Renovascular hypertension: the diagnosis and management of renal ischaemia

This paper is dedicated to Prof. Dr Dr Manfred Ziegler, plasia (intimal, medial, perimedial fibroplasia) or systemic arteritis. Atherosclerosis is common in older patients and on the occasion of his 65th birthday. accounts for 60–70% of all renal hypertensive cases in clinical practice. Renal artery aneurysms and arterioIntroduction venous fistulae are further pathologies which cause RH and may result in detrimental systemic cardiovascular According to the latest definition of the WHO, arterial hypertension is defined as a systolic blood pressure of eCects in the long-term [5,6]. Although the diagnosis and management of RH might not be under urological 140 mmHg and/or a diastolic blood pressure of 90 mmHg [1]. This definition is based on the quantitatguidance in every institution, every urologist should at least be familiar with this disease to initiate prompt ive relationship between arterial blood pressure and mortality; the higher the pressure the worse the progcurative therapy. nosis [2]. However, an elevation of blood pressure should always be established with repeated measurements The pathophysiology of RH before the diagnosis of hypertension is confirmed and further evaluation is instituted [3]. In most hypertensive Since the description by Goldblatt et al. in 1934 [7], many experimental and clinical studies have established patients the origin of the disease cannot be clearly defined (primary or essential hypertension). However, in the classical concept that the renin-angiotensin system (RAS) plays a major role in the onset and maintenance part of the hypertensive population, a circumscribed pathology can be identified as a cause for the elevation of RH [5,8]. The reduction in renal blood flow leads to renin secretion from the kidney into the circulation and of blood pressure (the secondary form of hypertension). Of those with hypertension, 3–15% also have renal the formation of the vasoconstrictor angiotensin II in the lungs, which re-enters the kidney and produces hypertension [4]; it represents the most frequent form of secondary hypertension. Its clinical importance is based constriction of the eCerent arterioles. Consequently, the glomerular filtration pressure is increased and the GFR on its potential curability. Published values for the prevalence of renovascular hypertension (RH) diCer remains constant under reduced blood flow. Circulating angiotensin II causes systemic arterial hypertension by because of diCerences in age distribution and the selection of patient groups. Thus the reported prevalence of direct vasoconstrictor action and stimulation of aldosterone secretion, which as a secondary eCect leads to RH is 1–20%, with peaks in children under the age of 10 years and in adults over the age of 40 years [4]. retention of sodium and free water [9]. More recent research modified the original concept Although the true incidence of RH is unknown it is estimated at #5% [5]. The continuing increase of the that systemic angiotensin II is formed only by renin, which is secreted from the ischaemic kidney. Molecular overall hypertensive population and the population in the older age groups emphasizes the importance of these biology studies clearly show that there is a complete, locally operating RAS in the kidney, in the blood vessels epidemiological data [4]. Renovascular hypertension is caused by renal artery and in the testes. The genes for the production of the components of the RAS are regulated by sodium balance disease, which leads to a significant reduction of renal blood flow. Perfusion impairment of the kidney results and reduction of renal perfusion pressure [10]. Intrarenal angiotensin II aCects the vascular tone of the eCerent in a reduction in GFR and consequent insuBciency of renal excretory function. The most frequent form of arterioles and vasa recta in the medulla, as well as tubular sodium reabsorption. At the eCector side renal artery disease is renal artery stenosis, caused either by atherosclerosis, diCerent forms of fibromuscular dysof the RAS, additional angiotensin peptide fragments (AngIII and Ang 1–7) with vasoconstrictor activity, and angiotensin receptor heterogeneity (subtypes AT1 and Accepted for publication 6 July 1999