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Background <p>Infective endocarditis-associated glomerulonephritis (IE-GN) causes acute kidney injury with unclear pathogenesis. Previous studies focused on glomerular lesions with limited understanding of tubulointerstitial involvement. We investigated clinicopathological characteristics of renal involvement in IE, focusing on distinct injury patterns in glomeruli and tubulointerstitium.</p> Methods <p>We conducted a retrospective case series of five male patients (age 46—74&#xa0;years) with confirmed infective endocarditis (IE) who underwent kidney biopsy at Toranomon Hospital between January 1, 2001, and August 31, 2024. The diagnosis of IE was made based on the modified Duke criteria (2011).</p> Results <p>Blood cultures were positive for <i>Streptococcus</i> (n = 4) and <i>Granulicatella</i> (n = 1). Acute kidney injury was present in three patients with eGFR of 6.5—23.9&#xa0;mL/min/1.73 m<sup>2</sup>. Light microscopy revealed two glomerular injury patterns: diffuse endocapillary proliferative glomerulonephritis with neutrophilic infiltration (n = 2) and necrotizing glomerulonephritis with fibrin deposition (n = 3). Patients with severe renal dysfunction demonstrated extensive tubulointerstitial inflammation with neutrophil and macrophage infiltration, while those with preserved renal function showed minimal tubulointerstitial involvement despite similar glomerular immune complex deposition. Immunofluorescence demonstrated granular IgA, IgM, and C3 deposits. Electron microscopy revealed inflammatory cell infiltration, endocapillary proliferation, and subendothelial and mesangial electron-dense deposits. Gram-positive bacteria were detected in one kidney specimen and in cardiac valve vegetation. Patients receiving surgical treatment (n = 3) achieved favorable outcomes.</p> Conclusions <p>This analysis of five cases suggests that IE-GN involves dual pathogenic pathways: immune complex-mediated glomerular injury and tubulointerstitial injury related to bacterial burden, with tubulointerstitial lesions more strongly associated with renal dysfunction.</p>

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Distinct glomerular and tubulointerstitial injury pathways in infective endocarditis-associated glomerulonephritis: a case series

  • 期刊论文

  • 发表日期：

    2026年6月16日

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  • Kei Kono,
  • Naoki Sawa,
  • Hiroki Mizuno,
  • Yusuke Yoshimura,
  • Yuki Oba,
  • Masayuki Yamanouchi,
  • Noriko Inoue,
  • Akinari Sekine,
  • Kiho Tanaka,
  • Eiko Hasegawa,
  • Tatsuya Suwabe,
  • Takeshi Fujii,
  • Yutaka Takazawa,
  • Kenichi Ohashi,
  • Yutaka Yamaguchi,
  • Takehiko Wada,
  • Yoshifumi Ubara

摘要

Background

Infective endocarditis-associated glomerulonephritis (IE-GN) causes acute kidney injury with unclear pathogenesis. Previous studies focused on glomerular lesions with limited understanding of tubulointerstitial involvement. We investigated clinicopathological characteristics of renal involvement in IE, focusing on distinct injury patterns in glomeruli and tubulointerstitium.

Methods

We conducted a retrospective case series of five male patients (age 46—74 years) with confirmed infective endocarditis (IE) who underwent kidney biopsy at Toranomon Hospital between January 1, 2001, and August 31, 2024. The diagnosis of IE was made based on the modified Duke criteria (2011).

Results

Blood cultures were positive for Streptococcus (n = 4) and Granulicatella (n = 1). Acute kidney injury was present in three patients with eGFR of 6.5—23.9 mL/min/1.73 m2. Light microscopy revealed two glomerular injury patterns: diffuse endocapillary proliferative glomerulonephritis with neutrophilic infiltration (n = 2) and necrotizing glomerulonephritis with fibrin deposition (n = 3). Patients with severe renal dysfunction demonstrated extensive tubulointerstitial inflammation with neutrophil and macrophage infiltration, while those with preserved renal function showed minimal tubulointerstitial involvement despite similar glomerular immune complex deposition. Immunofluorescence demonstrated granular IgA, IgM, and C3 deposits. Electron microscopy revealed inflammatory cell infiltration, endocapillary proliferation, and subendothelial and mesangial electron-dense deposits. Gram-positive bacteria were detected in one kidney specimen and in cardiac valve vegetation. Patients receiving surgical treatment (n = 3) achieved favorable outcomes.

Conclusions

This analysis of five cases suggests that IE-GN involves dual pathogenic pathways: immune complex-mediated glomerular injury and tubulointerstitial injury related to bacterial burden, with tubulointerstitial lesions more strongly associated with renal dysfunction.