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M Rambausek

Publications and source records attributed to M Rambausek.

At least 19 recordsLinked to original sources
PubMed1998

Smoking as a risk factor for end-stage renal failure in men with primary renal disease.

BACKGROUND: It is not known whether smoking increases the risk of end-stage renal failure (ESRF) in patients with primary renal disease. METHODS: We performed a retrospective multicenter case-control study including 582 patients from nine centers in Germany, Italy and Austria. The diseases investigated were IgA glomerulonephritis (IgA-GN) as a model of inflammatory renal disease and autosomal dominant polycystic kidney disease (ADPKD) as a model of non-inflammatory renal disease. Cases were patients who had progressed to ESRF and controls were patients who were not in ESRF, that is, whose serum-creatinine failed to progress to >3 mg/dl during the observation period and who did not require renal replacement therapy. Matching for renal disease (IgA-GN, ADPKD), gender, age at renal death and region of residence resulted in 102 individually matched pairs (IgA-GN N = 54, ADPKD N = 48). Multiple conditional logistic regression was used to estimate adjusted odds ratios for independent tobacco effects. RESULTS: In men (matched pairs: IgA-GN N = 44, ADPKD N = 28), a significant dose-dependent increase of the risk to progress to ESRF was found (non-adjusted). The baseline risk was defined as <5 pack-years (PY): (i) 5 to 15 PY, odds ratio 3.5 (95% CI 1.3 to 9.6), P = 0.017; (ii) >15 PY = 5.8 (2.0 to 17), P = 0.001. Systolic blood pressure, ACE inhibitor treatment and age at diagnosis emerged as potential confounders. After adjustment, the risk for ESRF in men with >5 PY was highly increased for patients without ACE inhibitor treatment [10.1 (2.3 to 45), P = 0.002] but not with ACE inhibitor treatment [1.4 (0.3 to 7.1), P = 0.65]. CONCLUSION: Smoking increases the risk of ESRF in men with inflammatory and non-inflammatory renal disease.

Adult↗
PubMed1995

The role of the parathyroid glands in the uremic syndrome.

The genesis of hyperparathyroidism in uremia has turned out to be quite complex, involving low calcitriol, low ionized calcium, and possibly direct effects of high phosphate as well as the action of local factors and modifier genes determining the hyperplastic response of the gland. Growth is initially polyclonal and later monoclonal. In addition, the response of target tissues to parathyroid hormone (PTH) is attenuated ("PTH resistance"), and this may be due, at least in part, to diminished phenotypic expression of PTH receptors. In a series of elegant studies, it has been shown that PTH acts not only on the classical target organs of calcium homeostasis (ie, bone and kidney), but also on nonclassical. The role of PTH excess in the genesis of several features of the uremic syndrome, for example muscle dysfunction, cardiomyopathy, leukocyte and T-cell dysfunction or insulin secretion by pancreatic islet cells, has been established. These studies have borne out the prediction that PTH is a "uremic toxin."

Animals↗
PubMed1995

More adverse renal prognosis of autosomal dominant polycystic kidney disease in families with primary hypertension.

Marked variability of age at renal death is noted in autosomal dominant polycystic kidney disease (ADPKD). The hypothesis that the coexistence of primary hypertension and ADPKD within families is associated with earlier renal death was tested. Of a total of 162 ADPKD patients treated in one Austrian and three German centers, 57 propositi were identified whose families provided (1) information concerning blood pressure; (2) documented presence of ADPKD (by sonography or autopsy) in one parent; and (3) age at renal death in the propositus. Hypertension of the unaffected parent was defined as blood pressure above 140/90 mm Hg or antihypertensive treatment before age 60 yr. Age at renal death in the propositus was defined as the start of renal replacement therapy. Median age at renal death of 23 offspring (11 male, 12 female) from families with a history of primary hypertension of the nonaffected parent was lower than that of 34 offspring (16 male, 18 female) from families without a known history of primary hypertension of the nonaffected parent, i.e., 49 yr (26 to 64) versus 54 yr (28 to 82) (P < 0.03). The data are consistent with the notion that genetic predisposition to primary hypertension is associated with an earlier onset of terminal renal failure in families with ADPKD.

Adult↗
PubMed1993

[Nonocclusive intestinal ischemia as a complication of hemodialysis treatment].

A 52-year-old man on haemodialysis treatment for chronic glomerulonephritis also had a nephrotic syndrome, hypercholesterolaemia, severe arterial hypertension and peripheral vascular disease in stage IIb. He also was a heavy smoker. Following a nonspecific diarrhoeal illness, which caused haemoconcentration, he developed abdominal pain and fever. WBC count (29,000/microliter) and serum lactate level (18.2 mmol/l) were elevated, and there were clinical signs of lower abdominal peritonitis. Laparotomy revealed multiple ischaemic segments. The arteries were not thrombosed but had severe atheromatous changes. There is an increasing incidence of such nonocclusive intestinal ischaemia because there are more elderly people and more patients with high-risk factors among those requiring dialysis.

Chronic Disease↗
PubMed1993

Structural causes of cardiac dysfunction in uremia.

While coronary heart disease is undoubtedly a major cause of cardiac morbidity and mortality in uremia, important noncoronary problems contribute to the common presence of cardiac problems. Based on clinical and experimental studies, we could show: (i) Left ventricular hypertrophy (LVH) can be dissociated, at least in part, from elevation of blood pressure. (ii) In uremia, PTH-dependent intermyocardiocytic fibrosis occurs; it may account, at least in part, for disturbed LV compliance and contribute to the arrhythmogenic potential. (iii) Blood pressure-independent abnormalities of intracardiac arterioles and reduced myocardial capillary supply are observed.

Animals↗
PubMed1992

Albuminuria of hypertensive patients.

Renal dysfunction as a consequence of malignant hypertension has been recognized for decades in patients with essential hypertension. It has been shown only recently, however, that albuminuria (including underlying albuminuria not detectable by conventional tests, i.e. microalbuminuria) has emerged as a frequent sequela of essential hypertension. Furthermore, renal dysfunction of the elderly as a result of ischemic nephropathy, in the absence of malignant hypertension, has turned out to be an important long-term outcome in the patient with essential hypertension. The presence of albuminuria is a strong predictor of cardiovascular events. Albuminuria is associated with more severe hypertension and with evidence of more advanced target organ damage (e.g. LVH). It is more prevalent in the elderly. It is unknown whether the predictive value of albuminuria reflects its association with more severe hypertension and end-organ damage, or whether albuminuria serves as an indicator of capillary leakiness which causes detectable abnormalities in the renal microcirculation but reflects more generalized endothelial barrier dysfunction predisposing to accelerated atherogenesis.

Adult↗
PubMed1991

Is control of secondary hyperparathyroidism optimal with the currently used calcium concentration in the CAPD fluid?

Progression of hyperparathyroidism and bone disease on CAPD has been noted by several authors. In our CAPD patients we observed that aluminium-containing phosphate binders were often required because administration of CaCO3 was limited by the development of hypercalcaemia particularly in patients concomitantly requiring calcitriol. We propose that CAPD fluids with lower calcium concentration should be evaluated to facilitate control of plasma phosphate and secondary hyperparathyroidism.

Calcitriol↗