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    A Rare Case: Improved Heart Failure with Anti-Complement Therapy in Complement-Dependent Hemolytic Uremic Syndrome
    (AVES, 2023) Özer, Hakan; Öztürk, Yasin; Türkmen, Kültigin; Tonbul, Halil Zeki; Selçuk, Nedim Yılmaz
    xtrarenal involvement occurs in approximately 20% of patients with complement-mediated hemolytic-uremic syndrome. The involvement is usually of the nervous system, and cardiac involvement occurs in 3%-10% of patients. Cardiac manifestations vary, including myocardial infarction, cardiomyopathy, and acute decompensated heart failure. Among these patients, thrombotic microangiopathy-related cardiac dysfunction is mainly due to the continuous activation of the complement system, which leads to endothelial damage and thrombosis in the coronary microvessels. We wanted to highlight the importance of cardiac evaluation at the time of diagnosis or during follow-up in thrombotic micro-angiopathy patients by presenting a case of heart failure with low ejection fraction in a 24-year-old young patient in whom we detected complement-mediated hemolytic-uremic syndrome, a secondary mutation of complement factor H receptor. It is still an unknown issue because of the rarity of cardiac involvement in complement-mediated hemolytic-uremic syndrome patients. Primary myocardial involvement is increasingly recognized as a possible concomitant feature of hemolytic-uremic syndrome. Failure to perform a detailed cardiac evaluation both at diagnosis and during follow-up in complement-mediated hemolytic-uremic syndrome patients can lead to fatal outcomes. Anti-complement therapy can also lead to good cardiac outcomes in these patients.
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    Two Different Presentation of C3 Glomerulonephritis Treated with Eculizumab: Two Cases and Brief Overview
    (Aves, 2023) Öztürk, Yasin; Özer, Hakan; Baloğlu, İsmail; Türkmen, Kültigin
    C3 glomerulopathy is a newly defined glomerular disease dominated by C3 complement storage and uncertain C1, C4, and immunoglobin accumulations. Hereditary mutations associated with Complement Factor H (CFH) causing hyperactivation of the alternative complement pathway were identified. Most mutations associated with C3 glomerulopathy are associated with the N-terminal end. Whether mutations are pathogenic or not will direct diagnosis and treatment. We present 2 cases, one 61-year-old and one 24-year-old attending our clinic at different times with hematuria, proteinuria, edema, and kidney failure. Both patients had C3 glomerulopathy diagnosed based on the results of kidney biopsy and were treated with eculizumab. Both cases had CFH-associated mutations.