Cardiac fibrosis triggered by the kidney: a case report.

Fibrosis, defined as an abnormal increase of tissue collagen fibres, is an important component of cardiac remodelling in patients with hypertension. Cardiac remodelling may in turn lead to increased myocardial stiffness, left ventricular (LV) dysfunctions, and ultimately to heart failure. A growing body of evidence indicates that the renin–angiotensin–aldosterone system (RAAS) plays an important role in the development of cardiac fibrosis [1–8]. Furthermore, experimental data suggest that angiotensin II (Ang II) and aldosterone can stimulate cardiac fibrosis independent of haemodynamic mechanisms through direct trophic effects on the myocardium, and probably also by inhibiting interstitial collagenases, thereby reducing collagen degradation [1,2,7,8]. However, less is known about the influence of the RAAS on cardiac fibrosis in humans. We report here the case of a patient with hypertension, and an activation of the RAAS, who demonstrated pronounced right ventricular (RV) fibrosis in the absence of pulmonary hypertension. Our observation suggests that an activation of the RAAS, per se, may promote the development of cardiac fibrosis independent of haemodynamic mechanisms in humans also.