Assessment of Renal Function, Mineral Metabolism Disturbances, and Anti‑Platelet Therapy in Chronic Kidney Disease: Clinical Significance of Urea, Creatinine, Calcium, Phosphorus, Alkaline Phosphatase, and Platelet Modulation

Abstract

Introduction: Chronic kidney disease (CKD) is associated with biochemical disturbances and increased cardiovascular risk. Antiplatelet therapy is widely used in CKD, but its impact on outcomes remains uncertain.

Aim: To evaluate biochemical derangements in CKD patients and correlate them with antiplatelet therapy outcomes for prognostic stratification.

Materials and Methods: A prospective observational study was conducted in 100 CKD patients. Serum urea, creatinine, calcium, phosphorus, and alkaline phosphatase were measured. Patients were stratified into four groups: aspirin, clopidogrel, dual therapy, and no antiplatelet therapy. Clinical outcomes including cardiovascular events, bleeding, and hospitalization were analyzed. Statistical associations were assessed using chi-square test.

Results: Elevated serum urea (>45 mg/dL) was observed in 50% of patients, creatinine (>1.3 mg/dL) in 70%, hypocalcemia in 28%, hyperphosphatemia in 44%, and high ALP in 45%. Cardiovascular events occurred in 20% of aspirin and clopidogrel groups, 25% in dual therapy, and 40% in untreated patients. Dual therapy was associated with higher bleeding (30%) and hospitalization (50%). Elevated urea, creatinine, hypocalcemia, and hyperphosphatemia were significantly correlated with adverse outcomes (p<0.05).

Conclusion: CKD patients exhibit marked biochemical disturbances that strongly predict cardiovascular and bleeding complications. Antiplatelet monotherapy reduces cardiovascular risk compared to no therapy, while dual therapy increases bleeding. Integrating biochemical markers with pharmacological outcomes may enhance prognostic stratification and guide individualized management in CKD.