<p>Here we present a case of bevacizumab-associated glomerular microangiopathy (Bmab-GMA), a rare and distinct glomerular pathology, in a middle-aged male patient who developed progressive renal impairment following adjuvant chemotherapy with bevacizumab for surgically resected lung adenocarcinoma. The patient presented with new-onset hypertension and mild elevation in serum creatinine. Renal biopsy revealed characteristic histopathological features, including pseudothrombotic deposits of periodic acid-Schiff (PAS)-positive hyaline material within glomerular capillaries on light microscopy, and subendothelial and mesangial electron-dense deposits with segmental widening of the subendothelial space on electron microscopy. The diagnosis of Bmab-GMA was established based on these clinicopathological findings. Management with bevacizumab discontinuation and antihypertensive therapy resulted in clinical stabilization. This case highlights the diagnostic challenges and management considerations of this rare entity, while identifying elevated soluble complement membrane attack complex (C5b-9) as evidence of complement activation, a potential pathological mechanism requiring further investigation for future therapeutic development.</p>

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Bevacizumab-associated glomerular microangiopathy: a case report and literature review

  • Rui Jiang,
  • Rui-zhi Yu,
  • Hai-feng Yang,
  • Li-xin Wang,
  • Jun-jie Lin

摘要

Here we present a case of bevacizumab-associated glomerular microangiopathy (Bmab-GMA), a rare and distinct glomerular pathology, in a middle-aged male patient who developed progressive renal impairment following adjuvant chemotherapy with bevacizumab for surgically resected lung adenocarcinoma. The patient presented with new-onset hypertension and mild elevation in serum creatinine. Renal biopsy revealed characteristic histopathological features, including pseudothrombotic deposits of periodic acid-Schiff (PAS)-positive hyaline material within glomerular capillaries on light microscopy, and subendothelial and mesangial electron-dense deposits with segmental widening of the subendothelial space on electron microscopy. The diagnosis of Bmab-GMA was established based on these clinicopathological findings. Management with bevacizumab discontinuation and antihypertensive therapy resulted in clinical stabilization. This case highlights the diagnostic challenges and management considerations of this rare entity, while identifying elevated soluble complement membrane attack complex (C5b-9) as evidence of complement activation, a potential pathological mechanism requiring further investigation for future therapeutic development.