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The patient developed aHUS and acute kidney injury (AKI), which resolved after appropriate therapy. Over 6years, she continued to have normal kidney function with no thrombocytopenia despite persistently elevated homocysteine and MMA levels. We question the roles of homocysteine and MMA as causative of aHUS/TMA in cblC deficiency as they remained elevated during follow-up but did not result in aHUS/TMA or AKI. Hyperhomocysteinemia and/or MMA caused by other metabolic diseases do not result in aHUS/TMA or AKI. This suggests tha