1. New drug toxicities in the onco-nephrology world
Mark A. Perazella, Hassan Izzedine 
Kidney International 
Volume 87, Issue 5, Pages (May 2015)
DOI: /ki
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2. Figure 1
Potential mechanisms of renal injury and hypertension induced by anti-angiogenic treatment. Systemic vascular endothelial cell dysfunction and localized kidney effects (glomerular endothelial cells and podocytes) of anti-angiogenesis drugs lead to clinical renal syndromes. Hypertension results from both systemic effects and renal effects (acute kidney injury reduces glomerular filtration rate (GFR) and natriuresis, thereby contributing to hypertension). VEGF, vascular endothelial growth factor; VEGFR, VEGF receptor.
Kidney International  , DOI: ( /ki )
Copyright © 2015 International Society of Nephrology Terms and Conditions

3. Figure 2
(a and b) Thrombotic microangiopathy associated with anti-angiogenesis drugs. (a) Light microscopy reveals luminal thrombosis within the glomerular capillary. The capillary basement membranes are thickened with double-contoured appearance of the capillary wall originally associated with mesangiolysis (Masson’s trichrome; original magnification × 200). (b) Electron microscopy reveals glomerular injury from thrombotic microangiopathy with endothelial swelling, schistocyte in the capillary loop, and fibrin with thrombus in the subendothelial space (original magnification × 2000).
Kidney International  , DOI: ( /ki )
Copyright © 2015 International Society of Nephrology Terms and Conditions

4. Figure 3
(a and b) Acute tubular injury/necrosis associated with crizotinib. (a) Light microscopy demonstrates tubular cell injury with dilatation, apical blebbing, and loss of brush border (hematoxylin and eosin; original magnification × 400). (b) Electron microscopy reveals tubular cell injury with blebbing and loss of brush border (original magnification × 5000).
Kidney International  , DOI: ( /ki )
Copyright © 2015 International Society of Nephrology Terms and Conditions