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Background <p>The coexistence of renal artery stenosis (RAS) and acute tubulointerstitial nephritis (ATIN) is exceptionally rare. While imaging studies are essential for diagnosing RAS, noninvasive tests such as renal artery ultrasound are highly sensitive to a patient’s hemodynamic status and fluid volume. This case illustrates how hemodynamic alterations associated with AKI, including ATIN, can lead to diagnostic challenges in identifying underlying RAS.</p> Case presentation <p>An 82-year-old male with chronic heart failure and chronic kidney disease presented with acute kidney injury (AKI) following the introduction of spironolactone and colchicine. Drug-induced ATIN was suspected on the basis of a skin rash, eosinophilia, elevated IgE levels, and positive gallium scintigraphy. Although magnetic resonance angiography suggested bilateral RAS, the initial renal artery ultrasound failed to meet diagnostic criteria. However, the initial intrarenal Doppler study showed prolonged acceleration time in the interlobar arteries, particularly on the right side, despite nondiagnostic peak systolic velocity findings. Renal function markedly improved following drug discontinuation and corticosteroid therapy. A subsequent renal biopsy revealed mild tubulitis on electron microscopy, providing limited histological support for a clinically suspected diagnosis of ATIN. After readmission for heart failure and subsequent hemodynamic stabilization, a follow-up ultrasound confirmed severe RAS. These findings suggest that altered intrarenal hemodynamics during AKI may have contributed to an initially nondiagnostic Doppler evaluation, although the precise mechanism remains speculative.</p> Conclusions <p>The coexistence of RAS and ATIN is exceptionally rare. This case suggests that, when possible renovascular disease coexists with acute parenchymal kidney injury, renal Doppler findings may be nondiagnostic during the acute phase. Accordingly, renal perfusion should be assessed comprehensively, including intrarenal waveform findings such as acceleration time and resistive index, rather than relying on peak systolic velocity alone. To ensure an accurate diagnosis of underlying RAS and to avoid potentially unnecessary initiation of renal replacement therapy, repeat evaluation after hemodynamic stabilization may be clinically important.</p>

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Acute kidney injury in the setting of the rare coexistence of bilateral renal artery stenosis and drug-induced acute tubulointerstitial nephritis: diagnostic challenges and a review of Doppler limitations

  • 期刊论文

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  • 发表日期：

    2026年5月1日

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  • Seiji Onodera,
  • Hiroki Ito,
  • Yutaka Matsumoto,
  • Kentaro Yano,
  • Yuya Suzuki,
  • Risa Ishikawa,
  • Toshiyuki Sato,
  • Tsubasa Yuki,
  • Go Anan,
  • Takuo Hirose,
  • Takefumi Mori

摘要

Background

The coexistence of renal artery stenosis (RAS) and acute tubulointerstitial nephritis (ATIN) is exceptionally rare. While imaging studies are essential for diagnosing RAS, noninvasive tests such as renal artery ultrasound are highly sensitive to a patient’s hemodynamic status and fluid volume. This case illustrates how hemodynamic alterations associated with AKI, including ATIN, can lead to diagnostic challenges in identifying underlying RAS.

Case presentation

An 82-year-old male with chronic heart failure and chronic kidney disease presented with acute kidney injury (AKI) following the introduction of spironolactone and colchicine. Drug-induced ATIN was suspected on the basis of a skin rash, eosinophilia, elevated IgE levels, and positive gallium scintigraphy. Although magnetic resonance angiography suggested bilateral RAS, the initial renal artery ultrasound failed to meet diagnostic criteria. However, the initial intrarenal Doppler study showed prolonged acceleration time in the interlobar arteries, particularly on the right side, despite nondiagnostic peak systolic velocity findings. Renal function markedly improved following drug discontinuation and corticosteroid therapy. A subsequent renal biopsy revealed mild tubulitis on electron microscopy, providing limited histological support for a clinically suspected diagnosis of ATIN. After readmission for heart failure and subsequent hemodynamic stabilization, a follow-up ultrasound confirmed severe RAS. These findings suggest that altered intrarenal hemodynamics during AKI may have contributed to an initially nondiagnostic Doppler evaluation, although the precise mechanism remains speculative.

Conclusions

The coexistence of RAS and ATIN is exceptionally rare. This case suggests that, when possible renovascular disease coexists with acute parenchymal kidney injury, renal Doppler findings may be nondiagnostic during the acute phase. Accordingly, renal perfusion should be assessed comprehensively, including intrarenal waveform findings such as acceleration time and resistive index, rather than relying on peak systolic velocity alone. To ensure an accurate diagnosis of underlying RAS and to avoid potentially unnecessary initiation of renal replacement therapy, repeat evaluation after hemodynamic stabilization may be clinically important.