hormone levels, caloric intake and increased blood urea nitrogen during the year of observation. These data show that comprehensive monitoring and suitable treatment must be performed in order to prevent growth retardation at any GFR level.
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PMID:Growth in young children with chronic renal failure. 270 11

The effects of 21 days of chronic renal failure (CRF) with and without excess parathyroid hormone (PTH) and those of 21 days administration of intact PTH on phospholipids and cholesterol contents of rat brain synaptosomes were examined. CRF and PTH treatment were associated with a significant (P less than 0.01-0.02) reduction in the synaptosomal contents of total phospholipids, phosphatidylinositol (PI), phosphatidylserine (PS), and phosphatidylethanolamine (PE). Parathyroidectomy (PTX) prior to the induction of CRF prevented the decrements in the synaptosomal contents of total phospholipids, PI, PS, and PE. The synaptosomal contents of these phospholipids in CRF-PTX rats were not different from those in normal rats despite CRF. There were no significant changes in the cholesterol content of the synaptosomes in the various experimental groups of animals. The data show that CRF affects synaptosomal metabolism of total phospholipids, PI, PS, and PE, and these derangements are due to the state of secondary hyperparathyroidism of renal failure. The decrements in the content of PI, PS, and PE could be, at least in part, responsible for the previously reported abnormalities in the neurotransmitter functions of brain synaptosomes in CRF and could underlie some of the abnormalities in central nervous system dysfunction in uremia.
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PMID:Effect of chronic renal failure and parathyroid hormone on phospholipid content of brain synaptosomes. 270 41


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