Serum ischemia‑modified albumin in patients with type 2 diabetes mellitus with and without diabetic nephropathy: A cross‑sectional study

Diabetic nephropathy is the leading cause of end‑stage renal disease worldwide, and ischemia‑modified albumin (IMA) has been proposed as a biomarker of oxidative stress in type 2 diabetes mellitus (T2DM). The present hospital‑based cross‑sectional study evaluated serum IMA levels together with biochemical, haematological, urinary and comorbidity profiles in patients with T2DM with and without nephropathy. The primary outcome was the between‑group difference in serum IMA; there was no healthy control group. A total of 50 patients were enrolled between November, 2021 and March, 2024, including 25 patients with T2DM without nephropathy (group A) and 25 patients with diabetic nephropathy (group B). Clinical and laboratory records were available for 19 patients in group A and 16 patients in group B; the others contributed IMA values only. In group B, chronic kidney disease (CKD) stage 5D was documented in 9 patients, CKD on maintenance haemodialysis in 1 patient, acute‑on‑chronic kidney disease in 1 patient, CKD of unspecified stage in 4 patients, and 10 patients had no clinical record. Serum IMA levels did not differ significantly between the groups [group A: Median, 0.332 absorbance units (ABSU); group B: Median, 0.317 ABSU; Mann‑Whitney test; P=0.727; mean difference (group A vs. B), 0.054 ABSU, 95% confidence interval, ‑0.08 to 0.19]; thus, a clinically relevant difference cannot be excluded. The result was similar following adjustment for serum albumin and in sensitivity analyses (all P>0.5). Blood urea (P=0.0003) and serum creatinine (P<0.0001) levels were higher in group B; the serum potassium level was nominally higher (P=0.040), but within the normal range in both groups. Among the patients with records, anaemia (14/18, 78% vs. 10/15, 67%) and infection (12/18, 67% vs. 9/15, 60%) were more frequent in group A than in group B. Heavy proteinuria (+++/++++) was recorded only in group B (2/7 tested) and all adverse in‑hospital outcomes occurred in group B; however, these comparisons rest on very small numbers. In the present small study without a healthy control group, serum IMA did not differ between patients with T2DM with and without nephropathy, and the findings are compatible with IMA reflecting systemic oxidative stress rather than nephropathy‑specific injury. Larger prospective studies with standardized IMA assays, albumin adjustment and comprehensive biochemical profiling are required to clarify the clinical utility of IMA in diabetic kidney disease.