High sensitivity C-reactive protein subsequent rise in urine albumin/creatinine ratio/fall in estimated glomerular filtration rate over 24 years in people with type 2 diabetes.

Systemic inflammation, which can be measured by high-sensitivity C-reactive protein (hsCRP), may play a crucial role in the progression of chronic kidney disease (CKD) in people with type 2 diabetes (T2D). In this study, we report longitudinal outcomes from 718 individuals with T2D, followed up for up to 24 years, to assess how hsCRP influences the development and progression of CKD, measured by urine albumin-to-creatinine ratio (uACR)/estimated glomerular filtration rate (eGFR). Longitudinal renal function analysis showed numerical trends towards greater mean eGFR decline (-20.6 ml/min in the lowest Q1 vs. -26.4 ml/min in the highest Q4 baseline hsCRP quartile) and greater fold increase in uACR (1.93 in Q1 vs. 2.91 in Q4) across hsCRP quartiles. However, in multivariate linear regression analyses, baseline hsCRP was not an independent predictor of eGFR decline (<i>P</i> = 0.267) or change in uACR (<i>P</i> = 0.884). We suggest that hsCRP may still serve as a single surrogate quantifiable analyte encompassing multiple risk/factors to denote individuals with a greater risk of rapid progression of diabetic nephropathy.