Additionally, enhancing the activity of a major selleck kinase inhibitor antioxidant enzyme, such as G6PD, may result in a reduction of complications secondary to increased oxidative stress in patients with ESRD. Background Because impairment of kidney function in patients with multiple myeloma can be caused by a variety of conditions, ascertaining the etiology of kidney dysfunction in patients with MM represents a challenging task for the practicing nephrologist. Patients with MM are at risk of ac quiring acute kidney injury as a result of light chain cast nephropathy, hypercalcemia, bisphosphonate induced tubular injury and lenalidomide nephrotoxicity. Similarly, syndromes of glomerular involvement can also occur in MM as a result of light or heavy chain deposition disease, amyloidosis or bisphosphonate induced podocytopathy.

Furthermore, patients with MM who un dergo hematopoietic stem cell transplantation are also at risk of acquiring renal syndromes inherent to HSCT, such as ischemic acute tubular necrosis and thrombotic microangiopathy. The clinical features of TMA syndromes include microangiopathic hemolytic anemia, thrombocytopenia, and organ injury. The pathological features are vascular damage manifested by arteriolar and capillary thrombosis with characteristic abnormalities in the endothelium and vessel wall. Renal pathology in TMA is characterized by thickened capillary walls, occlusion of vascular lumens, fibrin deposition and endothelial separation with expansion of suben dothelial zone. Over the last few years, multiple reports have unveiled an association between anti angiogenic therapy and TMA.

Antineoplastic drugs designed to target vascular endo thelial growth factor such as sunitinib, sorafenib, bevacizumab, and others, have been linked to the develop ment of a syndrome characterized by severe hypertension and or acute or chronic kidney injury, with or without proteinuria, and associated with histopathological evi dence of TMA in the kidney. Bortezomib is a prote asome inhibitor that was approved by the Food and Drug Administration in 2003 for the treatment of refrac tory MM and subsequently in 2008 as an initial treatment of patients with MM. Although it does not target VEGF directly, bortezomib has also been reported to be associ ated with TMA. In July 2012, a new member in its class, carfilzomib, was approved by the FDA for the treatment of relapsing or refractory MM.

In this report, we summarize the case of a patient with MM status post autologous HSCT and chronic kidney www.selleckchem.com/products/Sunitinib-Malate-(Sutent).html dis ease who experienced worsening hypertension along with a substantial increase in proteinuria shortly after the initi ation of carfilzomib for the treatment of refractory disease. We propose carfilzomib as a possible trigger of malignant hypertension and renal TMA in this case.