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Biomedical subjects

F Scheler

Publications and source records attributed to F Scheler.

At least 73 records · Page 4Linked to original sources
PubMed1985

[Alpha 1-microglobulin in the urine and serum in proteinuria and kidney insufficiency].

Alpha-1-microglobulin (alpha-1-m) is a low molecular weight glycoprotein (mw 25-33 KD) that is filtered through the glomeruli and reabsorbed in the proximal parts of the renal tubules where it is catabolized. Normal ranges were established for alpha-1-m (100 healthy controls) in serum (20-42 mg/l) and urine (3.5-8 mg/l). Alpha-1-m was then measured in 341 urine samples whose protein pattern had been classified as "pathologic" and "normal" according to microelectrophoresis. Increased alpha-1-m concentrations were found in 266 out of 280 pathologic urines (5% false negative) and in 3 out of 61 normal urines (4% false positive). Beta-2-microglobulin (beta-2-m), total protein or protein test strips showed a poorer correlation to the electrophoretic results. Measurement of alpha-1-m is, therefore, the most sensitive of these methods for the detection of proteinuria. In 90 patients with low molecular weight proteinuria and either with or without renal insufficiency alpha-1-m concentrations were determined in both urine and serum. While all patients had elevated urinary alpha-1-m concentrations, increased serum values were only found in renal insufficiency (Ccrea less than 100 ml/min). Independently of these results, we were also able to establish that increased alpha-1-m levels are found at decreased glomerular filtration rates (Ccrea less than 70 ml/min). Pathologic alpha-1-m concentrations therefore only allow the conclusion of isolated tubular impairment when the GFR is greater than 70 ml/min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

[Continuous ambulatory peritoneal dialysis. 5-year clinical experience].

Continuous ambulatory peritoneal dialysis (CAPD) is, next to conventional home dialysis, a world-wide method of treating chronic renal failure. This is the report of clinical experience of 34 CAPD patients who, from October 1978 to the end of 1983, had undergone 642 treatment months. The incidence of peritonitis after introduction of a new connector system in 1983 was reduced to 1 per 46 CAPD treatment months. In only 7 patients was it necessary to discontinue CAPD for reasons connected with the type of dialysis. No patient requested discontinuance of CAPD. Suitable bag and tube materials, adequate space, and well trained personnel are decisive for a successful CAPD programme, in addition to careful selection of patients. The latter aims at optimal patient motivation for the treatment method which, in principle, is more cost effective than home dialysis. In so far as patients fulfil the requirements for home dialysis they can be excellently rehabilitated.

Adolescent↗
PubMed1985

[Use of low molecular-weight heparin in hemodialysis patients].

Low-molecular-weight (LMW) heparin has been compared to standard unfractionated (UF) heparin in a total of 49 patients on hemodialysis and hemofiltration in order to determine the necessary therapeutic dose and its effect on the coagulation system. A LMW heparin dose corresponding to 50% of the normal UF heparin dose was found to produce similar plasma heparin levels (anti-FXa-U/ml) in particular on minimal heparinization. At higher doses, UF heparin produced a more marked increase in plasma-heparin than did LMW heparin. Highly significant differences were found between UF and LMW heparin in their effects on PTT and thrombin time. Partial thromboplastin time (PTT) increased under UF heparin by an average of 120 s whereas LMW heparin only produced an increase of 5-7 s. Thrombin time was increased by 250-280 s under UF heparin and by 5-8 s under LMW heparin. With this LMW heparin dose of 50% of the UF heparin dose, no thrombosis of the extracorporal system occurred and no macroscopic detectable thrombotic material was found in the dialyzers or filters. No significant differences were observed between the effects of UF and LMW heparin on Factor VIII activity and fibrin monomers, so that a difference in coagulation activation between the two heparins can be excluded. Furthermore, there were no changes in thromboplastin time according to Quick, fibrinogen, antithrombin III, plasminogen, and a2-antiplasmin.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood↗
PubMed1985

Neutral steroid metabolites in patients with uraemia and after renal transplantation: a quantitative and qualitative study in body fluids.

Steroid metabolites enriched from urine, haemofiltrate, and CAPD-dialysate (Continuous Ambulatory Peritoneal Dialysis) were identified by gas chromatography-mass spectrometry and quantified by capillary gas chromatography. The study included twenty healthy controls, twenty-six non-dialysed uraemics, thirty-nine patients on regular dialysis treatment, and twenty-two allograft recipients. Compared to the 24 h urinary excretion rates of controls the excretion rates of androsterone and etiocholanolone were in the lower normal range up to significantly decreased in the body fluids of all patients, and those of the corticoid metabolites were also significantly decreased. 11-Oxygenated androstanolones in urine from non-dialysed uraemics correlated significantly decreased. 11-oxygenated androstano-levels and were significantly increased, but normal in haemofiltrate and CAPD-dialysate, while in urine of allograft recipients the values were significantly lower.

Adrenal Cortex Hormones↗
PubMed1985

Effect of dialysate glucose load on plasma glucose and glucoregulatory hormones in CAPD patients.

The effect of a dialysate exchange with both 1.5 and 4.25% glucose solutions on plasma levels of glucose, insulin, gastric inhibitory polypeptide (GIP), and glucagon has been investigated in 5 continuous ambulatory peritoneal dialysis (CAPD) patients. Only in the case of the 4.25% solution did plasma glucose levels rise above 100 mg/dl. 4 of the 5 patients responded to this change with a marked insulin secretion. Employing the 1.5% solution, plasma glucose remained stable and only a slight insulin stimulation was observed in 2 patients. It is concluded that provided the 4.25% dialysates are used only occasionally, there will be no continuous stimulation of the pancreatic beta-cells due to absorption of glucose from the dialysate alone during CAPD treatment. GIP levels are highly elevated in CAPD patients. A dialysate exchange with either a 1.5 or a 4.25% glucose solution had no effect on this gastrointestinal hormone. Hyperglucagonemia was also observed in this collective. An initial suppression of glucagon levels occurred in 4 of the patients after a 4.25% dialysate exchange. The 5th patient demonstrated an initial rise followed by a later decrease in glucagon, a response similar to that reported in adult onset diabetes after an oral glucose tolerance test.

Adult↗
PubMed1984

[Bezafibrate-induced myolysis and myoglobinuria in patients with impaired renal function].

A muscular syndrome has been described in patients on clofibrate and fenofibrate therapy. The present paper describes four patients with impaired renal function in whom symptoms and signs of skeletal muscle damage developed during treatment with another clofibrinic acid derivative, bezafibrate. The syndrome was characterized by variable degrees of muscular cramps and paresis, excessive elevation of muscle enzymes in serum, myoglobinemia and myoglobinuria. Transient deterioration of renal function was also common. All patients had been overdosed with bezafibrate with regard to their renal function. It is concluded that bezafibrate like other lipid lowering agents of the clofibrate type may induce muscle damage, at least if doses are not adjusted to renal function. Extreme caution is warranted when treating patients with renal impairment with bezafibrate and strict dose adjustment to kidney function is necessary to avoid muscle damage.

Aged↗
PubMed1984

[Serum levels and urine excretion of L-carnitine in patients with normal and impaired kidney function].

The influence of age, sex, and renal function on serum levels and urinary excretion of free carnitine was studied in 187 subjects. Sixty-one subjects with normal renal function (creatinine clearance greater than 100 ml/min) showed a serum carnitine level of 72.2 +/- 23.2 mumol/l. The carnitine values of males (76.8 +/- 23.3 mumol/l, n = 39) were higher (p less than 0.05) than those of females (64.0 +/- 21.0 mumol/l, n = 22). Carnitine levels did not correlate with age. Values in patients with normal renal function did not differ from serum carnitine levels in healthy controls (74.7 +/- 17.5 mumol/l, n = 49). The mean urinary carnitine excretion per day was 163.5 mumol (range 63.7-419.6 mumol) in patients with intact renal function. Extreme impairment of glomerular filtration rate (creatinine clearance less than 20 ml/min) resulted in higher carnitine concentrations in serum (108.9 +/- 39.4 mumol/l, n = 18, p less than 0.05), lower carnitine elimination per day (78.5 mumol, range 14.5 - 424.3 mumol, n = 18, p less than 0.05) and a decreased carnitine clearance (0.8 ml/min, range 0.2 - 3.8 ml/min). These data together with earlier results obtained in dialysis patients suggest that carnitine metabolism in renal failure is altered by reduction of both endogenous carnitine biosynthesis and renal carnitine clearance.

Adolescent↗
PubMed1984

Favourable outcome of hepatic veno-occlusive disease in a renal transplant patient receiving azathioprine, treated by portacaval shunt. Report of a case and review of the literature.

Veno-occlusive disease (VOD) developed in a 45-year-old white male 2 years after cadaveric kidney transplantation while receiving combined immunosuppressive therapy with prednisone and azathioprine. Early clinical signs at presentation included ascites and tender hepatomegaly. The diagnosis of VOD was established at laparoscopy and by histological examination of liver biopsies. Azathioprine was discontinued. Gross ascites refractory to medical treatment and decreasing liver function required surgical treatment by portacaval shunt. Transient postoperative complications were hepatic encephalopathy and considerable hyperbilirubinaemia. 8 months later the patient is well, with stable renal function and no clinical signs of hepatic disease.

Azathioprine↗
PubMed1983

[Muscular carnitine-palmityl-transferase deficiency].

Deficiency in carnitine-palmityl-transferase (CPT) was demonstrated in a 20-year-old man with paroxysmal myoglobinuria, after failure to discover another cause. It is concluded that muscular CPT deficiency must be excluded before a recurrent myoglobinuria is classified as "idiopathic".

Acyltransferases↗
PubMed1983

Quantitative assessment of carnitine loss during hemodialysis and hemofiltration.

Carnitine deficiency has been claimed to be responsible for the myo- and cardio-myopathy observed in dialysis patients and has been attributed to the loss of carnitine during dialysis. To quantitate carnitine loss, we determined the carnitine concentrations in 29 patients on chronic hemodialysis, 10 patients on chronic hemofiltration, and 8 patients on CAPD. Mean plasma carnitine levels in hemodialysis and hemofiltration patients (39.8 +/- 2.7 mumoles/liter; N = 39) were significantly lower (P less than 0.01) than in controls (49.8 +/- 2.0 mumoles/liter; N = 43). Hemodialysis or hemofiltration led to a further reduction (33.2 +/- 3.5 mumoles/liter; P less than 0.001). There was no significant difference in the mean plasma carnitine level between CAPD patients (40.0 +/- 5.7 mumoles/liter) and controls. Hemofiltration treatment resulted in a weekly loss of 795 +/- 84 mumoles of carnitine. This was significantly lower (P less than 0.0001) than the urinary carnitine excretion in healthy controls (1534 +/- 134 mumoles per week; N = 27) and the carnitine elimination in the dialysate of CAPD patients (1905 +/- 236.6 mumoles per week; N = 8). It is concluded that carnitine deficiency in dialysis patients cannot be explained by loss into dialysate or filtrate. Because intestinal reabsorption of carnitine does not seem to be impaired, decreased endogenous carnitine synthesis is considered as the most plausible explanation for the moderate degree of carnitine deficiency observed in dialysis patients.

Adult↗