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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the value of bone Gla protein (BGP) as a biochemical marker of normal bone physiology and metabolic bone disorders, we have developed a radioimmunoassay (RIA) for the detection of BGP in human plasma. Antibodies were generated in rabbits immunized with purified calf BGP conjugated to thyroglobulin. Human plasma BGP reacted identically with the calf BGP standard, thus demonstrating the suitability of the assay to measure plasma BGP levels in man. The RIA is sensitive, accurate, and technically simple. Plasma BGP levels were determined in normal subjects (N = 35) and in patients with hypothyroidism (N = 10), hyperthyroidism (N = 22) and chronic renal failure (N = 35). The mean (+/- 1 SEM) concentration of plasma BGP in normal subjects was 1.27 +/- 0.07 nmol/l. Plasma BGP was significantly increased in patients with hyperthyroidism, 4.04 +/- 0.78 nmol/l (P less than 0.001) and chronic renal failure, 10.17 +/- 2.47 nmol/l (P less than 0.001). Low concentrations were found in patients with hypothyroidism, 0.74 +/- 0.11 nmol/l (P less than 0.01). Our studies indicate that plasma BGP provides a useful technique in the diagnosis of patients with bone disease.
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PMID:A radioimmunoassay for bone Gla protein (BGP) in human plasma. 349 71

In the past years dialyzers have been improved, and consequently pyrogenic reactions have become rare. However, some patients in our dialysis unit have shown symptoms during hemodialysis which we suspected could be caused by endotoxins. These patients, as well as controls without similar symptoms, had elevated levels of circulating endotoxin. We therefore measured endotoxin in blood from patients with chronic renal failure and different kinds of treatment. Serum samples were analyzed with a sensitive method described in the literature, using a chromogenic substrate and Limulus amebocyte lysate. In patients on hemodialysis (mean +/- SEM) the endotoxin value in samples taken immediately before dialysis was 40 +/- 4.7 ng/l and significantly elevated (p less than 0.001) compared with the endotoxin value (7 +/- 0.6 ng/l) found in the healthy reference group. Increased endotoxin levels were also seen in patients on hemofiltration (19 +/- 7.5 ng/l) and in patients with conservative treatment and various degrees of renal insufficiency (17 +/- 2.5 ng/l). Patients on peritoneal dialysis and renal-transplanted patients had levels not different from the controls. The mechanism behind endotoxemia in uremia is unknown but may partly be explained by reduced endotoxin elimination due to impaired liver macrophage function. The differences in endotoxin levels in patients on peritoneal or hemodialysis treatment may reflect that extracorporeal circulation enhances endotoxin entrance to the circulation and/or that endotoxin clearance is dependent on the dialysis regimen.
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PMID:Endotoxemia in chronic renal failure. 355 May 1

We produced antiserum to insulin-like growth factor I (IGF-I), and developed a specific and sensitive radioimmunoassay (RIA) for IGF-I using the biosynthetic IGF-I. This antiserum to IGF-I was specific for IGF-I; no cross-reactivities with multiplication stimulating activity, porcine insulin or human growth hormone (hGH) were detected. The sensitivity was 10-25 pg/tube with 50% displacement at 125 pg/tube. The intra- and inter-assay coefficients of variation for IGF-I were 5.4 and 9.7%, respectively. The plasma IGF-I levels as determined by RIA in normal adults (N = 46), patients with active acromegaly (N = 31), and pituitary dwarfs (N = 31) were 21.6 +/- 1.0, 157.3 +/- 17.0, and 2.5 +/- 0.3 ng/ml (Mean +/- SEM), respectively, indicating the levels were GH-dependent. The plasma IGF-I levels were significantly increased from 2.2 +/- 0.2 to 26.5 +/- 3.2 ng/ml after hGH administrations for three consecutive days in five pituitary dwarfs. The IGF-I levels were low in patients with hypothyroidism and liver cirrhosis, but were normal in patients with chronic renal failure. These data confirm previous reports and this radioimmunoassay proves useful in evaluating plasma IGF-I levels.
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PMID:Radioimmunoassay for insulin-like growth factor I (IGF-I) using biosynthetic IGF-I. 358 65

The bone histology in patients with chronic renal failure and aluminum-related bone disease does not always show the excess accumulation of unmineralized osteoid (matrix) characteristic of osteomalacia. Frequently, bone aluminum accumulation is associated with normal or reduced amounts of unmineralized osteoid and low bone formation and is referred to as aplastic bone disease. In this study, we compared static and dynamic bone histomorphometric parameters and plasma PTH and aluminum levels in 12 patients with osteomalacia and 18 patients with aplastic bone disease who had been receiving dialysis for the same duration to determine if the difference in osteoid accumulation in these 2 lesions might be explained by differences in aluminum accumulation or PTH levels. The stainable bone surface aluminum level was significantly higher in the patients with osteomalacia compared to that in the group with aplastic bone [61 +/- 5% (+/- SEM) vs. 43 +/- 4%; P less than 0.02]. The rates of bone apposition and bone formation were lower in the group with osteomalacia (P less than 0.01). Plasma amino-terminal PTH was not significantly different in the 2 groups. The increment in plasma aluminum levels after a single infusion of deferoxamine was higher in the osteomalacic group than in the aplastic group, suggesting that the patients with osteomalacia accumulated more total body chelatable aluminum than did those with aplastic bone disease during a comparable length of time on dialysis. We conclude that the excess unmineralized osteoid in aluminum-related osteomalacia results from the high rate of total body aluminum accumulation, which directly causes uncoupling of matrix mineralization and matrix production, independent of PTH levels. Patients with aplastic bone disease who have accumulated lesser amounts of total body aluminum fail to develop excess unmineralized osteoid because production and mineralization of matrix are more closely coupled than in the osteomalacic lesion, despite a decline in osteoblast numbers.
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PMID:Osteomalacia and aplastic bone disease in aluminum-related osteodystrophy. 358 92

Using a specific radioimmunoassay, we measured concentrations of plasma 7B2 (a novel pituitary polypeptide) immunoreactivity (7B2-IR) in normal human subjects, patients with chronic renal failure and those with liver cirrhosis. Mean (+/- SEM) values of plasma 7B2-IR in normal healthy men and women were 55.8 +/- 1.2 pg/ml (n = 266) and 56.1 +/- 0.9 pg/ml (n = 408), respectively. The elevation of plasma 7B2-IR showed a relationship with age of the subjects, in both men (r = 0.39, t = 6.86, p less than 0.001) and women (r = 0.35, t = 7.44, p less than 0.001). Plasma 7B2-IR concentrations were elevated in patients with chronic renal failure (536 +/- 45 pg/ml, Mean +/- SEM, n = 10) as well as those in liver cirrhosis (95 +/- 10 pg/ml, Mean +/- SEM, n = 15) compared to values in normal subjects, suggesting that 7B2 is mainly eliminated through the kidney and is partly metabolized in the liver.
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PMID:Age-related change in plasma concentration of 7B2 (a novel pituitary polypeptide) in normal humans. 361 60

Levels of immunoreactive (IR) oxytocin (OT)-associated or estrogen-stimulated neurophysin (ESN) and vasopressin-associated or nicotine-stimulated neurophysin (NSN) were measured in plasma of patients with chronic renal failure before and after hemodialysis (HD) and intermittent peritoneal dialysis (IPD), and during continuous ambulatory peritoneal dialysis (CAPD). ESN-IR in 17 patients before HD was 24.4 +/- 2.7 ng/ml (mean +/- SEM) and increased after HD to 33.2 +/- 4.1 ng/ml (P less than 0.001). ESN-IR in 17 patients with CAPD was 15.2 +/- 3.4 ng/ml, significantly lower than in patients undergoing HD, P less than 0.001. In patients receiving IPD (n = 6), ESN was 11.6 +/- 3.7 ng/ml and did not change significantly after IPD. Levels of ESN in patients with renal failure were increased compared with levels in normal individuals, 1.0 +/- 0.1 ng/ml. Levels of ESN were not correlated with laboratory parameters that may be abnormal in renal failure. NSN levels in 16 of 17 patients undergoing HD were 3.2 +/- 0.34 ng/ml and in 14 of 17 patients with CAPD were 2.9 +/- 0.4 ng/ml, respectively. ESN before HD (r = 0.63, P less than 0.01), after HD (r = 0.85, P less than 0.001), and in patients with CAPD (r = 0.83, P less than 0.001) and IPD (r = 0.81, P less than 0.05) correlated significantly with an OT-like peptide previously found to be increased in renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High-performance liquid chromatographic characterization of neurophysins in chronic renal failure. 365 23

To study the effect of specific beta 2-adrenergic stimulation on potassium metabolism in renal failure, we intravenously administered albuterol (Salbutamol) sulfate, 0.5 mg, to 20 patients with chronic renal failure (glomerular filtration rate, less than 5 mL/min) receiving maintenance hemodialysis. Within 30 minutes after albuterol administration, serum potassium level dropped from 5.6 +/- 0.2 (+/- SEM) to 4.5 +/- 0.2 mEq/L (5.6 +/- 0.2 to 4.5 +/- 0.2 mmol/L). There were no changes in plasma aldosterone levels or arterial pH, but blood glucose and serum insulin levels increased. Albuterol, however, induced similar decreases in serum potassium levels in three diabetic patients while free C peptide levels remained undetectable or subnormal after administration of the drug. Albuterol sulfate alone (0.5 mg intravenously) was also used to treat 24 patients with acute or chronic renal failure and hyperkalemia. Their serum potassium levels dropped from 7 +/- 0.2 mEq/L (7 +/- 0.2 mmol/L) to 5.6 +/- 0.2 mEq/L (5.6 +/- 0.2 mmol/L), 5.6 +/- 0.2 mEq/L (5.6 +/- 0.2 mmol/L), 6 +/- 0.2 mEq/L (6 +/- 0.2 mmol/L), and 6.2 +/- 0.2 mEq/L (6.2 +/- 0.2 mmol/L) at 30, 60, 180, and 360 minutes after receiving albuterol, respectively, and this was accompanied by reversal of the electrocardiographic manifestations of hyperkalemia. Despite inducing transient tachycardia, albuterol was remarkably well tolerated and no serious side effects were observed. beta 2-adrenergic stimulation of intracellular potassium uptake by albuterol is a safe and effective alternative for the treatment of hyperkalemia in renal failure.
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PMID:Potassium-lowering effect of albuterol for hyperkalemia in renal failure. 382 59

The purpose of this study was to characterize a new animal model of severe hypertension with azotemia. Hypertension was induced in rats by complete ligation of the aorta between the origin of the renal arteries. One month later chronic renal failure was induced by removing the right kidney. The serum creatinine concentration, mean arterial blood pressure (MABP), plasma renin activity (PRA) and plasma angiotensin II levels were monitored over the next two weeks. One month after aortic ligation, but before removal of the right kidney, the MABP, PRA, and plasma angiotensin II levels were significantly greater than in controls (P less than 0.05). Following nephrectomy serum creatinine concentration rose from 0.65 +/- 0.03 mg/100 ml (X +/- SEM) to 2.75 +/- 0.40 mg/100 ml and 1.78 +/- 0.22 mg/100 ml (P less than 0.05), 3 and 14 days after the right nephrectomy, respectively. Although the elevated MABP remained unchanged, the PRA and plasma angiotensin II concentrations significantly declined to levels indistinguishable from normotensive controls. These data indicate that combining aortic ligation with right nephrectomy produces a uremic model of severe hypertension in the rat. This model may facilitate studies designed to determine the best choice of antihypertensive drugs in the situation of severe hypertension and renal insufficiency.
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PMID:Unilaterally nephrectomized rat with aortic ligation: a uremic model of severe hypertension. 389 21

Serum gonadal hormones, gonadotrophins and zinc levels were studied in thirteen men aged 29-62 yr with chronic renal failure undergoing haemodialysis. All patients had decreased libido and impotence. Serum testosterone levels in patients (18.5 +/- 1.3 (SEM) nmol/l) were significantly lower (p less than 0.05) than in the control group (24.1 +/- 2.2 (SEM) nmol/l) although salivary testosterone levels were strictly within the normal range. Mean serum 17-beta-oestradiol and luteinizing hormone levels (0.19 +/- 0.03 (SEM) nmol/l, and 57.4 +/- 13.1 (SEM) IU/l, respectively) were significantly higher (p less than 0.05 and p less than 0.005, respectively) than in the control group (0.11 +/- 0.02 (SEM) nmol/l and 14.8 +/- 1.9 (SEM) IU/l, respectively). Mean progesterone and follicle-stimulating hormone levels in patients were not significantly different from those of control subjects. Mean prolactin values in patients (1,019 +/- 285 (SEM) mIU/l) were significantly higher (p less than 0.01) than in the control group (211 +/- 24 (SEM) mIU/l). Serum prolactin levels in five patients were extremely high (above 1,200 mIU/l). There was no statistically significant difference in serum zinc levels between patients and controls. As salivary testosterone is normal, it seems that hyperprolactinaemia and raised serum 17-beta-oestradiol levels may be responsible, at least in part, for sexual dysfunction in male patients with chronic renal failure receiving haemodialysis.
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PMID:Hormonal profile and serum zinc levels in uraemic men with gonadal dysfunction undergoing haemodialysis. 393 99

The clinical, radiological and hepatic histological features of 51 patients with hepatobiliary fibropolycystic disease were reviewed. Many of the patients had more than one of the diseases; the combination of both congenital hepatic fibrosis (CHF) and Caroli's disease was most striking. Twelve patients with CHF (50% male) presented at 6 +/- 2 years of age (mean +/- SEM) with hepatosplenomegaly or variceal bleeding. Their main problems were recurrent variceal bleeds and renal disease. Polycystic kidneys and renal stones were present in 79% and chronic renal failure in 30%. Six of the 8 patients with Caroli's disease were male (75%) and presented later (aged 37 +/- 8 years) with hepatomegaly or cholangitis. Recurrent cholangitis developed in most (7/8) and 2 had polycystic kidneys. Twelve patients had a combination of CHF and Caroli's disease presenting with hepatosplenomegaly, bleeding or cholangitis. As in Caroli's disease, most (83%) were male, but the age of presentation (15 +/- 4 years), and the incidence of polycystic kidneys (42%) and renal failure (8%) was intermediate between CHF and Caroli's disease. In these patients, bleeds always predated cholangitis. Histologically, acute cholangitis was superimposed on the changes of CHF. Adult polycystic liver disease (10 patients) presented later (43 +/- 3 years) in females (90%) with pain, a mass or incidentally; polycystic kidneys were present in 33%. Microhamartomas (10 patients), which were usually incidental findings, were diagnosed latest (50 +/- 6 years). Three choledochal cysts were seen. The hazard of cancer in these diseases was reflected by 2 bile duct cancers and 1 pancreatic cancer (incidence 6%). This study has confirmed that hepatobiliary fibropolycystic diseases form part of a family and are often associated together. However, the diseases are of greatly differing severity and the prognosis in an individual patient is determined by the fibropolycystic diseases present.
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PMID:Hepatobiliary fibropolycystic diseases. A clinical and histological review of 51 patients. 395 71


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