Non-Lupus Full House Nephropathy

Background:The presence of a full house pattern at immunofluorescence on kidney biopsy in a patient without clinical and laboratory features of systemic lupus erythematosus (SLE) has led to the descriptive term non-lupus full house nephropathy. This systematic review and meta-analysis focus on non-lupus full house nephropathy nomenclature, clinical findings and outcomes. Methods:In a reiterative process, all identified terms for non-lupus full house nephropathy and other MeSH terms were searched in PubMed. Out of 344 results, 57 records published between 1982 and 2022 were included in the analysis. Clinical data of single patients from different reports were collected. Patients were classified into three pathogenetic categories, which were compared according to baseline characteristics, treatments and outcomes. Results:Out of the 57 records, 61% were case reports. Non-lupus full house nephropathy was addressed with 17 different names. We identified 148 patients: 75(51%) were males; median age 35(23-58) years. Serum creatinine and proteinuria at onset were 1.4(0.8-2.5)mg/dL and 5.7(2.7-8.8)g/day. About half of patients achieved complete response. A causative agent was identified in 51(44%) patients, mainly infectious (41%). Secondary non-lupus full house nephropathy was mostly non-relapsing with worse kidney function at onset compared to idiopathic disease (P=0.001). Among the 57(50%) patients with idiopathic non-lupus full house nephropathy, complete response was comparable between patients treated with immunosuppression and supportive therapy; however, proteinuria and creatinine at onset were higher in patients treated with immunosuppression (P=0.09 and P=0.07). The remaining 7(6%) patients developed SLE after a median follow-up of 5.0(1.9-9.0) years. Conclusions:Our data support that SLE and non-lupus full house nephropathy are distinct clinical entities, with comparable outcomes. A small subset of patients develops SLE during follow-up. Non-lupus full house nephropathy is addressed by many different names in the literature. The identification of three pathogenetic categories provides further clues for the management of the disease.