Abstract
Blood and Urine Biomarkers for Assessing Dialysis Adequacy in Chronic and End-Stage Kidney Disease: A Systematic Review
Elmukhtar Habas, Hafedh Ghazouani, Ala Habas, Khaled Alarabi, Eshrak Habas, Amnna Rayani
Keywords: Dialysis adequacy, hemodialysis, peritoneal dialysis, biomarkers, uremic toxins, systematic review, personalized medicine
DOI: 10.63475/yjm.v5i1.0283
DOI URL: https://doi.org/10.63475/yjm.v5i1.0283
Publish Date: 07-04-2026
Download PDFDownloads: 1
Citation: 0
Author Affiliation:
1 Professor of Internal Medicine, Qatar University, Hamad General Hospital, Doha, Qatar
2 Quality and Patient Reviewer, Corporate Quality Improvement and Patient Safety Department, Hamad Medical Corporation, Doha, Qatar
3 Resident, Tripoli Central Hospital, University of Tripoli, Tripoli, Libya
4 Associate Consultant, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar
5 Resident, Tripoli University Hospital, University of Tripoli, Libya
6 Prof. Senior Consultant, University of Tripoli, Tripoli, Libya
Abstract
Background: Traditional dialysis adequacy assessment relies on urea-based kinetics, such as Kt/V, which overlooks aspects of uremic toxicity, including middle molecule buildup, inflammation, and tubular stress. Blood and urine biomarkers provide a more comprehensive and personalized approach. This systematic review evaluates their prognostic and diagnostic value for dialysis adequacy and clinical outcomes in adults with chronic kidney disease (CKD) stages 4 to 5 and end-stage kidney disease (ESKD).
Methods: Following PRISMA 2020 guidelines, we searched PubMed/MEDLINE, EMBASE, Cochrane Library, and Web of Science (January 2000–December 2025) for relevant studies. Two reviewers independently handled selection, extraction, and quality assessment via the Newcastle-Ottawa Scale and Grading of Recommendations Assessment, Development and Evaluation (GRADE).
Results: Of 2847 records, 48 studies (n = 41,326 patients) were included. Inflammatory biomarkers (e.g., sTNFR1, sTNFR2, CRP) were strongly associated with all-cause and cardiovascular mortality (pooled HR for sTNFR1, 1.86 [95% CI, 1.58–2.19]). Middle molecules (β2-microglobulin) and protein-bound toxins (indoxyl sulfate) are linked to mortality and cardiovascular events. Urinary tubular injury markers (NGAL, KIM-1) predicted residual kidney function (RKF) decline in hemodialysis and peritoneal dialysis, for example, 25% faster RKF loss per 50% urinary KIM-1 increase over 18 months in PD cohorts, with independent prognostic value for ESKD progression. Biomarkers often added value beyond Kt/V, though assay heterogeneity, timing, and normalization hindered comparisons.
Conclusions: Blood and urine biomarkers deliver pathophysiological insights surpassing urea kinetics, promising personalized dialysis. Translation requires assay standardization, decision thresholds, and interventional trials confirming that biomarker-guided strategies improve outcomes.
