Pulmonary hypertension has a 40% prevalence in hemodialysis patients and is driven by vascular access, volume overload, and endothelial dysfunction leading to pulmonary vessel obliteration.
This review highlights the high prevalence and complex pathophysiology of pulmonary hypertension in chronic kidney disease, emphasizing the need for targeted diagnostic and therapeutic strategies.
Pulmonary hypertension is defined as an increased systolic pulmonary pressure of >30 mm Hg, and it shows a 40% prevalence in hemodialysis patients due to vascular access (both central venous catheter and arteriovenous fistula). Secondary pulmonary hypertension in chronic kidney disease patients is strictly related to pulmonary circulation impairment together with chronic volume overload and increased levels of cytokines and growth factors, such as FGF, PDGF, and TGF-β, leading to fibrosis. Endothelial dysfunction, together with lower activation of NOS, increased levels of serum endothelin and fibrin storages, involves an extensive growth of endothelial cells leading to complete obliteration of pulmonary vessels. Pulmonary hypertension has no pathognomonic and distinctive symptoms and signs; standard transthoracic echocardiography allows easy assessment of compliance of the right heart chambers. The therapeutic approach is based on traditional drugs such as digitalis-derived drugs, vasodilatory agents (calcium channel blockers), and oral anticoagulants. New pharmacological agents are under investigation, such as prostaglandin analogues, endothelin receptor blockers, and phosphodiesterase-5 inhibitors.
Lullo et al. (Tue,) conducted a review in Pulmonary hypertension and right heart failure in chronic kidney disease. Pulmonary hypertension has a 40% prevalence in hemodialysis patients and is driven by vascular access, volume overload, and endothelial dysfunction leading to pulmonary vessel obliteration.