Renal steatosis in the tubulointerstitial compartment in primary glomerulopathies: biopsy evidence and correlation with disease severity.

Abstract

Background: While dyslipidemia is a well-established systemic risk factor in glomerular diseases, the clinical and histopathological relevance of compartmental intrarenal lipid deposition in primary glomerulonephritis (GN) remains insufficiently elucidated. Recent evidence suggests that lipid accumulation may directly contribute to glomerular and tubulointerstitial injury via pro-inflammatory and oxidative mechanisms.

Methods: In this single-center, cross-sectional analysis, we examined 31 adult patients with biopsy-proven primary GN-IgA nephropathy (IgAN), membranous nephropathy (MN), and focal segmental glomerulosclerosis/minimal change disease (FSGS/MCD)-diagnoses. Renal tissue specimens were subjected to Oil Red O staining to quantify lipid accumulation within tubular, interstitial, and vascular compartments. Clinical parameters and laboratory indices were assessed. Histopathologic correlations were performed using Oxford MEST-C classification (for IgAN) and Interstitial Fibrosis and Tubular Atrophy (IFTA) scoring.

Results: Intrarenal lipid deposition was prevalent across compartments: tubular (84%), interstitial (74%), and vascular (61%). In IgAN patients, both the extent and morphology of tubular steatosis were strongly correlated with composite MEST-C scores (P < .01). In MN, tubular lipid burden was significantly associated with systolic blood pressure and proteinuria levels (P < .01). Notably, interstitial and vascular lipid accumulation demonstrated positive associations independent of systemic lipid levels. In FSGS/MCD cases, tubular steatosis correlated with both low density lipoprotein (LDL) and interstitial lipid scores (P < .01), whereas vascular lipid presence was linked to the degree of proteinuria (P < .05).

Conclusions: Intrarenal lipid deposition is a prevalent histological finding in primary GN and correlates with both structural injury and clinical disease burden. These findings support the hypothesis that local lipid accumulation may represent a pathophysiologically relevant biomarker of disease activity.