Thrombotic Microangiopathy Associated with Pazopanib in a Kidney Transplant Recipient
| Autor: | Scott B. Campbell, Shabana Kalla, Brian Percy Doucet, Robert J. Ellis, Bibiana Tie, Nicole M. Isbel, Dev Jegatheesan |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
kidney transplant
medicine.medical_specialty Thrombotic microangiopathy medicine.medical_treatment 030232 urology & nephrology Urology urologic and male genital diseases Kidney Cancer: Case Reports Nephropathy Pazopanib 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine pazopanib RC254-282 Creatinine business.industry vascular endothelial growth factor inhibitors Neoplasms. Tumors. Oncology. Including cancer and carcinogens Immunosuppression medicine.disease Ciclosporin Diseases of the genitourinary system. Urology female genital diseases and pregnancy complications thrombotic microangiopathy Calcineurin chemistry 030220 oncology & carcinogenesis Prednisolone RC870-923 business medicine.drug |
| Zdroj: | Journal of Kidney Cancer and VHL Journal of Kidney Cancer and VHL, Vol 8, Iss 1 (2021) |
| ISSN: | 2203-5826 |
| Popis: | Thrombotic microangiopathy (TMA) is characterised by abnormalities in the walls of arterioles and capillaries, precipitated by hereditary or acquired characteristics, and culminating in microvascular thrombosis because of dysregulated complement activity. A number of drugs can precipitate TMA, including vascular endothelial growth factor (VEGF) inhibitors, because of their effects on endothelial repair. Pazopanib is a VEGF inhibitor used for the treatment of renal cell carcinoma (RCC); it is uncommonly associated with TMA. A 52-year-old male, 5 years post his second kidney transplant secondary to immunoglobulin (Ig) A nephropathy, presented with hypertension, fluid overload, and worsening graft function (peak creatinine 275 μmol/L, baseline 130–160 μmol/L) and nephrotic range proteinuria 2 months after commencing pazopanib for metastatic RCC. His maintenance immunosuppression included ciclosporin, mycophenolate, and prednisolone. Haematological parameters were unremarkable. Allograft biopsy demonstrated glomerular and arteriolar changes consistent with chronic active TMA, with overlying features of borderline cellular rejection. He was treated with intravenous methylprednisolone 250 mg for 3 days and commenced on irbesartan 75 mg daily. Drug-induced TMA from pazopanib was suspected, particularly given the documented association with other tyrosine kinase inhibitors (TKIs). In consultation with his medical oncologist, pazopanib was ceased, and an alternate TKI cabozantinib was commenced. Serum creatinine remained |
| Databáze: | OpenAIRE |
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