Erythrodermic psoriasis complicated by immune complex-mediated crescentic glomerulonephritis and atypical hemolytic uremic syndrome: a case report

Erythrodermic psoriasis (EP) is a severe, systemic inflammatory dermatosis. While kidney involvement is rare, the massive cytokine release associated with EP can induce systemic complications. We report a rare case of EP complicated by the simultaneous onset of immune complex-mediated crescentic glomerulonephritis (GN) and atypical haemolytic uraemic syndrome (aHUS), highlighting a severe form of complement-mediated renal injury in the context of dermatological inflammation. A 52-year-old male presented with a three-month history of diffuse erythrodermic psoriasis following herbal supplement ingestion, complicated by progressive anasarca and acute kidney injury. Laboratory findings showed nephrotic-range proteinuria, microscopic haematuria, thrombocytopaenia (platelets 41 × 10^9/L), microangiopathic haemolysis (elevated lactate dehydrogenase and schistocytes), and low complement C3 levels. Skin biopsy confirmed EP. Renal biopsy revealed diffuse endocapillary proliferation and crescent formation (20% of glomeruli) with immune complex deposition (granularIgG, IgA), alongside features of thrombotic microangiopathy (endothelial swelling, segmental double contours). The patient was successfully treated with corticosteroids, intravenous immunoglobulin, and the terminal complement inhibitor eculizumab, resulting in normalisation of haematological parameters and substantial renal recovery. This case underscores a critical pathogenic link between severe psoriasis-associated systemic inflammation, immune complex deposition, and complement-mediated microangiopathy. Early recognition of this overlap syndrome and prompt complement inhibition are crucial for preventing irreversible kidney disease.