Renal anemia is a frequent and significant complication in patients with end-stage kidney
disease undergoing hemodialysis, affecting over 90% of this population. Anemia adversely
impacts quality of life and is associated with increased cardiovascular risk,
hospitalization rates, and mortality. These patients also commonly experience
Malnutrition-Inflammation-Atherosclerosis (MIA) syndrome and have significantly elevated
cardiovascular mortality compared to the general population. While
Erythropoiesis-stimulating agents (ESAs) are a mainstay of therapy, concerns exist
regarding potential adverse events, particularly with high doses, highlighting the need
for alternative or complementary strategies.
Roxadustat is an oral hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHI)
that represents a newer class of agents for treating renal anemia. By inhibiting HIF
degradation, Roxadustat mimics a hypoxic state, leading to enhanced endogenous
erythropoietin synthesis and improved iron metabolism pathways. While its efficacy in
managing anemia is established, its potential effects on the interconnected issues of
cardiovascular disease (CVD) and MIA syndrome in the hemodialysis population remain
poorly understood and require further investigation.
This study hypothesizes that Roxadustat, compared to conventional anemia management, may
offer benefits beyond hemoglobin correction, potentially improving cardiovascular
parameters and ameliorating aspects of the MIA syndrome in hemodialysis patients.
This is a randomized, open-label, parallel-group, controlled clinical trial conducted at
the Urology and Nephrology center, Mansoura University. Eligible chronic hemodialysis
patients will be randomized 1:1 to receive either Roxadustat (intervention group) or
continue conventional anemia therapy (control group) for a duration of 6 months.
Conventional therapy typically includes ESAs and iron supplementation as per standard
clinical practice.
Key assessments will include evaluation of cardiovascular status (utilizing
echocardiography for structural and functional assessment, and Doppler ultrasound for
carotid intima-media thickness), markers relevant to MIA syndrome (including
anthropometric measurements, inflammatory markers like high-sensitivity C-reactive
protein (hs-CRP) and Endothelin-1, nutritional markers, lipid profiles, and measures like
normalized protein catabolic rate (nPCR)), and parameters related to anemia management
(hemoglobin, iron indices). Data will be collected at baseline and at the end of the
6-month study period. Safety monitoring will occur throughout the trial. Statistical
analysis will compare changes between the two groups using appropriate methods for
quantitative and qualitative data.
