Introduction: Atypical haemolytic uraemic syndrome (aHUS) is a rare, life-threatening thrombotic microangiopathy characterized by microangiopathic haemolytic anaemia, thrombocytopenia, and acute kidney injury , commonly resulting from dysregulation of the alternative complement pathway . We report two pediatric patients presented with distinct etiological triggers of aHUS: anti–factor H antibody–associated disease and Invasive pneumococcal infection associated disease. Case presentation: The first case involved a 10 year old boy presenting with abdominalpain,vomiting without preceding febrile illness or desentry . He was pale,lathergic with unremarkable other system examination.Investigations revealed Coombsnegative haemolytic anaemia, (Hb 7 .4g/dl,retic count 8.8%) thrombocytopenia,LDH(2566 U/L) and renalimpairement (creatinine 184micmol/L,Urea 28mmol/L),ANA and viral panel were negative. Immunological workup demonstrated ADAMTS 13 activity 100% and markedly elevated anti–factor H antibody titers (7800AU/ml) confirming immune-mediated complement dysregulation. The patient was managed with plasma exchange, corticosteroids, andsupportive therapy for acute renal impairement resulting in gradual hematological and renal recovery . The second case was a 3 years old girl admitted with severe cavitatory pneumonia and septic shock. Blood culture positive for Streptococcus pneumoniae.CRP 250mg/L, The clinical course was complicated by haemolytic anaemia(Hb 5g/dl,LDH 560 U/L,retic count 7%, thrombocytopenia and renal impairement(creatinine 158 micmol/L,Urea 26mmol/L) consistentwith pneumococcal-associated HUS. Direct Coombs test was positive. Child was managed with intravenous antibiotics,repeated cycles of plasmaparesis to reduce the antibody burden using Albumin(avoiding plasma products like FFP to prevent worsening haemolysis by T antigen exposure) leading to gradual recovery . Conclusion: These cases highlight the heterogenicity of aHUS and the importance of early recognition of underlying triggers for better outcomes.