ETIOLOGY AND CLINICO-MORPHOLOGICAL PRESENTATION OF MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS IN RUSSIAN POPULATION
THE AIM. Analysis of etiology, clinical and morphological manifestations, of membranoproliferative glomerulonephritis (MPGN). PATIENTS AND METHODS. Retrospective analysis focused on etiology, clinical presentation, light and electron microscopy, immunoglobulins (Ig) and C3 complement component (C3) deposits was done in the cohort of MPGN cases identified in the period 2000-2017. RESULTS. Two hundred and fourteen cases of MPGN were included in the study (mean age of 44 ± 16 years). Most patients had nephrotic syndrome and significant hematuria. In 58.4% of cases, eGFR was <60 mL/min/1.73 m<sup>2</sup>, and every fifth patient had CKD stages 4 or 5. The prevalence of MPGN among all biopsy-confirmed glomerulopathies was 9.3%. Idiopathic MPGN (iMPGN) was diagnosed in 30.4% of cases, while the proportion of iMPGN cases significantly reduced along the study period. Secondary MPGN (sMPGN) was identified in 69.6% of cases (autoimmune diseases - 34.1%, infectious diseases - 16.4%, monoclonal gammopathies - 9.3%, complement-mediated damage - 9.8%). Ig+C3+MPGN was mainly associated with autoimmune diseases and infections, however 26,6% of such cases remained “idiopathic”. C3-glomerulopathy or thrombotic microangiopathy were most often causes of Ig-C3+MPGN. Ig-C3-/Ig+C3-MPGN had heterogeneous etiology. CONCLUSION. MPGN is a severe variant of glomerular damage with a heterogeneous etiological structure. Targeted routine clinical and morphological diagnostics of MPGN allows identifying the cause of the disease in most cases. This approach is reliable for the adequate treatment choice and improvement of outcomes in sMPGN. Further improvement in diagnostic and classification approaches in idiopathic MPGN relies on progress in understanding of molecular etiopathogenesis of the disease.