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Biomedical subjects

M Rambausek

Publications and source records attributed to M Rambausek.

70 records · Page 4Linked to original sources
PubMed1985

Hypertension in mesangial IgA glomerulonephritis.

Blood pressure in 75 patients with IgA nephropathy (IgA-GN), confirmed by renal biopsy, was related to clinical, immunological and morphological findings. The findings were compared with an age-matched control group of patients with non-IgA-GN. Overall prevalence of hypertension (HT) was similar in IgA-GN and non-IgA-GN (38.7% vs 38.2%). The presence of HT in IgA-GN was related to age, renal function, immunohistological pattern and degree of glomerular sclerosis or vascular lesions respectively. No correlation was found between HT and elevated serum IgA, circulating IgA immune complexes and IgA skin deposits. The current observations underline the value of hypertension for predicting development of renal failure. Vascular lesions are not only strongly correlated with, but may even precede development of, hypertension as confirmed by longitudinal observations.

Adolescent↗
PubMed1985

Sicca syndrome in mesangial IgA glomerulonephritis.

Schirmer-test, history of conjunctivitis, salivary gland scintigraphy and SSA/SSB (Ro/La) antibodies were evaluated in 24 patients with mesangial IgA glomerulonephritis (IgA-GN), 58 patients with non-IgA-GN and 100 healthy controls. A sicca syndrome (positive Schirmer-test) was found in 46% of patients with IgA-GN and 17% of non-IgA-GN and 8% of controls (p less than 0.001). Only one of the IgA-GN patients volunteered a history of xerosis of the conjunctiva, but upon questioning 17% reported a history of ophthalmological treatment for recurrent conjunctivitis. The observation adds another extrarenal facet to the syndrome of mesangial IgA-GN. Diminished tear production may be another (immune?) abnormality of the oropharyngeal system.

Adolescent↗
PubMed1983

Deposition of polymeric IgA1 in idiopathic mesangial IgA-glomerulonephritis.

IgA deposits in kidney and skin biopsies from patients with idiopathic mesangial IgA-glomerulonephritis were characterized with immunofluorescence microscopy using monoclonal antibodies against the IgA subclasses IgA1 and IgA2. IgA1 was the major constituent in all biopsy specimens. Double immunofluorescence microscopy showed that IgA deposits were constantly associated with J-chain. Secretory component was never found in the deposited material. In vitro fixation of free secretory component, however, was observed in some biopsies. These findings indicate that most if not all of the deposited IgA in patients with idiopathic IgA-glomerulonephritis is polymeric in nature.

Adolescent↗
PubMed1983

[Mesangial IgA-glomerulonephritis].

IgA-glomerulonephritis represents the most frequent glomerulonephritis (GN; 20%) among our patients. In contrast to data from the literature the prognosis is not benign. Renal insufficiency developed in 17 out of 50 investigated patients within 4 to 96 months, 3 of these patients had to undergo dialysis. Eleven of the 17 patients still had a normal renal function at the time of diagnosis. Malignant hypertension was present in 5 patients. An unfavourable course was predictable in cases of male gender, proteinuria, hypertension, age above 30 years, and histological changes indicating glomerulosclerosis, tubular atrophy, interstitial fibrosis and vascular lesions. Increased serum IgA levels, circulating IgA complexes, association with certain HLA-B or -Dr antigens as well as clinical symptoms and signs of haematuria, dysuria and kidney pains were not helpful either for diagnosis or for prognosis. The value of skin biopsy was comparatively small. Positive IgA demonstration was possible in 12 out of 41 cases with IgA-GN, however, also in 4 out of 21 patients with non-IgA-GN. None of 50 probands without renal disease showed IgA. Five out of 7 skin biopsies demonstrated IgA2, one IgA1 and one both IgA1 and IgA2. Increased serum IgA levels were found in a high percentage (21 out of 38 patients). The same applied to circulating IgA-complexes (8 out of 33 patients).

Adolescent↗
PubMed1983

Glycogen metabolism in phosphorus-depleted rats.

Glycogen content as well as the enzymes of glycogenolysis and glycogen synthesis were examined in myocardium, skeletal muscle, liver and kidneys of rats with dietary phosphorus deprivation. Myocardial glycogen content was decreased and this was accompanied by activation of the enzymes of glycogenolysis and inhibition of the enzymes of glycogen synthesis. Beta blockade (nadolol) abolished the effect of phosphorus depletion (PD) on myocardial glycogen metabolism, documenting that the effect of PD is mediated, at least in part, by increased sympathetic activity. Furthermore, administration of insulin caused a marked increase of glycogen content in the heart of both control and phosphorus-depleted (PD) animals. There was no change of glycogen content or the activities of enzymes of glycogen metabolism in skeletal muscle or kidney, but a decrease of glycogen content of the liver was observed in PD animals.

Adrenergic beta-Antagonists↗
PubMed1983

Clinical and serological features of mesangial IgA glomerulonephritis.

IgA-glomerulonephritis (IgA-GN) accounts for approximately 20 per cent of all glomerulonephritis in our unit. Seventeen out of 50 patients with IgA-GN developed renal failure, which appeared in 11 out of 17 over the course of a mean follow-up of 68 months. Haemodialysis was required in three patients. Twenty-two out of 50 patients had hypertension, five with malignant hypertension. Perivascular IgA deposits were found in skin biopsies of 29 per cent of patients with IgA-GN and also in 19 per cent of patients with other GN, but not in healthy controls. Mucosal (salivary and nasal) secretory IgA concentrations were normal. In cutaneous and glomerular IgA/IgM deposits, IgA1 was demonstrated using monoclonal antibodies. No excess of HLA-A, B or DR antigens and no relation of clinical course and HLA-Bw35 were found.

Adolescent↗
PubMed1983

Cardiac function in experimental uremia.

In acutely uremic animals, the contractile force of the heart is consistently increased; such an increase can be dissociated from changes of afterload or catecholaminergic drive. It is associated with diminished sarcolemmal Na,K-ATPase activity in the heart which, in turn, may be related to increased levels of endogenous digitalis-like substances (endigens) that have been postulated to represent a natriuretic factor. In patients with chronic uremia, myocardial contractility is usually normal, but occasionally there may be heart failure unrelated to pre-existing hypertension, coronary heart disease, anemia, fluid overload, or other recognizable factors. So far, the experimental basis for this clinical observation is uncertain. Possible causes for the clinical syndrome include an excess of parathyroid hormone or cardiodepressor substances. There is experimental evidence of impaired cardiac response to beta adrenergic agonists, e.g., decreased isoproterenol-dependent calcium uptake, diminished inotropic and chronotropic responses. In acutely uremic rats, cardiac cyclic AMP levels are high but can be reversed by beta blockers. Heart calcium content is variable and heart weight is constantly increased in acutely uremic rats, despite decreased skeletal muscle mass. The change in heart weight is not related to anemia, to an excess of parathyroid hormone, or to sympathetic activity; its cause remains unknown. Experimental studies to date have shown a variety of abnormalities, but do not provide a uniform concept of the mechanisms or an explanation for the cardiac dysfunction so often observed in patients with uremia.

Animals↗
PubMed1982

Vascular effects of parathyroid hormone (PTH).

PTH causes dose dependent transient vasodilatation in various vascular beds, specifically renal, coeliac, coronary, but not osseous. It has an acute dose-dependent hypotensive effect in the intact animal which is not mediated by alpha- or beta-adrenergic, cholinergic or histaminergic mechanisms. Aortic medial smooth muscle cells respond to PTH with an increase of cAMP, cGMP and, presumably via protein kinase, with activation of phosphorylase B kinase. The acute vasodilatory effect of PTH is antagonised by indomethacin and diclofenac as well as by ouabain, suggesting that the membrane Na-K pump and prostaglandins are involved in PTH-induced vasodilatation. Parathyroidectomy and a high calcium diet attenuate the rise of arterial pressure in experimental hypertension, pointing to some permissive effect of PTH for development hypertension. This is most likely due to long term effects of PTH on vessel wall calcium content and exchange. This chronic effect of PTH may explain the high prevalence of hypertension in patients with primary hyperparathyroidism.

Animals↗
PubMed1981

[Treatment of advanced metastasizing carcinoma of the prostate with estracyt (author's transl)].

We treated 41 patients with advancing metastatic carcinoma of the prostate in our hospital for 21 days by giving 2 X 150 mg Estracyt intravenously per day. We saw good clinical results in 32 of the 41 patients (= 78%). We found a statistically significant (P less than 0.05) decrease of the acid and prostatic phosphatases. There was a significant (P less than 0.05) increase of the alkaline phosphatases. We did not see any renal or hematologic toxicity. Ten % of our intravenously treated patients experienced thrombophlebitis at the site of injection. Estracyt showed good clinical results.

Acid Phosphatase↗