Pulmonary hypertension and renal dysfunction: a narrative review

Abstract

Pulmonary hypertension (PH) is a severe and highly prevalent complication of chronic kidney disease (CKD). Conversely, patients with pulmonary arterial hypertension (PAH) frequently develop renal dysfunction. These cardio–renal interactions predict poorer outcomes, yet their mechanisms are not entirely understood. This narrative review explores the pathophysiological interactions between the pulmonary circulation and the kidney and the impact on patient care. PH in CKD is driven by a combination of left heart disease, volume overload and endothelial dysfunction. Molecular mechanisms include an imbalance of endogenous vasoactive agents favouring increased vasoconstriction, as well as vascular remodelling induced by mediators of mineral bone metabolism (parathyroid hormone, fibroblast growth factor 23, α-Klotho). In haemodialysis patients, arteriovenous fistulas (AVFs) contribute to PH via a high cardiac output state. Management of CKD-PH relies on strict volume control, treating underlying comorbidities and modulating high AVF flow. Targeted PAH therapies are generally contraindicated in CKD-PH. Kidney transplantation can reverse PH in a significant proportion of patients. Pulmonary vascular remodelling in PAH can induce renal dysfunction through reduced renal perfusion and increased venous congestion (the right heart cardio–renal syndrome). Impaired kidney function in PAH predicts increased mortality and warrants more aggressive vasodilator therapy. The association of PH and CKD is frequent and confers a poor prognosis. Accurate diagnosis and effective management require a multidisciplinary approach involving pulmonologists, cardiologists and nephrologists.