Sunitinib- and Sorafenib-lnduced Nephrotic Syndrome in a Patient with Gastrointestinal Stromal Tumor
| Autor: | Nedim Turan, Selcuk Cemil Ozturk, Suleyman Buyukberber, Galip Guz, Bulent Cetin, Mustafa Benekli, Salih Inal, Leyla Memiş |
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| Rok vydání: | 2012 |
| Předmět: |
Niacinamide
Oncology Sorafenib medicine.medical_specialty Indoles Nephrotic Syndrome Gastrointestinal Stromal Tumors Pyridines Angiogenesis Inhibitors urologic and male genital diseases Internal medicine Sunitinib medicine Humans Pyrroles Pharmacology (medical) Stromal tumor Gastrointestinal Neoplasms GiST business.industry Phenylurea Compounds Benzenesulfonates Middle Aged medicine.disease female genital diseases and pregnancy complications Female business Nephrotic syndrome medicine.drug |
| Zdroj: | Annals of Pharmacotherapy. 46:1438-1438 |
| ISSN: | 1542-6270 1060-0280 |
| Popis: | Objective TO report a case of nephrotic syndrome (NS) induced by both sunitinib and sorafenib therapy. Case Summary A 61-year-old woman with metastatic gastrointestinal stromal tumor (GIST) presented with NS and hypertension following therapy with sunitinib 400 mg/day. Because of grade 3 toxicity, the drug was discontinued. After sunitinib discontinuation, NS and hypertension resolved. However, NS recurred on rechallenge. A similar picture developed following therapy with sorafenib 800 mg/day. A renal biopsy revealed a focal segmental glomerulosclerosis (FSGS). A few months after sorafenib cessation, resolution of NS and hypertension was again achieved. Discussion Several cases of NS have been reported among patients receiving sunitinib and sorafenib. However, renal histopathologic data were obtained in only a few patients. Although biopsy-proven cases of FSGS associated with sunitinib have been reported, this is, to our knowledge, the first reported case of biopsy-proven FSGS associated with sorafenib. The Naranjo probability scale indicated probable causality for NS developing with sorafenib, and definite causality with sunitinib. The clinical and histopathologic findings have led us to agree with the class effect proposal that all antiangiogenic drugs share a similar toxicity profile. Evidence supporting this hypothesis includes worsening of hypertension and proteinuria by both drugs, with full recovery occurring within a few months after cessation of the drugs, which favors the role of vascular endothelial growth factor receptor inhibition in FSGS development. Conclusions The clinical adverse spectrum of antiangiogenic drugs may be broader than initially observed because of a lack of renal biopsy data and routine screening for proteinuria. It can be speculated that proteinuria, as well as hypertension, is a class effect of all antiangiogenic drugs. |
| Databáze: | OpenAIRE |
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