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criteria were prospectively followed up for 6 months with relevant clinical data and laboratory investigations. Electron microscopy and genetic testing was done wherever feasible. At 6 months of follow up the outcomes were analyzed. Factors affecting disease progression were studied. Results: We had 33 patients out of which 27 had C3GN and 6 had atypical HUS. Majority were in age group 31-40yrs. 57.6% were males. The most common clinical syndrome was acute nephritic illness (30.3%). Positive family history was present in 9.09%. 29 patients had hypertension at onset of disease. 27 patients had proteinuria > 1 g per day. Micro hematuria was present in 91%. Abnormal GFR at presentation was seen in in 25 patients. The mean serum creatinine at onset was 3.8AE2.76 mg/dl. 93.9% had low serum C3. The mean hemoglobin of 6.33AE0.63g/dl and mean platelet count of 0.56AE0.30 lakhs/mm3 in aHUS group.The most common pattern on light microscopy was MPGN (8 patients). Crescents in biopsy was seen in 26.66% and 23.3% had severe IFTA. The most frequent deposits were subendothelial in electron microscopy. Genetic study was done for 13 patients and 10 of them (76.9%) had positive mutation. The most frequent mutations were in CFHR genes. 87.8% of patients (29/33) received steroids. 9 patients (27.27%) received MMF while 4 patients (12.12%) received CNI and 3 patients with Crescentic GN (9.09%) received cyclophosphamide. 5 aHUS patients received therapeutic plasma exchange and 1 received only plasma infusion in addition to steroids. Most of the patients received at least 4-6 months of immunosuppression. 21% of patients had dialysis requiring renal failure at onset. At 6 months 29 patients survived out of which 37.9% progressed to ESRD. 3 of them underwent transplant. 4 patients died during follow up.44.44% of patients with no ESRD had persistent micro hematuria and hypertension. The total remission with steroids only was 71.4%, with steroids plus MMF was 66.6% and with steroids plus CNI was 75%. In atypical HUS only 40% achieved remission with TPE and immunosuppression. Multivariate regression analysis showed serum creatinine at diagnosis and IFTA on biopsy as predictors of disease progression. Conclusions: Alternate complement pathway dysregulation in this study resulted in C3GN and atypical HUS. There was 33% progression to ESRD. We have limited access to complement therapeutics and hence less costlier but effective treatment strategies are definitely the need of the hour.

difference in the development of de novo HLA-DSA, HLA-Ab and rejection between the group and the results were consistent in a model adjusted for all potential confounders. Kaplan-Meier survival curve showed no difference in graft survival in between the group with a mean days in transfusion vs non-transfusion were 2961.6 and 2935.0 respectively with a p value of 0.420. This result was consistent despite being adjusted for age, gender, pre-existing preformed HLA-DSA and the formation of new HLA-Ab. Conclusions: Blood transfusion under strong immunosuppressive cover within 1 week perioperative period post transplantation is safe with no significance association with the development of de novo HLA-DSA, HLA-Ab or clinical rejection.