Selective continuous extracorporal elimination of low-density lipoproteins with heparin at acidic pH.
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Biomedical subjects
Publications and source records attributed to F Scheler.
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Carnitine concentrations were measured in plasma, haemofiltrate, dialysate and urine of patients on regular dialysis treatment and in normal controls. Patients on haemofiltration and on haemodialysis exhibited moderately decreased plasma values, whereas in eight patients on CAPD mean values did not differ from controls. Carnitine loss into the haemofiltrate was significantly lower than urinary carnitine excretion in normal subjects. Major disturbances of intestinal carnitine absorption in patients on regular dialysis treatment were not observed. It is concluded that patients on regular dialysis are in a state of moderate carnitine deficiency and that therapeutically induced carnitine losses or grossly impaired intestinal absorption are not major factors in the development of carnitine deficiency in these patients.
Haemodialysis had become impossible or possible only using high doses of heparin in 20 patients with dialysis-dependent renal insufficiency due to lowering of antithrombin III (AT III). In order to assess the value of AT III substitution for effective heparin treatment and concomitant diminution of the danger of haemorrhage AT III substitution was done in these patients. Six patients. Six patients with acute renal failure and disseminated intravascular coagulation were able to undergo dialysis using only 750-1000 IU heparin/h after normalisation of AT III without complications. In 3 patients thrombosing of the extracorporeal system had occurred despite increasing doses of heparin; only after 1500 U AT III subsequent haemodialysis could be performed without thromboses. Dialysis was performed with continuous substitution of the AT III-heparin-complex in 6 patients prone to haemorrhage. 250-500 U of AT III-heparin-complex were sufficient and proved as safe and well manageable possibility of minimal anticoagulation. In 5 patients repeated thrombosing of the haemofilter per day had occurred during continuous arteriovenous haemofiltration. After AT III administration haemofilters could be left in situ for 18-46 hours.
Systematic blood coagulation analyses were conducted in 32 severely hypertensive patients treated with the angiotensin converting enzyme inhibitor captopril. Two hours after the first captopril dose, fibrin monomer complexes had already increased. This rise was even more distinct after 26 h and 1 week. Tests after 6 and 12 months of therapy showed a regression of fibrin monomer complexes to pretreatment values. In several patients with a marked increase in fibrin monomer complexes, the partial thromboplastin time (PTT) became shorter and antiplasmin activity increased. The most pronounced increase in fibrin monomer complexes was seen in patients with a rapid and excessive blood pressure reduction. The concentration of fibrin monomer complexes also rose in 15 healthy normotensive subjects, after a single oral dose of captopril (25 mg). Additionally, the PTT was shortened and antiplasmin significantly rose. An inhibition of fibrinolysis by captopril could be demonstrated by the effect on fibrin plates and thrombus weight after streptokinase. Out of 58 patients with severe hypertension and atherosclerosis treated with captopril, 7 patients suffered vascular complications during antihypertensive therapy: myocardial infarction (n = 2), coronary insufficiency (1), cerebral ischemia (1), renal insufficiency (3). These ischemic lesions may be partly explained by the alterations of coagulation and fibrinolysis under captopril therapy.
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During the past few years continuous ambulatory peritoneal dialysis (CAPD) has become well established in the home treatment of uremia. CAPD, however, may induce certain biochemical abnormalities. Using glucose as an osmotic agent of the dialysate the peritoneal glucose load may vary between 75 and 200 g per day, depending upon how often high osmotic dialysate is needed. If the latter is restricted to one bag per day a long-term disturbance of the glucoregulatory hormones insulin, GIP an glucagon seem to be inprobable. Investigations into glucose tolerance after 23 til 34 months of CAPD treatment in 4 patients did not indicate any exhaustion of the pancreatic beta-cells. Long-term evaluation into the metabolism of lipoproteins, total plasma proteins, aminoacids and trace elements did not show significant abnormalities induced by CAPD itself. Biochemical alterations observed are more or less related to the uremic state of the patients.
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A patient with typical features of late onset McArdle's disease is described. During forearm ischemic work test the patient exhibited an exaggerated increase in ammonia release, largely exceeding normal values. It is suggested, that this is due to an activation of the myokinase/myoadenylate deaminase pathway. Besides lack of lactate release increased ammonia release during ischemia may be a typical feature of McArdle's disease.
The effect of an oral glucose tolerance test (oGTT) on serum levels of branched-chain keto acids (BCKA), i.e. alpha-keto-isocaproic acid (KICA), alpha-keto-isovaleric acid (KIVA) and alpha-keto-beta methyl-n-valeric acid (KMVA) as well as on serum insulin, C-peptide and blood glucose levels was determined in uremic patients and in healthy control subjects. In controls, blood levels of KICA, KMVA and KIVA declined significantly following oral administration of 100 glucose. In uremic patients no decline of KICA was observed. The fall of KMVA was diminished, while suppression of KIVA blood levels in response to the oGGT remained unimpaired. Although serum insulin and C-peptide levels in uremic patients were not significantly different from the controls before and throughout the oGTT, six out of eight displayed abnormal glucose tolerance. It is suggested that the response of blood BCKA levels to an oGTT is altered in uremia, an abnormality restricted primarily to KICA and possibly explained by insulin antagonism and/or by insufficient insulin secretion.
Acute rhabdomyolysis with myoglobinuric renal failure occurred in a 66-year-old woman who was in hyperosmolar non-ketotic diabetic coma. No previous description of such a case has been found. The clinical picture was characterized by the typical findings of hyperosmolar coma, in addition to excessive serum creatine kinase and myoglobin levels and massive myoglobinuria with acute renal failure. The rhabdomyolysis became fully manifest only under insulin treatment, possibly the result of insulin-induced hypophosphataemia, which seems to be of importance in the causation of the rhabdomyolysis.
In 44 patients with chronic renal failure of varied etiology serum immunoreactive myoglobin was measured and compared to values obtained in patients with normal renal function. Irrespective of the underlying disease a highly significant linear correlation was found between serum immunoreactive myoglobin and serum creatinine concentration. In patients with serum creatinine concentrations above 550 mu mol/1 (6.2 mg%) serum myoglobin was as a rule elevated above the range found in the controls with normal renal function. This was also true in dialysis patients. These result demonstrate that serum myoglobin may only be used with restrictions in the diagnosis of myocardial infarction in patients suffering from advanced chronic renal failure.
Twenty intensive care patients, who as an additional complication developed acute oliguric renal failure were treated solely with continuous arteriovenous haemofiltration (CAVH). The mean spontaneous filtration rate was 8.8 +/- 3.5ml/min. IV substitution of the ultrafiltrate by K+-free Ringer's lactate solution resulted in a steady state plasma creatinine level of 6.4 +/- 3.5mg/dl. Duration of treatment was three to 24 days (10.5 +/- 7.9 days). Eight patients recovered kidney function and survived. Clinical experience in five intensive care units with more than 150 applications of CAVH allows the following conclusions: optimal control of water and electrolyte balance; unlimited parenteral nutrition; continuous fluid withdrawal better tolerated than intermittent withdrawal by means of dialysis. With skilled puncture of the femoral artery there was no risk of bleeding. Low dose continuous heparin administration (10IU/kg/hr) into the arterial blood line is sufficient for extracorporeal anticoagulation. Haemofilters can be used for a long time (two to ten days). Specially trained dialysis personnel and investment costs for machines are not necessary.