Assessment of Glomerular and Tubular Function in the Evaluation of Diabetic Nephropathy: A Cross-sectional Study.

Background: Diabetic nephropathy (DN) occurs in 20%-40% of patients with diabetes, and it is characterized by proteinuria and progressive loss of renal functions ultimately leading to end-stage renal disease. Classically, albuminuria is regarded as a consequence of diabetes-induced glomerular damage. It is now being appreciated that the renal tubulointerstitium also plays a role in the development of DN.[1] Urinary cystatin C (UCC) is an emerging marker of DN. It is totally catabolized by proximal tubular cells and is not normally present in the urine. However, in the presence of tubulopathy, it is excreted in urine, and serum levels also are elevated due to lack of catabolism.

Materials And Methods: The present study was conducted to evaluate the presence of glomerulopathy and tubulopathy in patients with type 2 diabetes mellitus (T2DM) and to correlate them with established risk factors for nephropathy. We aimed at evaluating the level of UCC as a marker of tubulointerstitial damage in patients with T2DM in relation to the level of albuminuria and other parameters. Seventy-two patients with T2DM (mean age, 47.44 ± 10.40 years) and 45 healthy age- and sex-matched subjects were evaluated for UCC, serum creatinine, and urinary albumin-creatinine ratio (UACR) along with other parameters.

Results: Of the 72 patients included in the study, microalbuminuria was found in 26% and macroalbuminuria in 10% of cases. UCC was significantly higher in micro- and macro-albuminuric groups in comparison with normoalbuminuric patients and correlated positively with UACR. Among the 46 patients with normoalbuminuria, 11 had elevated UCC levels indicating early tubular dysfunction.

Conclusions: This finding may support the hypothesis of a "tubular phase" of diabetic kidney disease preceding overt DN, and hence, the use of UCC measurement for early evaluation of renal involvement.