For a study, it was determined to include patients at risk of kidney failure, clinical trials in nephrology were enriched for patients with micro- or macroalbuminuria. Patients with normoalbuminuria, on the other hand, could develop renal failure. TNF receptor-1, TNF receptor-2, and kidney injury marker-1 (KIM-1) had all been linked to the advancement of kidney disease in people with micro- or macroalbuminuria. TNF receptor-1, TNF receptor-2, and KIM-1 were evaluated as prognostic biomarkers for CKD progression in patients with type 2 diabetes and normoalbuminuria. Immunoassays were used to detect NF receptor-1, TNF receptor-2, and KIM-1 in plasma samples from patients with type 2 diabetes who were at high cardiovascular risk and taking part in the Canagliflozin Cardiovascular Assessment Study trial. Researchers estimated the hazard ratios per doubling of each biomarker for the renal outcome using multivariable-adjusted Cox proportional hazards analyses, stratified the population by the fourth quartile of each biomarker distribution, and evaluated the number of events and event rates.
During a median follow-up of 6.1 (interquartile range, 5.8–6.4) years in patients with normoalbuminuria (n=2553), 51 renal outcomes were documented (event rate, 3.5; 95% CI, 2.6 to 4.6 per 1000 patient-years). Each doubling of baseline TNF receptor-1 (hazard ratio, 4.2; 95% CI, 1.8 to 9.6) and TNF receptor-2 (hazard ratio, 2.3; 95% CI, 1.5 to 3.6) levels were linked with an increased risk of renal outcome. KIM-1, urine albumin-creatinine ratio, and eGFR at baseline were not linked to renal outcomes. The highest quartile of TNF receptor-1 (2992 ng/ml) and TNF receptor-2 (11,394 ng/ml) incident rates were 5.6 and 7.0 events per 1000 patient-years, respectively, compared to 2.8 and 2.3 in the lowest 3 quartiles. TNF receptor-1 and TNF receptor-2 were linked to renal outcomes in type 2 diabetes patients with normoalbuminuria.