SAT-158 Early Diagnosis of Diabetic Kidney Disease through Histopathology Biomarkers

Abstract

Background: Diabetic kidney disease (DKD) is universally spotted on the standards of persistent albuminuria. However, numerous diabetic patients may remain normoalbuminuric upon reaching a persistent glomerular filtration rate (GFR) of <60 mL/min. The objective of the present research study was to examine the occurrence and grouping of DKD renal microstructure insults in patients with diabetes mellitus (DM). Material and Methods: In this prospective study, we performed kidney biopsy of 29 patients; DM type 1 (3, 10.3%) and type 2 (26, 89.7%) with DM history >5 years and HbA1c above 6.5%. Serum creatinine, eGFR, albuminuria (>30mg/dL) and serum cholesterol were included as part of laboratory and clinical parameters. The mean age of the subjects was 52.3 ± 7.9 years. The creatinine (1.00 ± 0.15) and proteinuria (10.6 ± 4.6) of the patients were well within normal range and eGFR was >60mL/min/1.73m2. Overall, 79.3% of the subjects had hypertensive history, while 65.5% demonstrated dyslipidemia. CKD Class II was found to be the major Class affecting the studied subjects; 75.9%. Coronary Artery Disease (CAD) was the predominant etiology of death (34.5%). Out of 29 patients with DM history >5 years and HbA1c greater than 6.5%, 24 (82.8%) patients had renal histopathological insults proving DKD in the absence of proteinuria and eGFR <60mL/min/1.732. The kidney size was found to be normal for both right (11.4 ± 1.0) and left (11.3 ± 0.9) kidneys through Ultrasonography investigation. Class IIa (48.3%) was found to be the leading DKD Class in our patients. Overall, the mean GBM thickness was demonstrated to be 248.7 ± 114.3 nm. The mean percentage of global glomerulosclerosis was 12.4 ± 7.8 In the absence of proteinuria and early stages of CKD (Class I and II, eGFR >60mL/min/1.73m2) in DM patients, renal histopathological evidence confirms DKD in 82.8% of our study population. The kidney biopsy would not only be helpful in identifying silent DKD, but would also allow risk stratification and treatment of DM patients with early stages of CKD who otherwise might progress to ESRD.