Exploring the Role of Serum Lysyl Oxidase (LOX) Levels and LOX Gene Polymorphism (G473A) in Diabetic Nephropathy

Diabetic Nephropathy (DN) is a leading microvascular complication of diabetes with poor prognosis. Extra cellular matrix accumulation (ECM) leading to renal fibrosis is the key manifestation of diabetic kidney. Lysyl oxidase (LOX) plays an important role in cross linking of collagen. Altered LOX expression and LOX depended cross links with Diabetes have been documented both in rat and human model. Evidence of LOX gene polymorphism (G473A) has been shown limited to Diabetic foot ulcer. Studies on association of single nucleotide polymorphism (SNP) (G473A) of LOX gene with Diabetic nephropathy is scarce. A pilot study was proposed with an objective to find out association of serum LOX and LOX gene polymorphism (G473A) in Diabetic Nephropathy. This cross-sectional study was conducted in the Dept. of Biochemistry, AIIMS Bhubaneswar. Serum LOX level, LOX gene polymorphism (G473A) by PCR-RFLP and its association with disease process was assessed in Diabetes as well as Diabetes Nephropathy cases. Results were analysed using SPSS-26 version. Serum LOX registered a significant rise having positive association with glycaemic status and inverse relationship with eGFR, whereas LOX gene polymorphism (G473A) did not reveal significant association with serum LOX and the disease process in DN cases. Increased serum LOX level might have contributed to disordered ECM with resultant lowering of kidney function in DN. LOX gene polymorphism (G473A) might not have influenced serum LOX level. A probable regulatory effect of hyperglycaemia through other mediators on LOX expression may exist that needs further exploration.