To the Editor: Ozen et al.(July 6 issue) 1 describe 11 study participants with loss-of-function variants in CD55 and complement hyperactivation, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome). CD55-deficient mice recapitulate some of the clinical characteristics of this newly identified syndrome2, 3 and have a predisposition to glomerular injury, 4 which is consistent with the presence of proteinuria in 2 of the 11 patients. Therefore, urinary protein loss may represent a feature of the CHAPLE syndrome (since CD55 is expressed in human glomeruli) and may lead to hypoalbuminemia, hypogammaglobulinemia, and edema. A comparison of the clinical symptoms among the 11 patients described by Ozen et al. showed that the 2 patients with proteinuria (Patients 4.1 and 6.1) also had pronounced hypoalbuminemia and hypogammaglobulinemia. Additional data regarding renal function and proteinuria among the series of patients could enable a better understanding of the degree of renal involvement in this rare condition and the role of CD55 in human glomerular physiology. Similarly, we wonder about the effects of eculizumab (which inhibits the complement component C5) on renal function and proteinuria in the 3 patients with the CHAPLE syndrome who are described in the letter by Kurolap et al. 5 in the same issue of the Journal.