High-dose enalapril treatment reverses myocardial fibrosis in experimental uremic cardiomyopathy.

Aims: Patients with renal failure develop cardiovascular alterations which contribute to the higher rate of cardiac death. Blockade of the renin angiotensin system ameliorates the development of such changes. It is unclear, however, to what extent ACE-inhibitors can also reverse existing cardiovascular alterations.

Reversal of glomerulosclerosis after high-dose enalapril treatment in subtotally nephrectomized rats.

Interventions to block the renin-angiotensin system (RAS) halt the progression of renal lesions in renal damage models. It has recently also been reported that established glomerulosclerosis can be reversed by pharmacologic blockade of the RAS. It was the aim of this study to confirm that high doses of angiotensin-converting enzyme (ACE) inhibitors reverse established glomerulosclerosis and to extend the findings by providing quantitative information on glomerular geometry, podocytes and other glomerular cells, renal vessels and tubulointerstitial tissue.

Morphology of the heart and arteries in renal failure.

In patients with renal failure, cardiovascular complications are a major clinical problem; cardiac death is the main cause of death in these patients. Cardiac risk is increased by a factor of 20 in uremic patients, compared with matched segments of the general population. It has been known for a long time that atherosclerosis, particularly plaque in the epicardiac coronary conduit arteries, are more frequent in patients with chronic renal failure.

Cardiomyocyte loss in experimental renal failure: prevention by ramipril.

Background: The development of left ventricular hypertrophy (LVH) and of structural abnormalities of the heart is a key abnormality in renal failure that potentially contributes to the high rate of cardiac death. In renal failure, the behavior of cardiomyocyte volume and number in the development of LVH has so far not been investigated. A potential role of the (local) renin-angiotensin system (RAS) in the genesis of LVH has been suspected.

Hyperphosphatemia aggravates cardiac fibrosis and microvascular disease in experimental uremia.

Background: Hyperphosphatemia is a known predictor of cardiovascular death and specifically of cardiac death in hemodialysis patients. The pathomechanisms involved have not been completely clarified. While a number of observations suggest an important role of hyperphosphatemia and positive calcium balance on atherosclerosis and calcification of the coronary conduit arteries, independent effects on postcoronary microvessels and on cardiac fibrosis have not been excluded.

Cardiovascular changes in renal failure.

In patients with renal failure cardiovascular complications are an important clinical problem and cardiac death is the main cause of death in these patients. It is well documented that cardiac risk is increased by a factor of 20 in uremic patients compared with age- and sex-matched segments of the general population. This finding in patients with renal failure can be at least partially explained by the well-described structural and metabolic abnormalities of the myocardium.