The evidence regarding thrombotic microangiopathy (TMA) related to Coronavirus Infectious
Disease 2019 (COVID-19) in patients with complement gene mutations as a cause of acute
kidney injury (AKI) are limited. We presented a case of a 23-year-old male patient
admitted with an asymptomatic form of COVID-19, but with uncontrolled hypertension
and AM. Kidney biopsy showed severe lesions of TMA. In evolution patient had persistent
microangiopathic hemolytic anemia, decreased level of haptoglobin and increased LDH
level. Decreased complement C3 level and the presence of schistocytes were found for
the first time after biopsy. Kidney function progressively decreased and the patient
remained hemodialysis dependent. Complement work-up showed a heterozygous variant
with unknown significance in complement factor I (CFI) c.-13G>A, affecting the 5'
UTR region of the gene. In addition, the patient was found to be heterozygous for
the complement factor H (CFH) H3 haplotype (involving the rare alleles of c.-331C>T,
Q672Q and E936D polymorphisms) reported as a risk factor of atypical hemolytic uremic
syndrome. This case of AM associated with severe TMA and secondary hemolytic uremic
syndrome highlights the importance of genetic risk modifiers in the alternative pathway
dysregulation of the complement in the setting of COVID-19, even in asymptomatic forms.
