| Autor: |
Persu A; Pole of Cardiovascular Research, Institut de Recherche Expérimentale et Clinique and Division of Cardiology, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, Brussels, Belgium (A.P.)., Canning C; Department of Vascular Medicine and Surgery, St. James's Hospital, Dublin, Ireland (C.C.)., Prejbisz A; Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.P., P.D., M.J., A.J.)., Dobrowolski P; Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.P., P.D., M.J., A.J.)., Amar L; Université de Paris, INSERM CIC1418, France (L.A., M.A.).; AP-HP, Hôpital Européen Georges-Pompidou, Hypertension Department and DMU CARTE, Reference Centre for Rare Vascular Disease, Paris, France (L.A., M.A.)., Chrysochou C; Renal Department, Salford Royal NHS Foundation Trust, Manchester, United Kingdom (C.C.)., Kądziela J; Department of Interventional Cardiology and Angiology, National Institute of Cardiology, Warsaw, Poland (J.K.)., Litwin M; Department of Nephrology and Arterial Hypertension, The Children's Memorial Health Institute, Warsaw, Poland (M.L.)., van Twist D; Zuyderland Medical Centre, Sittard/Heerlen, the Netherlands (D.v.T.)., Van der Niepen P; Department of Nephrology and Hypertension, Vrije Universiteit Brussel, Universitair Ziekenhuis Brussel, Belgium (P.V.d.N.)., Wuerzner G; Service of Nephrology and Hypertension, Lausanne University Hospital and University of Lausanne, Switzerland (G.W.)., de Leeuw P; Department of Internal Medicine and Gastroenterology, Zuyderland Medical Center, Heerlen, the Netherlands (P.d.L.).; Department of Internal Medicine, Division of General Internal Medicine (P.d.L.), Maastricht University Medical Center, Maastricht University, the Netherlands.; CARIM School for Cardiovascular Diseases (P.d.L.), Maastricht University Medical Center, Maastricht University, the Netherlands., Azizi M; Université de Paris, INSERM CIC1418, France (L.A., M.A.).; AP-HP, Hôpital Européen Georges-Pompidou, Hypertension Department and DMU CARTE, Reference Centre for Rare Vascular Disease, Paris, France (L.A., M.A.)., Januszewicz M; Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.P., P.D., M.J., A.J.).; II Department of Clinical Radiology, Medical University of Warsaw, Poland (M.J.)., Januszewicz A; Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.P., P.D., M.J., A.J.). |
| Abstrakt: |
Renovascular hypertension is one of the most common forms of secondary hypertension. Over 95% of cases of renovascular hypertension are due either to atherosclerosis of the main renal artery trunks or to fibromuscular dysplasia. These two causes of renal artery stenosis have been extensively discussed in recent reviews and consensus. The aim of the current article is to provide comprehensive and up-to-date information on the remaining causes. While these causes are rare or extremely rare, etiologic and differential diagnosis matters both for prognosis and management. Therefore, the clinician cannot ignore them. For didactic reasons, we have grouped these different entities into stenotic lesions (neurofibromatosis type 1 and other rare syndromes, dissection, arteritis, and segmental arterial mediolysis) often associated with aortic coarctation and other arterial abnormalities, and nonstenotic lesions, where hypertension is secondary to compression of adjacent arteries and changes in arterial pulsatility (aneurysm) or to the formation of a shunt, leading to kidney ischemia (arteriovenous fistula). Finally, thrombotic disorders of the renal artery may also be responsible for renovascular hypertension. Although thrombotic/embolic lesions do not represent primary vessel wall disease, they are characterized by frequent macrovascular involvement. In this review, we illustrate the most characteristic aspects of these different entities responsible for renovascular hypertension and discuss their prevalence, pathophysiology, clinical presentation, management, and prognosis. |
