Biomedical subjects

M Hörl

Publications and source records attributed to M Hörl.

22 records · Page 2Linked to original sources

PubMed1982

[Alterations of fat metabolism in renal disease - pathogenetic mechanisms (author's transl)].

Hypertriglyceridaemia is often observed in patients (1) with chronic renal insufficiency, (2) on haemodialysis and (3) after successful renal transplantation. HDL cholesterol is reduced in all three groups of patients and plasma cholesterol is elevated after renal transplantation. In these three patient groups type IV hyperlipoproteinaemia is found most frequently and after renal transplantation there is a relative increase in the incidence of type II hyperlipoproteinaemia. The role of glucagon resistance and carnitine deficiency in the alteration of fat metabolism seen in patients with chronic renal failure and patients on haemodialysis is discussed. Other factors which may influence fat metabolism in uraemia include calcium and vitamin D status as well as beta adrenergic receptor blocking agents and diuretics. Steroid therapy may be one cause of the hypercholesterolaemia and hypertriglyceridaemia seen after renal transplantation. PHLP lipase activity is reduced in all three groups of patients. In nephrotic syndrome, if hypercholesterolaemia occurs, the HDL cholesterol fraction is increased and thus the cardiovascular risk may be lower than in the three patient group mentioned above.

Adrenergic beta-Antagonists↗

PubMed1982

[Fat and renal failure--therapeutic aspects].

There is current debate as to whether or not the hyperlipidaemia seen in patients (1) with chronic renal insufficiency, (2) on regular dialysis treatment and (3) after successful renal transplantation should be specifically treated. The reduced HDL cholesterol fraction suggests that the risk of cardiovascular complications may be increased. Therapeutic possibilities include increased physical exercise and a reduction of carbohydrate intake. If these measures fail, then treatment with clofibrate or bezafibrate should be considered. The recommended dosage of clofibrate is 1.0-1.5 g/week (with CPK-control), and of bezafibrate is 400-500 mg/week in patients with chronic renal insufficiency (creatinin-clearance below 20 ml/min). In patients on regular dialysis treatment plasma lipids are reduced by adding carnitine. Most investigators believe that a specific therapy of the hypercholesterolaemia and hypertriglyceridaemia of patients with nephrotic syndrome is not necessary since the disturbances in fat metabolism are associated with an increased levels of HDL-cholesterol. With remission of the nephrotic syndrome an improvement of the hyperlipoproteinaemia is observed. If patients with acute renal failure are under parenteral nutrition fat infusion is recommended once per week to avoid a deficiency of essential fatty acids which is augmented by daily dialysis therapy.

Acute Kidney Injury↗

PubMed1982

[Protein catabolism and tourniquet shock: the role of proteolytic enzymes].

In the plasma and/or serum ultrafiltrates of a 20-year-old patient with tourniquet shock and post-traumatic acute renal failure it was possible to identify free proteolytic activity during the oligoanuric phase. Plasma alpha 2-macroglobulin values were significantly lowered, whereas the plasma concentrations of antithrombin III were unchanged. alpha 1-Antitrypsin values, however, were markedly enhanced. In contrast, urinary excretion of alpha 1-antitrypsin and antithrombin III were enhanced during the oligoanuric phase. Addition of kallikrein and/or trypsin resulted in strong inhibition of urinary proteolytic activity. These effects were not seen during the polyuric and recovery phase. From our results it can be concluded that proteolytic enzymes may be involved in protein catabolism of patients with tourniquet shock and hypercatabolic acute renal failure.

Acute Kidney Injury↗

PubMed1981

Evidence for the participation of proteases on protein catabolism during hypercatabolic renal failure.

In ultrafiltrated plasma (molecular weight less than 50,000) obtained from four patients with multiple muscular trauma and acute post-traumatic renal failure, it was possible to verify a subcomponential specific digestion of the subunits alpha and gamma of phosphorylase kinase isolated from rabbit skeletal muscle. The activity of free proteolytic enzymes in ultrafiltrated plasma as well as an increase of plasma alpha 1-antitrypsin values were correlated with the severity and unfavourable course of the illness. In contrast, the plasma levels of alpha 2-macroglobulin were drastically lowered. The mean total protein concentration in the sera of patients with post-traumatic ARF was lowered, whereas the mean ultrafiltrate protein concentration was significantly enhanced. In ultrafiltrated plasma of two patients with hyperuricaemic ARF, three patients with ARF after drug over-dosage, one patient with acute pancreatic necrosis combined with acute renal failure and one patient with chronic pancreatitis, no proteolytic activity could be detected using phosphorylase kinase as substrate. Studies on the trypsin binding capacity of the plasma protease inhibitors revealed a significantly lowered level in patients with post-traumatic acute renal failure as compared to healthy controls, patients with chronic renal insufficiency and patients on regular dialysis treatment Proteolytic activity was found in ca. 100-fold concentrated diafiltrates (molecular weight greater than 10,000) of patients on regular dialysis treatment. Our data suggest a participation of proteases on protein catabolism in hypercatabolic states. Whilst the blood coagulation system can largely be excluded as a source of proteases, it is possible that proteolytic enzymes may be released from muscle lysosomes and/or macrophages after multiple muscular trauma.

Acute Kidney Injury↗