The Neuroendocrine-Cardiovascular Axis in Chronic Kidney Disease: The Role of Prolactin and Gonadal Dysfunction.

backgroundChronic kidney disease (CKD) is accompanied by endocrine disturbances, including elevated prolactin and disruption of the hypothalamic-pituitary-gonadal axis. Their reproductive consequences are well recognized, whereas their cardiovascular relevance remains uncertain. SUMMARY: Reduced renal metabolism, altered dopaminergic regulation, the uremic milieu, inflammation, and comorbidity may increase prolactin and suppress gonadal function. In men, testosterone deficiency becomes more common as kidney function declines. In women, the dominant phenotype is loss of cyclicity, menstrual disturbance, anovulation, and a shortened reproductive lifespan; a single low estradiol value does not adequately characterize this heterogeneous state. Experimental studies identify candidate endothelial, nitric-oxide, inflammatory, thrombotic, and body-composition pathways. Clinical evidence, however, is predominantly observational, is more extensive in men than women, and is inconsistent for prolactin. Non-dialysis CKD and dialysis cohorts are therefore considered separately. Hormone measurement also requires attention to assay method, biological variability, acute illness, medication exposure, menstrual status, and timing relative to dialysis. KEY MESSAGES: Prolactin and gonadal dysfunction are best viewed as components of a hypothesis-generating neuroendocrine-cardiovascular framework rather than established causal cardiovascular risk factors. No evidence supports routine dopamine-agonist treatment of asymptomatic CKD-related hyperprolactinemia or hormone therapy for cardiovascular prevention. Symptom-directed endocrine evaluation, rigorous diagnosis, and CKD-specific prospective and interventional studies are needed.