Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The possibility that abnormalities of skeletal muscle may limit the exercise tolerance of patients with chronic renal failure was investigated in patients undergoing regular haemodialysis. 2. Blood flow to the calf, a vascular bed consisting predominantly of skeletal muscle, was measured in six patients before and after exercise and compared with values obtained from 12 control subjects. 3. The patients were limited on exertion and had an abnormal response of calf blood flow to bicycle exercise. Resting calf blood flow was similar in patients and control subjects, but the mean increase in calf blood flow in response to submaximal exercise was 0.55 (SEM 0.12) ml min-1 100 ml-1 in the patients and 1.43 (SEM 0.17) ml min-1 100 ml-1 in the control subjects. The increase after symptom-limited maximal exercise was 1.50 (SEM 0.80) ml min-1 100 ml-1 in the patients and 4.20 (SEM 0.40) ml min-1 100 ml-1 in the control subjects. 4. Skeletal muscle biopsies from eight haemodialysis patients were studied by histochemistry and electron microscopy. 5. Oxidative enzyme activity was increased and there were large subsarcolemmal aggregates of structurally normal mitochondria. Necrotic capillaries were observed as empty basement membrane tubes containing fragments of degenerating endothelium. 6. The changes were compatible with a response to a chronic reduction in skeletal muscle blood flow.
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PMID:Impaired nutritive skeletal muscle blood flow in patients with chronic renal failure. 216 72

A radioimmunoassay has been developed for measuring plasma neuropeptide-Y immunoreactivity using extraction on Sep-Pak C18 cartridges. Neuropeptide-Y concentrations (mean +/- SEM) in plasma from 15 normotensive individuals were 223.6 +/- 14.7 ng/l. Plasma concentrations were raised in 10 patients with heamodialysis-dependent chronic renal failure with values of 417.6 +/- 13.6 ng/l and in 3 patients with phaeochromocytoma the concentrations were 237 ng/l, 574 ng/l and 747 ng/l. Plasma neuropeptide-Y immunoreactivity was also measured in 10 normotensive individuals in response to a, hand-in-ice, cold pressor test. Despite an immediate significant elevation in blood pressure, neuropeptide-Y immunoreactivity was not significantly raised until after the removal of the hand from the ice by which time the blood pressure had returned towards the basal levels. This dissociation in neuropeptide-Y immunoreactivity and blood pressure responses probably reflects a delay in the diffusion of synaptic neuropeptide-Y into the general circulation. This study suggests that the measurement of neuropeptide-Y immunoreactivity may be a useful index of sympathetic activation.
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PMID:Radioimmunoassay for plasma neuropeptide-Y in physiological and physiopathological states and response to sympathetic activation. 226 96

The concentration and molecular form of pancreastatin-like immunoreactivity (PST-LI) in urine of normal subjects and patients with noninsulin-dependent diabetes mellitus or chronic renal failure were examined. PST-LI output (mean +/- SEM) in urine of normal subjects was 74.6 +/- 8.5 pmol/day and 87.1 +/- 11.7 pmol/g creatinine. That in patients with noninsulin-dependent diabetes mellitus was 78.1 +/- 9.0 (SEM) pmol/day and 85.6 +/- 9.0 pmol/g creatinine and was not significantly different from that in normal subjects. Gel filtration analysis showed that PST-LI molecules excreted in urine of these two groups were smaller than human pancreastatin (43-52) (hPST-10) of C-terminal fragment. The PST-LI molecular forms were deduced to be nonbioactive from the result that hPST-10 did not inhibit pancreatic exocrine secretion. PST-LI excretion in patients with chronic renal failure was 258.5 +/- 62.9 pmol/day and 713.2 +/- 219.6 pmol/g creatinine. A molecular form corresponding to hPST-52 and a larger form eluted in the high mol wt region (approximately mol wt 15 K) were detected by gel filtration of urine from these patients, indicating that PST-LI is excreted in urine without degradation in patients with chronic renal failure. These results support the suggestion that the kidney may play an important role in PST degradation or metabolism.
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PMID:Pancreastatin-like immunoreactivity in urine. 240 13

1. The initial rate of L-lysine influx into erythrocytes from 13 patients with chronic renal failure has been measured using 14C-labelled lysine. Ten patients were on maintenance haemodialysis and three had never been dialysed. The results are compared with data obtained from 12 normal individuals. 2. The rate of lysine influx into washed cells from buffered saline containing 0.02-0.5 mmol of L-lysine/l has been calculated. The results can be fitted with a model in which influx has a single saturable component obeying Michaelis-Menten kinetics, and a linear non-saturable component. 3. In uraemic erythrocytes the saturable component had a mean Vmax. of 0.762 mmol h-1 litre-1 of cells (n = 13, SEM 0.072) and a mean Km of 68.2 mumol/l (SEM 5.7). These values in normal erythrocytes were 0.566 mmol h-1 litre-1 of cells (n = 12, SEM 0.033) and 70.5 mumol/l (SEM 4.1), respectively. The mean apparent diffusion constant (KD) for the linear component of influx was 0.224 h-1 (SEM 0.039) in uraemic cells and 0.178 h-1 (SEM 0.028) in normals. 4. The 35% increase in mean Vmax seen in uraemic erythrocytes was statistically significant (P = 0.02). A similar increase in Vmax. in uraemic cells compared with controls was seen in erythrocytes which were studied in zero-trans conditions after depletion of intracellular amino acids. The mean values of Km and KD were not significantly different in uraemia. The origins of this increased membrane transport capacity for lysine in uraemia are discussed.
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PMID:Increased lysine transport capacity in erythrocytes from patients with chronic renal failure. 249 48

This study evaluates the use of calcium carbonate in chronic renal failure. Forty-eight patients (25 male, 23 female, mean age 54.3 years, six pre-dialysis. 12 CAPD, 30 haemodialysis) on phosphate restriction and requiring aluminum hydroxide (mean 2.4 +/- 0.8 g/day) to control serum phosphate, were converted to an equivalent dose of calcium carbonate (2.5 +/- 0.6 g/day). None received vitamin D analogues. Three months post-conversion there was a significant decrease in mean (+/- SEM) serum phosphate (1.86 +/- 0.08 versus 1.66 +/- 0.05 mmol/l P less than 0.01) and serum aluminum (28.3 +/- 5.4 versus 13.2 +/- 3.0 micrograms/l, P less than 0.0001): calcium/phosphate product was unchanged. Post-conversion there was an increase in serum bicarbonate, (20.6 +/- 0.5 versus 22.1 +/- 0.6 mmol/l, P less than 0.01) and serum calcium (2.32 +/- 0.02 versus 2.45 +/- 0.03 mmol/l, P less than 0.0001). No change in serum creatinine, alkaline phosphatase or parathormone occurred. No adverse effects were reported but nine (18%) patients became hypercalcaemic (2.7 to 2.93 mmol/l), eight of whom responded to dose reduction. Hypercalcaemia did not correlate with pre-conversion serum calcium, parathyroid hormone, alkaline phosphatase or aluminium. Calcium carbonate is an effective alternative to aluminium-based phosphate binders. It produces a beneficial increase in serum calcium and bicarbonate and a significant decrease in serum aluminium. Hypercalcaemia is unpredictable but is easily reversible in the majority of patients.
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PMID:The use of calcium carbonate to treat the hyperphosphataemia of chronic renal failure. 251 82

1. Plasma levels of immunoreactive N-terminal pro-atrial natriuretic peptide (N-terminal ANP) have been measured in 25 normal subjects, 29 patients with essential hypertension, six cardiac transplant recipients, seven patients with dialysis-independent chronic renal failure and 11 patients with haemodialysis-dependent chronic renal failure. Plasma was extracted on Sep-Pak cartridges and N-terminal ANP immunoreactivity was measured using an antibody directed against pro-ANP (1-30). 2. Plasma levels of N-terminal ANP (means +/- SEM) were 235.3 +/- 19.2 pg/ml in normal subjects and were significantly raised in patients with essential hypertension (363.6 +/- 36.3 pg/ml), in cardiac transplant recipients (1240.0 +/- 196.2 pg/ml), in patients with chronic renal failure not requiring dialysis (1636.6 +/- 488.4 pg/ml) and patients with chronic renal failure on maintenance haemodialysis (10336.1 +/- 2043.7 pg/ml). 3. There were positive and significant correlations between the plasma levels of N-terminal ANP and alpha-human ANP (alpha-hANP) with individual correlation coefficients of 0.68 within the normal subjects, 0.47 in patients with essential hypertension, 0.78 in patients with dialysis-independent chronic renal failure and 0.68 in patients with haemodialysis-dependent chronic renal failure (P less than 0.05 in every case).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunoreactive N-terminal pro-atrial natriuretic peptide in human plasma: plasma levels and comparisons with alpha-human atrial natriuretic peptide in normal subjects, patients with essential hypertension, cardiac transplant and chronic renal failure. 253 Oct 55

In order to evaluate the possible role of vasoactive hormones in the mechanism of exaggerated sodium loss due to reduced renal mass we measured plasma concentration of atrial natriuretic peptide (ANP), aldosterone, plasma renin activity (PRA), plasma noradrenaline, and dopamine, in 12 children with advanced chronic renal failure (mean CIn 17.8 +/- 2.6, mean +/- SEM, CPAH 93.5 +/- 17 ml/min per 1.73 m2, FENa 7.0 +/- 0.95%). No patient had clinical signs of volume overload. Plasma concentrations of ANP were not significantly different from those of healthy age-matched controls (29.2 +/- 7.2 vs 23.2 +/- 3.1 fmol/ml) and did not correlate with urinary sodium excretion. Plasma concentrations of aldosterone, PRA and noradrenaline, were also within the physiological range, while plasma dopamine levels were elevated (260 +/- 36 vs 98 +/- 11 pg/ml, less than 0.001). Our data do not support the notion that ANP or the renin-aldosterone axis play a major role in the adaptation of remaining nephrons to maintain long-term sodium balance in normotensive children with chronic renal failure.
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PMID:Atrial natriuretic peptide and sodium homeostasis in chronic renal failure. 253 71

Ion pumping by the erythrocyte Na, K-ATPase has been measured using ouabain-sensitive 86Rb flux in 11 non-dialysed patients with chronic renal failure (CRF), 13 patients on haemodialysis (HD), 13 patients on peritoneal dialysis (CAPD) and 15 patients with functional transplants (FT). Flux measurements were performed in plasma and simultaneous estimates of specific 3H-ouabain binding were made. The results indicate that, compared to normal controls, Na,K pump flux was reduced by 21% in CRF (p less than 0.01), 30% in HD (p less than 0.01), 15% in CAPD (p less than 0.02), and was normal in FT. Mean specific ouabain binding sites per cell (+/- SEM) were; controls 366 +/- 16; CRF, 290 +/- 16; HD, 344 +/- 17; CAPD, 321 +/- 18; FT, 345 +/- 26. Calculation of mean turnover rate per pump site indicated that patients on HD showed a 30% reduction compared to controls (influx 55 K ions/s versus 79 K ions/s, p less than 0.01). Cross-incubation experiments suggest that the lowered pump flux seen in the CRF and HD groups was due to plasma factors. This work shows that erythrocyte Na,K pump number is reduced in CRF, while patients on maintenance HD have normal pump numbers per erythrocyte but reduced pump turnover.
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PMID:Effects of dialysis and transplantation on red cell Na pump function in renal failure. 255 64

Plasma pancreastatin (PST)-like immunoreactivity in normal subjects and patients with various diseases was estimated by a RIA, using antiserum raised against a synthetic C-terminal peptide of human PST deduced from the sequence of human chromogranin-A. The mean level +/- SEM was 13.2 +/- 0.6 pmol/L in normal subjects, but was significantly higher in patients with chronic renal failure (526.7 +/- 48.5). An immunoreactive form corresponding to a human PST-like sequence [human chromogranin-A-(250-301)] and a larger form were detected by gel filtration of plasma from these patients, suggesting accumulation of the larger molecular form in these patients. A significant increase in PST-like immunoreactivity was also found in patients with liver cirrhosis (20.8 +/- 3.0 pmol/L), but not in patients with noninsulin-dependent diabetes mellitus, chronic pancreatitis, or pancreatic cancer. Elevated levels were found in 16 of the 21 patients with small cell lung carcinoma examined. High levels were also found in 3 of 11 patients with islet cell tumor.
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PMID:Plasma pancreastatin-like immunoreactivity in various diseases. 255 88

1. Methylguanidine is a suspected uraemic toxin that accumulates in renal failure. 2. We measured methylguanidine in the plasma of dogs with acute ischaemic-induced renal failure and in the plasma and urine of dogs with spontaneous chronic renal insufficiency, using a highly sensitive method involving solid-phase extraction followed by h.p.l.c. with post-column fluorescence detection. 3. Constriction of the remaining renal artery of four uninephrectomized dogs for 90 min resulted in a significant (P less than 0.01) increase in plasma creatinine concentration after 24 h (from 113 +/- 3 to 303 +/- 50 mumol/l; mean +/- SEM). Over the next 14 days, plasma creatinine fell towards baseline concentrations. Plasma methylguanidine also increased significantly (P less than 0.05) 24 h after renal occlusion (from 0.16 +/- 0.04 to 0.86 +/- 0.32 mumol/l) and showed a similar pattern to the plasma creatinine concentration. 4. In a further four dogs, administration of mannitol (2 g/kg) at the time of reperfusion significantly attenuated these responses. 5. Dogs with chronic renal failure demonstrated increased plasma concentrations and urinary excretion of methylguanidine, and the levels appeared to be related to the severity of renal insufficiency. Thus, the dogs with the highest plasma creatinine concentrations and lowest creatinine clearances had the highest plasma methylguanidine concentrations. The clearance of methylguanidine exceeded that of creatinine, indicating that the toxin undergoes renal tubular secretion.
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PMID:Production of methylguanidine in dogs with acute and chronic renal failure. 260 68


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