Patients who reached the study endpoint had significantly higher PLA2R1-ab, higher serum creatinine levels, lower eGFR, more extended tubular atrophy and interstitial fibrosis at baseline, while during follow-up they more often failed to deplete PLA2R1-ab and had significantly less often a complete remission of proteinuria compared to patients who did not reach the study endpoint (Table 2). The gene discussed is PLA2R1; the disease is Atrophy.