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Addition of nonalbumin proteinuria to albuminuria improves prediction of type 2 diabetic nephropathy progression.
BACKGROUND: Albuminuria is generally accepted as a sensitive marker of diabetic nephropathy but has limitations in predicting its progression. The aim of this study was to evaluate the use of nonalbumin proteinuria in addition to albuminuria for predicting the progression of type 2 diabetic nephropathy.
METHODS: In this retrospective observational study, the urine albumin-to-creatinine ratio (ACR) and the nonalbumin protein-to-creatinine ratio (NAPCR) were measured in 325 patients with type 2 diabetes and estimated glomerular filtration rates (eGFR) ≥30 mL/min/1.73 m(2). The patients were divided into four groups based on the cutoff points for the urinary ACR (30 mg/g) and NAPCR (120 mg/g). The renal outcomes were chronic kidney disease (CKD) progression and accelerated eGFR decline.
RESULTS: During the 4.3-year follow-up period, 25 (7.7%) patients showed CKD progression and 69 (21.2%) patients showed accelerated eGFR decline. After adjusting for nine clinical parameters, the group with a NAPCR greater than 120 mg/g exhibited higher cumulative incidences of CKD progression (hazard ratio 6.84; P = 0.001) and accelerated eGFR decline (hazard ratio 1.95; P = 0.011) than the group with a NAPCR < 120 mg/g. In patients with normoalbuminuria, the group with NAPCR levels greater than 120 mg/g also exhibited a higher cumulative incidence than that with NAPCR levels <120 mg/g of CKD progression (hazard ratio 21.82; P = 0.005). The addition of NAPCR to ACR improved the model fit for CKD progression and accelerated eGFR decline.
CONCLUSION: Nonalbumin proteinuria showed additional value over and above that of albuminuria for predicting the progression of CKD in patients with type 2 diabetes.
METHODS: In this retrospective observational study, the urine albumin-to-creatinine ratio (ACR) and the nonalbumin protein-to-creatinine ratio (NAPCR) were measured in 325 patients with type 2 diabetes and estimated glomerular filtration rates (eGFR) ≥30 mL/min/1.73 m(2). The patients were divided into four groups based on the cutoff points for the urinary ACR (30 mg/g) and NAPCR (120 mg/g). The renal outcomes were chronic kidney disease (CKD) progression and accelerated eGFR decline.
RESULTS: During the 4.3-year follow-up period, 25 (7.7%) patients showed CKD progression and 69 (21.2%) patients showed accelerated eGFR decline. After adjusting for nine clinical parameters, the group with a NAPCR greater than 120 mg/g exhibited higher cumulative incidences of CKD progression (hazard ratio 6.84; P = 0.001) and accelerated eGFR decline (hazard ratio 1.95; P = 0.011) than the group with a NAPCR < 120 mg/g. In patients with normoalbuminuria, the group with NAPCR levels greater than 120 mg/g also exhibited a higher cumulative incidence than that with NAPCR levels <120 mg/g of CKD progression (hazard ratio 21.82; P = 0.005). The addition of NAPCR to ACR improved the model fit for CKD progression and accelerated eGFR decline.
CONCLUSION: Nonalbumin proteinuria showed additional value over and above that of albuminuria for predicting the progression of CKD in patients with type 2 diabetes.
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