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Biomedical subjects

W Höfer

Publications and source records attributed to W Höfer.

At least 19 recordsLinked to original sources
PubMed1986

Effect of long-term administration of 1,25-dihydroxyvitamin D3 and 1 alpha-hydroxyvitamin D3 on the calcium content of the aorta, heart and kidney of normal and uremic rats.

Studies in uremic rats were performed to see whether or not the long-term administration of therapeutical doses of 1,25-Dihydroxyvitamin D3 or 1 alpha-hydroxyvitamin D3 would induce histological changes in the aorta or increase the calcium content of the aorta or the heart. In contrast to observations of others, no effect of both vitamin D sterols could be observed on both investigated tissues. However, the remnant kidneys of the rats treated with both vitamin D compounds showed a significantly increased calcium content. According to these results one cannot exclude that the chronic application of active vitamin D metabolites has induced a calcium deposition in the remnant kidney. This finding deserves special attention, although we found, on the other hand, no evidence that an underlying arterial disease is aggravated by this therapy.

Animals↗
PubMed1985

Endotoxin-induced acute renal failure in mice. Effects of indomethacin and the thromboxane-synthetase antagonist UK 38.485.

Functional acute renal failure (ARF) was induced within 24 h following i.p. injection of 200 micrograms E. coli endotoxins (ET) into C3H/HeHan mice. Pre- and post-treatment with either UK 38.485, a selective thromboxane (TX)-synthetase inhibitor, or with the cyclo-oxigenase inhibitor, indomethacin (IM), does not prevent acute renal failure in these mice. Histologically, only very little fibrin degradation and few microthrombi are present 24 h later in the kidneys, so that disseminated intravascular coagulation (DIC) mechanisms cannot have caused the significant azotemia. Slight histological changes are accentuated in the UK 38.485-treated group. Only the indomethacin group has a significantly increased mortality as compared to all other groups. We conclude from our study that with low dosages of endotoxins functional ARF can be induced in mice without a circulatory shock and early mortality and that both UK 38.485 and IM are of little value in preventing it.

Acute Kidney Injury↗
PubMed1984

Effect of diets containing varying concentrations of essential fatty acids and triglycerides on renal function in uremic rats and NZB/NZW F1 mice.

Influences of essential fatty acids (EFA) and triglycerides as reasons for the progression of chronic renal failure are still in debate. We studied the outcome of four diets containing different concentrations of triglycerides and EFA in 5/6 nephrectomized rats and in NZB/W mice up to 45 weeks. The results showed no significant differences in the outcome of survival rate, proteinuria, urea, and creatinine levels as well as histological findings in the different groups of both animal models. We conclude that diets containing EFA up to C18:2 or being free of EFA or that triglyceride-enriched diets have no influence on the natural course of the renal disease in these both experimental models.

Animals↗
PubMed1979

[Clinico-pathological correlations in lupus nephritis with reference to therapeutic and prognostic aspects (author's transl)].

Since 1970 in 27 out of 46 patients with the diagnosis of systemic lupus erythematosus (SLE) a renal biopsy could be taken. The morphological outcome was followed in 14 patients with a total of 18 repeated biopsies. By light- and electron microscopy renal involvement was demonstrable in all patients. Four histologic subgroups could be differentiated: Mesangio-proliferative (MESLN, 14), focal proliferative (FLN, 6), diffus proliferative (DLN, 6), and membranous lupus nephritis (MLN, 1). Some biopsies demonstrated linear deposits with IgG/IgA-specificity. 2/27 patients only showed a clinical deteriorating course with progressive renal insufficiency despite steroid or steroid-azathioprine therapy. One patient with DLN died in terminal renal failure. The morphological follow-up showed an unfavourable course in 3/14 patients only. One MESLN demonstrated a transition to DLN, one DLN an increase of proliferative lesions and a second DLN focal and local sclerosis. In our experience renal involvement in SLE can adequately characterised and controlled by repeated be clinico-pathological correlations an aggressive therapeutic regimen is not indicated and can be avoided.

Azathioprine↗
PubMed1978

[Anticoagulation and immunosuppression in rapidly progressive glomerulonephritis of poststreptococcal type (author's transl)].

In the majority of cases acute poststreptococcal glomerulonephritis is characterized by a good prognosis. Only relatively rare courses of this disease with clinical symptoms of rapid progressive glomerulonephritis and morphological signs of extracapillary glomerulonephritis together with crescent formation are sometimes prone to an infavorable outcome. A widely accepted medication does not exist up to now. Our own observations including clinical and morphological follow up studies are suggesting a combination of anticoagulants and immunosuppressive drugs. Indication and usefullness of that regimen are discussed.

Adolescent↗
PubMed1977

[Renal vein thrombosis: a complication of the nephrotic syndrome? (author's transl)].

The nephrotic syndrome is complicated by an increased thromboembolic risk. This is related to changes in one or more factors of the Virchow triad (vessel wall, blood flow, coagulation). The hypercoagulability may be enhanced by iatrogenic manipulations as for instance vessel punctures, application of steroids and diuretics. The preferential location of thrombus formation are the veins of the leg, pelvis, kidney, and the cerebral sinuses. In contrast the "primary" renal vein thrombosis has long been considered not as a complication of the nephrotic syndrome but as its cause. In the meantime there have been accumulated histological, experimental and clinical facts showing the nephrotic syndrome causative for the renal vein thrombosis. This is revealed too by our own cases.

Adolescent↗