Objective: In this prospective cohort study, 26 sporadic SRNS patients (17 male and 9 females) aged 2 years to 25 years and five age matched individuals as control were included. Using Next generation sequencing technique, a panel of 62 genes associated with SRNS were analyzed. Ten patients underwent kidney biopsy also. Methods: We detected mutations in 12 patients (12/25) and one control (1/5). Most common mutation was in collagen genes, seen in 7/26 (27%). Mutations in Col4A3 was seen in 5/26(19.23%), Col4A4 in 1/26(3.80%) and Col4A5 in 2/26(7.69%). Other mutations detected were in membrane associated guanylate Kinase-2 gene (MAGI2) 2/26(7.70%), 1-Phosphatidylinositol-4,5-bisphosphate phosphodiesterase epsilon-1 (PLCE1) gene in 2/26(7.70%); NPHS1, Laminin β2 gene, FAT atypical cadherin-1, APOL 1, Nucleoporin 93 and Anillin actin binding protein gene in one each [1/26(3.80%)]. [Table 1] In cases where kidney biopsy was performed, most common histopathological diagnosis was FSGS seen in 6/10 biopsies (60%) followed by MCD 2 /10 biopsies (20%). All mutations were heterozygous and ‘novel mutations according to American College of Medical Genetics and Genomics (ACMG) criteria. Mutation was present in 4/6 cases of FSGS (66%) and in both cases of MCD (100%) while MPGN was not associated with mutations (0/2). [Table 2] Results: SRNS is significantly associated with novel mutations, most commonly collagen genes in our cohort. Mutations frequently associated with SRNS in other studies worldwide were uncommon in our population. FSGS and MCD were commonly associated with genetic mutations. Conclusions: Objective: Steroid resistant nephrotic syndrome (SRNS) occurs in 10% - 20% of nephrotic syndrome (NS) cases. Most of them progress to end stage kidney disease over the next 10-15 years. Genetic mutations are responsible for up to 30% SRNS. Knowledge of genetic mutations may lead to identification of newer mutations, avoidance of kidney biopsies and unnecessary exposure to immunosuppressants. Methods: In this prospective cohort study, 26 sporadic SRNS patients (17 male and 9 females) aged 2 years to 25 years and five age matched individuals as control were included. Using Next generation sequencing technique, a panel of 62 genes associated with SRNS were analyzed. Ten patients underwent kidney biopsy also. Results: We detected mutations in 12 patients (12/25) and one control (1/5). Most common mutation was in collagen genes, seen in 7/26 (27%). Mutations in Col4A3 was seen in 5/26(19.23%), Col4A4 in 1/26(3.80%) and Col4A5 in 2/26(7.69%). Other mutations detected were in membrane associated guanylate Kinase-2 gene (MAGI2) 2/26(7.70%), 1-Phosphatidylinositol-4,5-bisphosphate phosphodiesterase epsilon-1 (PLCE1) gene in 2/26(7.70%); NPHS1, Laminin β2 gene, FAT atypical cadherin-1, APOL 1, Nucleoporin 93 and Anillin actin binding protein gene in one each [1/26(3.80%)]. [Table 1] In cases where kidney biopsy was performed, most common histopathological diagnosis was FSGS seen in 6/10 biopsies (60%) followed by MCD 2 /10 biopsies (20%). All mutations were heterozygous and ‘novel mutations according to American College of Medical Genetics and Genomics (ACMG) criteria. Mutation was present in 4/6 cases of FSGS (66%) and in both cases of MCD (100%) while MPGN was not associated with mutations (0/2). [Table 2] Conclusions: SRNS is significantly associated with novel mutations, most commonly collagen genes in our cohort. Mutations frequently associated with SRNS in other studies worldwide were uncommon in our population. FSGS and MCD were commonly associated with genetic mutations.