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Biomedical subjects

T Risler

Publications and source records attributed to T Risler.

At least 127 records · Page 7Linked to original sources

Renal, major histocompatibility complex antigens and cellular components in rapidly progressive glomerulonephritis identified by monoclonal antibodies.

Identification of crescent-forming cells in rapidly progressive glomerulonephritis (RPGN) is very difficult, and controversial results on the participation of different epithelia as well as of monocytes have been reported. In the present study different monoclonal antibodies were used to analyze cellular infiltrates of crescents and the interstitium as well as the distribution of well-defined renal antigens and major histocompatibility complex (MHC) encoded antigens along the human nephron in cryostat sections of renal biopsies from patients with RPGN. The results demonstrate that monocytes/macrophages infiltrate Bowman's space and that cellular components of crescents present with phenotypes of parietal glomerular and proximal tubular cells. T lymphocytes are significantly found in glomeruli and also in interstitium with predominance for CD4+ lymphocytes. Reduction of MHC class-II antigens within diseased glomeruli correlates with changes in renal antigen expression. Tubular cells, however, often presented an abnormal expression of MHC class-II antigens. Differences of renal and MHC-encoded antigen expression may be due to rapid regeneration episodes of renal parenchymal cells in RPGN.

Adult↗

Influence of strenuous exercise on albumin excretion.

Renal albumin excretion rate was 7.3 mg/24 h (SEM 0.5, range 0.6-21.0) in 66 healthy subjects. This rate increased markedly during and shortly after strenuous exercise on a bicycle ergometer (before: 5.5 +/- 0.6 micrograms/min; during and just after: 16.9 +/- 2.2 micrograms/min; P less than 0.001; n = 30). However, albumin excretion/24 h was not significantly higher during 24 h with a period of strenuous exercise than during 24 h without such exercise (10.3 +/- 0.9 mg/24 h vs 8.5 +/- 0.7 mg/24 h).

Adult↗

[Digitalis therapy in medical practice. Research on indications and dosage criteria in general practice].

Two hundred digitalized patients under nine freely practising physicians were investigated. One hundred and ninety-six patients received digoxin or one of its derivatives. Of these, 50% did not have therapeutic serum glycoside concentrations, 48% were in the mostly subtherapeutic range and 2% were in the potentially toxic range. Signs of glycoside intoxication were not found. A substantiated indication for glycoside therapy was found in the final analysis in 55% of the patients. In 128 patients, the methyldigoxin dose calculated (0.16 +/- 0.030 mg/d) was markedly in excess of that actually prescribed (0.13 +/- 0.050 mg/d; p less than 0.001), so that there were indications of a general underdigitalization. In addition, it was not possible to anchor the restrictive kidney function as a reason for reduction of digoxin dosage in the prescription behavior. In the long run, only 36% of the patients with justified indication and therapeutic serum glycoside concentration as well as (with reservations) the 3% with potentially toxic serum glycoside concentration profited from the glycoside therapy.

Atrial Fibrillation↗

Drug monitoring of quinine by HPLC in cerebral malaria with acute renal failure treated by haemofiltration.

The monitoring of quinine by HPLC in 3 patients suffering from cerebral malaria with acute renal failure and treated by haemofiltration is reported. The recommended dose of quinine in this situation is reduced to 10 to 15 mg.kg-1.day-1. However, in the first patient, when given quinine 10 mg kg-1.day-1 the plasma concentration was mainly below the recommended therapeutic range of 5 to 15 mg/l. In consequence, the dose of quinine in the second patient was elevated to quinine dihydrochloride 15.1 mg.kg-1.day-1 which produced plasma concentrations in the low therapeutic range. In the third patient, an unreduced dose of quinine dihydrochloride 25.7 mg.kg-1.day-1 was employed, resulting in plasma concentrations above 15 mg/l, which is generally assumed to be toxic, although, no sign of acute quinine toxicity was seen. The antimalarial effect in all three patients was satisfactory. Quinine was estimated in the haemofiltrate in two patients and was found to be below the limit of sensitivity (0.25 mg/l). Plasma quinine did not change during or shortly after haemofiltration. It is concluded that in case of acute renal failure in cerebral malaria the dose of quinine should be reduced, but that the common recommendation of 10 to 15 mg.kg-1.day-1 may be too low, and that haemofiltration has no marked influence on the total body clearance of quinine.

Acute Kidney Injury↗

The renin-angiotensin-aldosterone system during haemodialysis with acetate or bicarbonate at different dialysate sodium concentrations.

The hormones of the renin angiotensin aldosterone system were measured during regular haemodialysis with acetate or bicarbonate at dialysate sodium concentrations of 135, 140, 145, and 150 mmol/l. Plasma renin activity and aldosterone concentration were higher during acetate haemodialysis than during bicarbonate haemodialysis. At lower dialysate sodium concentrations, plasma renin activity (acetate dialysis and bicarbonate dialysis) and aldosterone concentration (only acetate dialysis) were higher than they were at higher dialysate sodium concentrations. Plasma renin activity increased during acetate dialysis, but did not change during bicarbonate dialysis. Aldosterone and potassium concentrations were positively correlated. Aldosterone decreased during haemodialysis (increase to predialysis values at the end of haemodialysis (4 h) at lower dialysate sodium concentrations). It is concluded that the renin angiotensin aldosterone system is activated more during acetate dialysis than during bicarbonate dialysis. Aldosterone concentrations seem to be related more closely to serum potassium than to renin-angiotensin-aldosterone system and to serum sodium intradialytically.

Acetates↗

Effects of membrane plasma exchange on the hemostatic system and on thyroid hormones in critically ill patients.

The present study examined the effects of repeated plasma exchanges with membrane filtration (Plasmaflux P2 membrane, 4.3 I human albumin solution) on the hemostatic system and on thyroid hormones in critically ill patients. Clotting factors V, VII, VIII, IX, X, XI, XII, XIII, fibrinogen, antithrombin III (ATIII), prothrombin time (PT), activated partial thromboplastin time (PTT), total (TT3) and free tri-iodothyronine (FT3), total (TT4) and free thyroxine (FT4), and thyroxine binding globulin (TBG) were determined before, immediately after, 1, 3, 6 and 24 h after plasma exchange in 6 patients (3 with glomerulonephritis, 2 with IgG myeloma, 1 with chronic polyneuritis) during 18 plasma exchanges. After plasma exchange levels of clotting factors and ATIII were markedly lowered but except for fibrinogen and factor XIII, they were not reduced by repeated exchange procedures. Thyroid hormones and TBG were reconstituted after 24 h. Pre-exchange levels, except for TT4 and TBG, were not lowered by repeated exchange procedures. Risk of bleeding or thrombosis is small and there is no appreciable risk of loss of thyroid hormones during repeated plasma exchanges.

Adult↗

Enzyme-linked immunosorbent assay for urinary albumin at low concentrations.

We describe an enzyme-linked immunosorbent assay (ELISA) for urinary albumin. It requires only commercially available reagents, can detect as little as 16 micrograms of albumin per liter, and analytical recovery ranges from 92 to 116%. The assay is simple, rapid, and inexpensive. Albumin excretion was 6.2 (SD 4.1) mg/24 h in healthy subjects (n = 40), 14.7 (SD 7.2) mg/24 h in albumin-test-strip-negative Type I diabetics (n = 11), and 19.7 (SD 16.2) mg/24 h in patients with essential hypertension (n = 12).

Adult↗

Treatment of non anti-GBM-antibody mediated, rapidly progressive glomerulonephritis by plasmapheresis and immunosuppression.

A retrospective study was conducted to evaluate the efficacy of plasmapheresis in combination with different immunosuppressive drugs ("pulse" therapy, azathioprine or cyclophosphamide together with steroids) in nine patients presenting with rapidly progressive glomerulonephritis (RPGN) not mediated by antibody to glomerular basement membrane. Six of these patients had to be initially dialysed. All patients underwent renal biopsy, which revealed that seven patients had a minimum of 80% crescents and five had interstitial fibrosis. Recovery of renal function was observed in seven patients (78%). All patients without interstitial fibrosis were recompensated for at least 14 months after the acute onset of RPGN. Those who presented with interstitial fibrosis declined to endstage renal failure after 13 months requiring chronic hemodialysis treatment or cadaveric kidney transplantation. On the basis of these findings interstitial fibrosis seems to be a limiting factor for the prognosis of non-anti-GBM-antibody mediated RPGN.

Adult↗

[Spontaneous regression of residential stenosis of the infarct vessel following successful percutaneous transluminal coronary recanalization].

In 64 out of 90 patients with thrombolysis by intracoronary streptokinase (PTCR) in the acute stage of myocardial infarction coronary angiography was performed in the chronic stage after 28 +/- 20 days. 52 of 56 successfully treated patients had a patent infarct vessel in the chronic stage. 36 of these patients showed a spontaneous regression from the subacute to the chronic stage. In 49 of the 56 patients (age: 53.4 +/- 10.4 years) a residual stenosis of more than 75% after PTCR was found; in the chronic stage only 31 patients had a stenosis of more than 75%. Of 10 patients with a spontaneous regression of 25% or more (age: 48.0 +/- 14.9 years) 8 had a one-vessel disease. The infarct vessel was in 6 patients the left anterior descending, in 4 patients the right coronary artery and in no case the left circumflex branch. The results suggest that the indication for invasive interventions, such as acute coronary angioplasty or bypass surgery, does not only depend on the degree of the residual stenosis directly after reperfusion. If possible, the decision for further invasive treatment should depend on the clinical follow-up.

Adult↗

[Renal and extracorporeal elimination of digoxin and its methylated and acetylated derivatives].

This study was performed to get more informations on the renal and extracorporeal elimination of digoxin. The first part of this study demonstrated that a radioimmunoassay for digoxin or a specific tritium label of digoxin is necessary to measure renal digoxin clearances. Randomly labeled 3H-digoxin may loose its label and thus give incoherent results. A comparison of digoxin and inulin clearances in patients demonstrates glomerular filtration as the major renal excretion pathway of digoxin, but a major fraction of the glycoside is excreted by tubular secretion. Opposite to digoxin, beta-methyl-digoxin undergoes less tubular secretion but eventually additional tubular reabsorption. The insertion of digoxin and quinidine may be a further prove for the existence of a tubular secretion of digoxin. While the renal clearance of digoxin is significantly bigger than the renal clearance of creatinine, additional quinidine therapy reduces the renal clearance of digoxin to the one of creatinine. We studied the renal excretion mechanism of digoxin additionally in an animal model of acute prerenal failure. After a 33% reduction of renal arterial pressure glomerular filtrate dropped 68%. Under these circumstances the renal excretion mechanism of digoxin measured as the digoxin to inulin clearance ratio did not change. We evaluated the efficiency of hemodialysis, hemofiltration and hemoperfusion to eliminate digoxin. Although digoxin is eliminated by all three methods, even the most effective, hemoperfusion, can reduce total body content of digoxin less than 3%. Thus we conclude that all these methods have no indication in the treatment of digoxin intoxications.

Acetyldigoxins↗

On the interaction between digoxin and disopyramide.

Combined oral therapy with digoxin (0.375 mg/dl) and disopyramide (300 and 600 mg/dl) in nine subjects did not alter steady-state digoxin serum concentrations just before the daily single digoxin dose. Digoxin and creatinine clearances were not changed. After a bolus IV dose of 0.8 mg digoxin, volume of distribution (from 672 +/- 176 l to 407 +/- 153 l) and elimination t1/2 beta of digoxin were reduced significantly in five subjects after 600 mg oral disopyramide daily (from 40.2 +/- 11.7 hr to 22 +/- 7.3 hr). Total clearance and digoxin distribution t1/2 alpha did not change significantly. The clinical significance of this interaction is not clear.

Adult↗