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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have established a simplified assay system for the measurement of urinary kallikrein activity by utilizing the sensitive and specific radioimmunoassay system of kinins previously reported from our laboratory. Kinins were generated by incubating urine samples (50 microliter) with kininogen (1500 ng) in the presence of kininase inhibitors, and the generated kinins were measured by radioimmunoassay. Since the cross reactivity of kininogen in the kinin radioimmunoassay system was not recognized at dose up to 1.0 microgram, the amount of untreated kininogen in the radioimmunoassay samples did not interfere with the measurement of kinins. This eliminated the necessity for a kininogen extraction procedure. A good linear correlation (r = 0.939, p less than 0.001) was observed between the urinary kallikrein activity determined by this assay system (kininogenase activity) and that by esterolytic acitvity. Urinary kallikrein activity was 3.3 +/- 0.9 microgram/min/24 hour urine (mean +/- SEM), 1.4 +/- 0.4 microgram/min/24 hour urine and 0.25 +/- 0.06 microgram/min/24 hour urine in 6 normal subjects, 7 patients with non-complicated essential hypertension and 4 patients with chronic renal failure, respectively. Thus, urinary kallikrein activity was significantly lower in the patients with essential hypertension (p less than 0.05) and the patients with chronic renal failure (p less than 0.01) than in the normal subjects.
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PMID:Measurement of urinary kallikrein acitvity by kinin radioimmunoassay. 10 45

Echocardiographic and systolic time intervals changes found after hemodyalisis in 16 patients with chronic renal failure are analysed and discussed. Echocardiogram shows: significant (p less than 0.05), no change statistically significant of end-systolic diameter, fractional shortening, mean velocity of circumferential shortening (VcF), and amplitude of septal motion. Systolic time intervals show: significant reduction (p less than 0.001) of total electromechanical systole (SEM), mechanical systole (SM) and left ventricular ejection time (LVET), and increase (p less than 0.05) of pre-ejection period (PEP) and the ratio PEP/LVET (p less than 0.005). The reason of these changes is the post-dialytic fluid's loss (2140 +/- 760 g) followed by left ventricular end-diastolic diameter and volume reduction which decreases stoke volume and LVET (according to Frank-Starling's law). It has not been possible to draw concordant and definitive conclusions on the post-dialytic left ventricular function. PEP lengthening would give evident for myocardial involvement (but pre-load and after-load changes modifies it), while the other data are slightly affected (VcF, fractional shortening, and amplitude of septal motion) or improved (amplitude and peak velocity of posterior wall motion).
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PMID:[The left ventricle in chronic renal failure patients. Ecocardiographic and poligraphic study before and after hemodialysis (author's transl)]. 16 34

Serum vitamin B12 concentrations were measured in 60 patients undergoing repetitive hemodialysis and in undialyzed patients with chronic renal failure. Dialysis patients had significantly lower serum vitamin B12 levels than the nondialyzed group 321 +/- SEM 38 pg/ml versus 793 +/- 100), and 19 of 60 dialysis patients had vitamin B12 Concentrations less than 200 pg/ml. Folic acid concentration was 5 times greater in dialysis than in nondialysis patients, presumably because the latter received daily supplementation with folic acid. Serum vitamin B12 concentrations fell progressively during the patient's course of dialysis. Neither inadequate dietary intake nor vitamin B12 malabsorption accounted for the differences in the serum vitamin B12 concentrations seen in the two groups. Serum vitamin B12 levels and nerve conduction velocities in 51 dialyzed patients showed a significant correlation. Six dialyzed patients with low serum vitamin B12 levels and slow nerve conduction velocities showed improvement in nerve conduction (+ 14.6 +/- 3.3 m/sec) following the parenteral use of pharmacological doses of vitamin B12. The cause of the low serum vitamin B12 concentration is not clear, nevertheless, alterations in serum vitamin B12 seen in some dialysis patients may be a factor in the persistence of abnormal nerve conduction and may be reversed with large doses of parenteral vitamin B12.
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PMID:Vitamin B12 levels and nerve conduction velocities in patients undergoing maintenance hemodialysis. 18 Jul 88

The effects in man of liver disease, renal failure and hepatic microsomal enzyme induction on the elimination kinetics of antipyrine in saliva have been examined. Antipyrine (10 mg/kg) was given orally and assayed in saliva by gas-liquid chromatography. The mean antipyrine half-life from saliva in nine epileptic subjects receiving long term anticonvulsant drug therapy (6 hr +/- 0-9 SEM) was significantly shorter than in twenty normal healthy volunteers (10-7 +/- 0-6). Therapy included phenytoin and phenobarbitone, two drugs known to induce hepatic microsomal enzymes. Five subjects with chronic renal failure exhibited no significant difference in salivary anti-pyrine half-life (11-7 +/- 1-9) compared to the control group, whereas six subjects with chronic liver disease and impaired hepatic function had significantly increased half-life values (42-4 +/- 10). The results suggest that differences in the activity of hepatic microsomal enzymes are reflected by changes in salivary antipyrine elimination kinetics. Chronic renal failure appeared to have no effect on the function of these enzymes.
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PMID:Salivary antipyrine kinetics in hepatic and renal disease and in patients on anticonvulsant therapy. 27 Sep 89

The MCR and half-disappearance time of exogenously administered somatostatin have been measured during and after cessation of a constant infusion. Studies were performed on normal volunteers and patients with chronic liver disease and failure. Immunoreactive somatostatin was measured by a sensitive and specific RIA using an antiserum directed against the core of the molecule. Normal subjects had a mean MCR of 1949 +/- 250 ml/min (28.4 +/- 4.2 ml/min . kg BW) (mean +/- SEM), similar to values found in five patients with chronic liver disease. However, patients with chronic renal failure showed a highly significant (P less than 0.001) lowering of the MCR (501 +/- 32.7 ml/min or 7.8 +/- 0.6 ml/min . kg). The rate of disappearance of somatostatin after infusion was linear for 7-10 min, after which a much slower component was observed. In normal subjects, the t 1/2 of the first component varied from 1.1-3.0 min, in patients with liver disease it varied from 1.2-4.8 min, and in patients with chronic renal failure it varied from 2.6-4.9 min. Exogenously administered somatostatin is rapidly cleared in normal subjects and patients with chronic liver disease, but the MCR in end stage chronic renal failure is markedly lowered. The kidney may have a role in the metabolic clearance of exogenously administered somatostatin, or uremia may impair catabolism nonspecifically.
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PMID:Metabolic clearance and plasma half-disappearance time of exogenous somatostatin in man. 42 6

1 alpha, 25-Dihydroxycholecalciferol (1,25-(OH)2D3) has been measured in human serum by radioimmunoassay. The assay uses a high titre antiserum raised in sheep against 1,25-(OH)2D3-25-hemisuccinate, conjugated to bovine serum albumin. The sensitivity of the assay is 10 pg/tube. Other hydroxylated forms of vitamin D3 cross react with the antiserum and are therefore removed from serum extracts by chromatography on Sephadex LH 20 followed by high pressure liquid chromatography. The mean (+/- SEM) serum 1,25-(OH)2D3 concentration for a group of healthy adult subjects was 41 +/- 2.5 pg/ml. None was detected in anephric patients and the concentration was low or undetectable in patients with chronic renal failure.
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PMID:Measurement of 1,25-dihydroxycholecalciferol in man by radioimmunoassay. 48 20

To delineate the potential role of disordered glucose and glucose-precursor kinetics in the abnormal carbohydrate metabolism of chronic renal failure, alanine and glucose production and utilization and gluconeogenesis from alanine were studied in patients with chronic compensated renal insufficiency and in normal volunteers. With simultaneous primed injection-continuous infusions of radiolabeled alanine and glucose, rates of metabolite turnover and precursor-product interrelationships were calculated from the plateau portion of the appropriate specific activity curves. All subjects were studied in the postabsorption state. In 13 patients with chronic renal failure (creatinine = 10.7+/-1.2 mg/100 ml; mean+/-SEM), glucose turnover was found to be 1,035+/-99.3 mumol/min. This rate was increased 56% (P = 0.003) over that observed in control subjects (664+/-33.5 mumol/min). Alanine turnover was 474+/-96.0 mumol/min in azotemic patients. This rate was 191% greater (P = 0.007) than the rate determined in control subjects (163+/-19.4 mumol/min). Gluconeogenesis from alanine and the percent of glucose production contributed by gluconeogenesis from alanine were increased in patients with chronic renal failure (192% and 169%, respectively) as compared to controls (P < 0.05 for each). Alanine utilization for gluconeogenesis was increased from 40.2+/-3.86 mumol/min in control subjects to 143+/-39.0 mumol/min in azotemic patients (P < 0.05). The percent of alanine utilization accounted for by gluconeogenesis was not altered in chronic renal insufficiency. In nondiabetic azotemic subjects, mean fasting glucose and immunoreactive insulin levels were increased 24.3% (P = 0.005) and 130% (P = 0.046), respectively.These results in patients with chronic renal failure demonstrate (a) increased glucose production and utilization, (b) increased gluconeogenesis from alanine, (c) increased alanine production and utilization, and (d) a relative impairment to glucose disposal. We conclude that chronic azotemia is characterized by increased rates of glucose and glucose precursor flux and by a relative impairment to glucose disposal. These findings may suggest an underlying hepatic and peripheral insensitivity to the metabolic action of insulin in patients with chronic renal insufficiency.
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PMID:Abnormal carbohydrate metabolism in chronic renal failure. The potential role of accelerated glucose production, increased gluconeogenesis, and impaired glucose disposal. 65 34

Creatinine appearance, defined as the sum of daily creatinine excretion in urine (average over 5 days) plus accumulation in body water, measured over the same interval, was calculated in 27 patients with severe chronic renal failure (creatinine clearance less than 0.15 liter/kg/day). Creatinine appearance per kg body weight in patients with the lowest clearances decreased to values as low as one third of values predicted from age and sex. The absolute value of measured cratinine accumulation was only 11 +/- 2% of creatinine appearance and thus could not account for such deficits in appearance and therefore renal excretion. One explanation for these results is that extrarenal clearance, CM, remains constant, that is, that the quantity of creatinine degraded, M, is proportional to serum creatinine, S: CM = M/S. When the values for extrarenal clearance necessary to account for the measured deficit in creatinine appearance were calculated, they were found to be quite constant: 0.042 +/- 0.004 liter/kg/day (SEM, n=13) in males and 0.041 +/- 0.004 liter/kg/day (SEM, n=14) in females. Renal creatinine clearance in these patients, predicted from age, sex, serum creatinine, and the assumed constant value for extrarenal clearance, corresponded closely to observed clearance (r = 0.93). From these calculations, decreased creatinine appearance (and excretion) of uremic patients may be explained by a constant extrarenal clearance, indicating degradation.
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PMID:A proposed mechanism for reduced creatinine excretion in severe chronic renal failure. 71 98

Here we report a highly sensitive and convenient ligand binding assay for the determination of 1,25(OH)2D3 in small volumes of human plasma. This method involves: (1) extraction of vitamin D3 and its metabolites using methanol-methylene chloride with separation of phases by centrifugation; (2) gel chromatography and high pressure liquid chromatography for the quantitative isolation of 1,25-(OH)2D3; and (3) a sensitive ligand binding assay for 1,25-(OH)2D3 employing cytosol receptor from the intestinal mucosa of rachitic chicks. Using modified rachitogenic chick diets allows early (less than 4 wks) harvesting of active receptor for 1,25-(OH)2D3 in high yield. The method includes a rapid and effective procedure for stable and long-term storage of the active cytosol receptor. A convenient dextran-charcoal means is used for the separation of receptor bound from free 1,25-(OH)2D3 resulting in the achievement of a lower (less than 5%) background (i.e., nonspecific binding) than reported for other 1,25-(OH)2D3 assays. Analysis of this receptor shows it to be a saturable, single class of binding sites with a dissociation constant (Kd) of approximately 3.7 x 10-11. The final recovery of 1,25-(OH)2D3 following extraction and chromatography is 80 +/- 3% and triplicate determinations can be made on a 3 ml plasma sample. The ligand binding assay routinely detects less than or equal to 5pg of 1,25-(OH)2D3 per assay tube and the inter- and intraassay variation, based on repeated determinations of 1,25-(OH)2D3 in pooled normal human plasma, is less than 5%. Preliminary studies indicate that our methodology will permit measurement of plasma 1,25-(OH)2D3 levels in all normal subjects and in pathophysiologic states where 1,25-(OH)2D3 levels may be below or above normal values. 1,25-(OH)2D3 values (pg/ml +/- SEM) in human plasma obtained from both normals and patients with various untreated calcium homeostatic disorders were: normals = 33.5 +/- 1.8; end-stage chronic renal failure = 5.1 +/- 1.2; primary hypoparathyroidism = 18.3 +/- 2.8; primary hyperparathyroidism = 61.4 +/- 7.1; and hyperthyroidism with associated hypercalcemia = 42.1 +/- 8.4.
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PMID:An improved method for the measurement of 1,25-(OH)2D3 in human plasma. 75 33

In patients with chronic renal failure (CRF) (CCr less than 20 ml/min), we have previously demonstrated greater rates of Na excretion (ex) when Na intake was nearly all NaHCO3 as compared to NaCl (both 200 mEq Na daily). Chloride (Cl) wasting on NaHCO3 (with severe Cl restriction) occurred, however, and may in part explain the results. To avoid Cl restriction in 6 patients with CRF (CCr 10-15 ml/min) on an estimated 10 mEq Na and Cl diet, electrolyte ex was compared on NaCl supplements of 200 mEq/day versus a daily mixture of NaHCO3 (100mEq) and NaCl (100 mEq). Periods on NaCl and the mixture lasted 4 days (order randomized) separated by re-equilibration to baseline weight (wt). Mean +/- SEM ex of Na, Cl, HCO3 mEq/day and CCr and deltawt (lbs) are compared below for the 4th day of NaCl vs NaHCO3 intake. (see article). Also there were no significant differences in K excretion, blood pressure, or plasma renin activities. Mean serum HCO3 increased from 21.2 to 25.8 mEq/l (day 1 vs 5, P less than 0.01) reflecting the net positive HCO3 balance on the mixture indicated above. Thus increments of Na intake above a fixed NaCl intake were excreted similarly whether given as NaCl or NaHCO3. Greater Na ex on NaHCO3 may depend on severe Cl restriction and/or higher serum HCO3 levels. If dietary NaCl intakes are near maximum tolerance, NaHCO3 supplementation should be accompanied by reductions in NaCl intake to maintain Na balance,
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PMID:NaHCO3 and NaCl tolerance in chronic renal failure II. 83 32


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