Prevalence and Predictors of Progression of Chronic Kidney Disease in Type 2 Diabetes Mellitus — A Prospective Observational Stud
Keywords:
Chronic Kidney Disease, Diabetic Nephropathy, Disease Progression, eGFR Decline, Proteinuria, Type 2 Diabetes.Abstract
Background: Diabetic nephropathy is the leading cause of end-stage renal disease worldwide. Early identification of patients at risk for rapid disease progression is critical for timely therapeutic intervention, yet predictive data from Indian tertiary care settings remain scarce. Methods: This prospective observational study enrolled 180 type 2 diabetes mellitus patients with established CKD stages 2 through 4 (eGFR 15 to 89 mL/min/1.73 m squared) between January and December 2023 at a tertiary nephrology unit in India. Serum creatinine, eGFR (CKD-EPI formula), 24-hour urine protein, HbA1c, lipid profile, and haemoglobin were measured at baseline and every 3 months for 12 months. Rapid progression was defined as an annual eGFR decline exceeding 5 mL/min/1.73 m squared per year. Multivariate Cox regression was used to identify independent predictors. Results: Mean age was 56.4 plus or minus 10.8 years and 58.9% were male. The median baseline eGFR was 42.6 mL/min/1.73 m squared. Over 12 months the median eGFR decline was 3.8 mL/min/1.73 m squared per year. Rapid progression occurred in 62 patients (34.4%). On multivariate analysis, baseline 24-hour proteinuria above 1 g per day (hazard ratio 3.18, 95% CI 1.84 to 5.50, p less than 0.001), baseline eGFR below 30 (HR 2.74, p equals 0.002), HbA1c above 8% (HR 2.16, p equals 0.012), uncontrolled systolic hypertension above 150 mmHg (HR 1.94, p equals 0.024), and haemoglobin below 10 g/dL (HR 1.82, p equals 0.036) were independent predictors. Use of ACE inhibitors or ARBs was protective (HR 0.54, p equals 0.008). Conclusion: One in three diabetic CKD patients demonstrated rapid progression over 12 months. Heavy proteinuria and advanced baseline CKD stage were the strongest predictors. Aggressive proteinuria reduction with RAAS blockade, tight glycaemic control, and anaemia correction are recommended to slow progression.
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