Purpose of Review <p>Renal involvement is a major determinant of morbidity and mortality in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). Accurate assessment of disease activity and renal prognosis remains challenging due to the complex interplay between immune-mediated injury and chronic damage. This review summarizes recent advances in understanding the pathogenesis of renal involvement in AAV and the contributions of renal biopsy and urinary biomarkers to disease assessment and outcome prediction.</p> Recent Findings <p>Current studies have elucidated key mechanisms underlying renal injury in AAV, including endothelial damage, complement pathway amplification, neutrophil activation, and dysregulated immune responses. Although renal biopsy remains the diagnostic gold standard, histopathological classifications and prognostic tools have refined prediction of kidney failure but are limited by sampling variability and invasiveness. AAV-glomerulonephritis activity evaluation still relies on evaluation of kidney function biomarkers (serum creatinine or cystatin-C), along with proteinuria and hematuria. Emerging urinary biomarkers, such as monocyte chemoattractant protein-1 (MCP-1), kidney injury molecule-1 (KIM-1), and soluble CD163, among others, reflect glomerular and tubular injury and show promise for non-invasive disease monitoring. However, heterogeneity in study design, small sample sizes, and lack of standardization limit their clinical application.</p> Summary <p>Integrating histopathological data with urinary biomarkers offers a more precise evaluation of renal activity and chronicity in AAV. Future research should focus on validating biomarker panels in large, longitudinal cohorts and combining them with biopsy findings to develop personalized monitoring and treatment strategies. Such integration may enable early detection of renal relapse, reduce treatment toxicity, and improve long-term outcomes for patients with AAV.</p>

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The Assessment of Disease Activity and Renal Prognosis in AAV – The Contribution of Urinary Biomarkers and Renal Biopsy

  • Juan Manuel Mejía-Vilet,
  • Marco A. Alba,
  • Andrea Hinojosa-Azaola

摘要

Purpose of Review

Renal involvement is a major determinant of morbidity and mortality in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). Accurate assessment of disease activity and renal prognosis remains challenging due to the complex interplay between immune-mediated injury and chronic damage. This review summarizes recent advances in understanding the pathogenesis of renal involvement in AAV and the contributions of renal biopsy and urinary biomarkers to disease assessment and outcome prediction.

Recent Findings

Current studies have elucidated key mechanisms underlying renal injury in AAV, including endothelial damage, complement pathway amplification, neutrophil activation, and dysregulated immune responses. Although renal biopsy remains the diagnostic gold standard, histopathological classifications and prognostic tools have refined prediction of kidney failure but are limited by sampling variability and invasiveness. AAV-glomerulonephritis activity evaluation still relies on evaluation of kidney function biomarkers (serum creatinine or cystatin-C), along with proteinuria and hematuria. Emerging urinary biomarkers, such as monocyte chemoattractant protein-1 (MCP-1), kidney injury molecule-1 (KIM-1), and soluble CD163, among others, reflect glomerular and tubular injury and show promise for non-invasive disease monitoring. However, heterogeneity in study design, small sample sizes, and lack of standardization limit their clinical application.

Summary

Integrating histopathological data with urinary biomarkers offers a more precise evaluation of renal activity and chronicity in AAV. Future research should focus on validating biomarker panels in large, longitudinal cohorts and combining them with biopsy findings to develop personalized monitoring and treatment strategies. Such integration may enable early detection of renal relapse, reduce treatment toxicity, and improve long-term outcomes for patients with AAV.