Journal of community hospital internal medicine perspectives · 2026
Slipping Through the Chasm of Multicenter Hand-offs-Rare Incidence of Nintedanib Induced Renal Failure: Case Report.
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Abid Muhammad Mohsin, Khan Muhammad Ijaz, Jain Tanvi, Daniel Amrita, Flack Tristan M, Posner Jeffrey N
Аннотация
INTRODUCTION: Nintedanib, a receptor tyrosine kinase inhibitor (TKI), is approved for idiopathic pulmonary fibrosis (IPF). While its common adverse effects include gastrointestinal symptoms and elevated liver enzymes, renal toxicity is rare. We report a case of nintedanib-induced kidney failure.
CASE: An 82-year-old man with IPF and no prior kidney disease developed acute kidney injury (AKI), nephrotic-range proteinuria, volume overload, metabolic acidosis, and hyperkalemia 10 days after starting nintedanib. Extensive serologic investigations were unremarkable. Kidney biopsy showed acute tubular injury, minimal change disease (MCD), focal global glomerulosclerosis, and interstitial fibrosis. Nintedanib and other potential nephrotoxins were stopped, and the patient was started on hemodialysis. Kidney function recovered within six weeks. Five months later, the patient was unintentionally restarted on nintedanib during a phone follow-up. He presented five weeks later with worsening edema, anuria, and weakness. Renal ultrasound was normal. Repeat biopsy revealed MCD, global glomerulosclerosis, extensive tubular necrosis, and 60 % interstitial fibrosis-worse than prior findings. Immunofluorescence was negative, and no other nephrotoxins were involved. Hemodialysis was reinitiated. By three months, kidney function and urine output returned to baseline.
DISCUSSION: FDA-approved in 2014 for IPF, nintedanib exemplifies multi-kinase TKIs; renal toxicity, particularly with it, is uncommon. To date, only four post-marketing cases of nintedanib-induced renal injury exist. Histologic findings such as MCD and glomerular sclerosis, previously noted with other VEGF inhibitors, have not been reported with nintedanib.
CONCLUSION: This case underscores the need for vigilance regarding nintedanib's nephrotoxicity and highlights the value of interdisciplinary care to prevent medicationrelated harm.
CASE: An 82-year-old man with IPF and no prior kidney disease developed acute kidney injury (AKI), nephrotic-range proteinuria, volume overload, metabolic acidosis, and hyperkalemia 10 days after starting nintedanib. Extensive serologic investigations were unremarkable. Kidney biopsy showed acute tubular injury, minimal change disease (MCD), focal global glomerulosclerosis, and interstitial fibrosis. Nintedanib and other potential nephrotoxins were stopped, and the patient was started on hemodialysis. Kidney function recovered within six weeks. Five months later, the patient was unintentionally restarted on nintedanib during a phone follow-up. He presented five weeks later with worsening edema, anuria, and weakness. Renal ultrasound was normal. Repeat biopsy revealed MCD, global glomerulosclerosis, extensive tubular necrosis, and 60 % interstitial fibrosis-worse than prior findings. Immunofluorescence was negative, and no other nephrotoxins were involved. Hemodialysis was reinitiated. By three months, kidney function and urine output returned to baseline.
DISCUSSION: FDA-approved in 2014 for IPF, nintedanib exemplifies multi-kinase TKIs; renal toxicity, particularly with it, is uncommon. To date, only four post-marketing cases of nintedanib-induced renal injury exist. Histologic findings such as MCD and glomerular sclerosis, previously noted with other VEGF inhibitors, have not been reported with nintedanib.
CONCLUSION: This case underscores the need for vigilance regarding nintedanib's nephrotoxicity and highlights the value of interdisciplinary care to prevent medicationrelated harm.