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

Glucose intolerance is a common concomitant of untreated chronic renal failure, but the effect of long-term treatment on the insulin resistance believed to be behind it is as yet not clarified. Peripheral tissue sensitivity to insulin was therefore examined in 7 dialyzed uraemic patients, 8 undialyzed uraemic and 8 matched healthy subjects using the hyperinsulinaemic euglycaemic clamp technique. The dialyzed subjects had been on maintenance haemodialysis for a mean of 4 yr (range, 3-131 months) and were studied both before and after a single random dialysis. The clamping was performed during 150 min using a glucose controlled insulin infusion system (Biostator). Insulin was infused at a rate of 2.0 mU/kg/min. Tissue sensitivity to insulin was expressed as glucose uptake (M) at steady state (90-150 min) over steady state serum insulin concentration (I). While M was significantly greater in healthy subjects (12.52 +/- 1.02 mg/kg/min, mean +/- 1 SEM) than in dialyzed uraemics (9.59 +/- 0.78 mg/kg/min and 9.36 +/- 0.70 mg/kg/min, both p less than 0.05), M/I was similar in chronically dialyzed patients (before and after dialysis: 0.098 +/- 0.017 mg/kg/min per microU/ml vs 0.104 +/- 0.020 mg/kg/min per microU/ml) and in controls (0.111 +/- 0.015 mg/kg/min per microU/ml; p greater than 0.20). In contrast M/I ratio of uraemic subjects who had never been dialyzed (0.062 +/- mg/kg/min per microU/ml) was significantly reduced (both p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of tissue sensitivity to insulin in uraemic patients on long-term haemodialysis therapy. 404 32

We compared the ionic activity of sodium, as measured with glass electrodes, with sodium concentration in 23 healthy persons, 15 persons with acute renal failure, and before and after dialysis in 46 patients with chronic renal failure. In healthy persons the mean (+/- SEM) sodium concentration was 139.1 +/- 0.6 mmol/L, whereas the ionic activity was equal to that of a 145.2 +/- 0.5 mmol/L solution of sodium chloride. Variation in the concentration of plasma protein was the most important factor influencing the sodium activity coefficient (the ratio between activity and concentration). The sodium activity coefficient in plasma water (corrected for the non-aqueous phase of the plasma) was fairly constant, being 96% of that in a 140 mmol/L solution of sodium chloride. Thus sodium binds to non-protein molecules and sodium ions interact with other substances in uremic plasma only to a very limited extent. The sum of the molar activities of sodium, potassium, urea, and creatinine was closely and linearly correlated with plasma osmolality, both before and after dialysis.
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PMID:Sodium activity, sodium concentration, and osmolality in plasma in acute and chronic renal failure. 405 50

Measurement of oxalate levels in 14 patients with chronic renal failure, treated by maintenance hemodialysis, revealed elevated plasma oxalate concentrations in all patients 1,075.7 +/- (SEM) 253 micrograms/dl. In 7 of these subjects the oxalate concentration was more than three times higher than the upper limit of normal. Furthermore, a strong positive correlation (r = 0.75) between serum creatinine and plasma oxalate concentration was found. A combination of hemodialysis and hemoperfusion procedure was carried out in a dialysis patient with primary oxalosis as a cause of renal failure. The average oxalate clearance of the hemodialyzer during seven hemodialysis/hemoperfusion procedures was 91 ml/min and that of the charcoal detoxifier was 24 ml/min. The amount of oxalate removed during 4 1/2 h of the hemodialysis/hemoperfusion procedure was 429 mg. This amount was calculated to be produced in about 87 h, with an oxalate generation rate of 4.9 mg/h.
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PMID:Hyperoxalemia in renal failure and the role of hemoperfusion and hemodialysis in primary oxalosis. 405 24

Elevation of plasma glucagon concentration has been observed in starvation and illnesses associated with increased catabolism such as diabetes mellitus and severe infections. Thus, we examined plasma glucose, immunoreactive insulin (IRI, microunits per milliliter) and glucagon (IRG, picograms per milliliter) responses to a beef meal (1 g/kg body wt) and intravenous glucose (1.5 g/min for 45 min) in patients with chronic renal failure (CRF). After the beef meal (n = 6), plasma glucose did not change, IRI rose from 10.1+/-1.2 to 16.3+/-1.1 (P < 0.01), and IRG rose from a fasting value of 225+/-26 to 321+/-40 (P < 0.01) by 90 min (mean+/-SEM). Intravenous infusion of glucose in CRF patients resulted in significant elevations and prolonged disappearance of plasma glucose and insulin when compared to control subjects (P < 0.01). Glucose infusion failed to suppress elevated plasma glucagon concentrations to normal levels.6 wk of chronic hemodialysis in five patients resulted in normal plasma glucose and insulin responses to the same intravenous glucose load. In contrast, plasma glucagon concentration remained unchanged after hemodialysis and there was no correlation of plasma glucagon levels with carbohydrate intolerance.
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PMID:Hyperglucagonemia of renal failure. 481 42

It has been suggested that an inappropriate relationship between renin and exchangeable sodium is responsible for the hypertension of patients with chronic renal failure. Long-term blockade of the renin system by captopril made it possible to test this hypothesis in 8 patients on maintenance hemodialysis. Captopril was administered orally in 2 daily doses of 25 to 200 mg. Previously, blood pressure averaged 179/105 +/- 6/3 (mean +/- SEM) pre- and 182/103 +/- 7/3 mm HG post-dialysis, despite intensive ultrafiltration and conventional antihypertensive therapy. The 4 patients with the highest plasma renin activity normalized their blood pressure with captopril alone, whereas in the 4 remaining patients, captopril therapy was complemented by salt subtraction which consisted in replacement of 1-2 liters of ultrafiltrate by an equal volume of 5% dextrose until blood pressure was controlled. After an average treatment period of 5 months, blood pressure of all 8 patients was reduced to 134/76 +/- 7/5 mm Hg (P less than 0.001) pre- and 144/81 +/- 9/5 mm Hg (P less than 0.001) post-dialysis without a significant change in body weight. The present data suggest that captopril alone or combined with salt subtraction normalizes blood pressure of patients on chronic hemodialysis with so called uncontrollable hypertension.
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PMID:Uncontrollable hypertension in patients on hemodialysis: long-term treatment with captopril and salt subtraction. 626 27

The circulating concentrations of 1,25-dihydroxyvitamin D and 24,25-dihydroxyvitamin D are abnormally low in patients with chronic renal failure (CRF). To determine the importance of substrate (25-hydroxyvitamin D) concentration in this phenomenon, five patients with end stage renal disease treated with hemodialysis were given 25-hydroxyvitamin D3 (25-OH-D3) orally for 4 weeks. The serum concentration of 25-OH-D3 increased from a mean (+/- SEM) of 26 +/- 5 ng/ml immediately before therapy to a maximum of 108 +/- 5 ng/ml 4 weeks after beginning administration of 25-OH-D3. The concentrations of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), 24,25-dihydroxyvitamin D3 (24,25(OH)2D3), and 25,26-dihydroxyvitamin D3 (25,26(OH)2D3) increased from 6.6 +/- 0.8 pg/ml, 0.29 +/- 0.10 ng/ml, and 0.36 +/- 0.06 ng/ml, respectively, immediately before 25-OH-D3 administration to 21.7 +/- 2.2 pg/ml, 0.48 +/- 0.09 ng/ml; and 0.78 +/- 0.12 ng/ml, respectively, after 4 weeks of administration of 25-OH-D3. These results suggest that substrate availability may be an important determinant of the circulating concentrations of these metabolites in patients with CRF. It seems possible that the therapeutic effects of 25-OH-D3 administration to the CRF patient may be mediated through the normal actions of 1,25-dihydroxyvitamin D3, 24,25-dihydroxyvitamin D3, and perhaps other metabolites rather than through analog effects of 25-OH-D3.
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PMID:Plasma vitamin D metabolite concentrations in chronic renal failure: effect of oral administration of 25-hydroxyvitamin D3. 633 30

In this study, we have investigated plasma pyridoxal 5'-phosphate (PLP) concentrations in undialyzed and dialyzed uremic patients and in kidney transplant subjects, using an enzymatic technique with thermal deproteinization to liberate PLP from plasma proteins. The specificity of the reaction indicates no interference with pyridoxal and only 3% interference with pyridoxamine phosphate. In 17 hemodialyzed patients, a deficiency of about 50% of plasma PLP concentration is found as compared to 25 healthy subjects (22.2 +/- 2.47 vs. 48.8 +/- 3.00 nmol . l-1), as mean +/- SEM). In seven undialyzed uremic patients with end-stage renal failure, the plasma PLP concentration is also decreased (29.3 +/- 1.74 nmol . l-1). The absence of PLP in plasma ultrafiltrates demonstrates that no loss of PLP occurs due to hemodialysis. The daily oral supplementation with 250-750 mg pyridoxal induces a supraphysiological increase in plasma PLP concentration in hemodialyzed as well as in undialyzed patients. In 116 non-uremic kidney transplant subjects, the mean plasma PLP concentration was 33.8 +/- 3.50 nmol . l-1). In 65% of these patients, a marked deficit (below 20 nmol . l-1) was observed. In conclusion, uremic patients have a deficient vitamin B6 state. Its correction with pyridoxal to restore physiological plasma PLP concentration necessitates oral supplementation with lower doses that those widely used at present. In kidney transplant patients a similar plasma PLP deficiency is observed in the absence of chronic renal failure.
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PMID:Pyridoxal 5'-phosphate deficiency in uremic undialyzed, hemodialyzed, and non-uremic kidney transplant patients. 633 52

Rejection of an allograft usually is preceded by activation of T lymphocytes, in which state such cells may be identified by their ability to form thermostable rosettes with sheep erythrocytes (TE-R). The objective of the present work, therefore, was to determine whether or not enumeration of TE-R in the peripheral blood was of any value in the diagnosis of rejection. The results showed no significant differences between TE-R (mean +/- SEM) in normal subjects (9.9 +/- 1.3; n = 25), renal allograft recipients without rejections (13.5 +/- 1.7; n = 5) and in patients who suffered from acute tubular necrosis in the posttransplant period (12.4 +/- 2.5; n = 8). In contrast, recipients who had rejection episodes showed a marked rise in TE-R levels (43.0 +/- 4.0; n = 11) about two to seven days prior to the diagnosis of rejection by clinical and chemical criteria. Furthermore, TE-R remained high if the rejection episodes turned out to be irreversible after therapy (42.2 +/- 3.7) but fell if the episodes were reversible (19.9 +/- 3.2). TE-R values were elevated in patients with chronic renal failure on maintenance hemodialysis (45.7 +/- 4.9; n = 23). Neither acute dialytic runs or acute infections altered TE-R values. In conclusion, those results show that enumeration of TE-R may be helpful in the early diagnosis of allograft rejection, before clinical and chemical stigmata are apparent.
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PMID:Thermostable erythrocyte rosettes in chronic renal failure and allograft rejection. 635 76

Plasma renin activity (PRA), aldosterone, vasopressin and catecholamines were measured in 15 children (ages 7.3 to 16.2 years) with chronic renal failure (CRF) before and after one session of hemodialysis and in 15 control children. Basal levels of PRA and aldosterone in children with CRF did not differ significantly from control values, but showed a wider range. Uremic patients with nephronophthisis showed the highest basal PRA and aldosterone levels. In children with CRF, basal vasopressin levels were significantly higher (9.7 +/- [SEM] 2.0 ng/liter) than control values (3.2 +/- 0.8 ng/liter). Plasma noradrenalin and adrenalin concentrations were similar in children with CRF and controls. During hemodialysis, a fall in blood pressure and a rise in heart rate was observed in all children. PRA and catecholamines increased twofold to fivefold during dialysis while aldosterone and vasopressin showed a variable response. In contrast to reports in adults, there is no evidence for an insufficiency of vasoactive hormones or of the sympathetic nervous system in children on hemodialysis.
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PMID:Vasoactive hormones in children with chronic renal failure. 636 49

Secretion of pancreatic polypeptide (PP) is regulated mainly by cholinergic mechanisms and we have studied this in patients with chronic renal failure (CRF). Basal serum PP concentrations in 25 patients with CRF (401 +/- 80; 116-2100 pmol/l; mean +/- SEM and range) were significantly higher than in 65 normal subjects (33 +/- 2; 21-120 pmol/l, P less than 0.001). Ingestion of a standard test meal induced significantly larger increases in serum PP in 11 patients with CRF (304 +/- 45; 155-640 pmol/l) than in 11 normal subjects (140 +/- 33; 51-440 pmol/l, P less than 0.005). Insulin-hypoglycaemia (0.1 U/kg i.v.) provoked similar increases in serum PP in five patients with CRF (404 +/- 79; 170-665 pmol/l) as in five normal subjects (449 +/- 92; 180-706 pmol/l). Administration of atropine (1 mg i.v.) did not normalize the elevated basal serum PP concentrations in five patients with CRF. On the other hand, administration of the same dose of atropine 60 min after ingestion of food decreased postprandial serum PP levels to basal values within one hour both in five patients with CRF and in six normal subjects. Sephadex G-50 column chromatography of basal, postprandial and post-atropine sera from three patients with CRF revealed at least three different molecular forms. The PP peak coeluting with the 4200 molecular weight human PP standard comprised more than half of total PP immunoreactivity and was the only peak to be influenced by feeding or atropine. We conclude that in patients with CRF, PP secretion stimulated by cholinergic mechanisms is normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cholinergic regulation of pancreatic polypeptide secretion in chronic renal failure. 637 35


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