1. Volume 79, Issue 1, Pages 33-45 (January 2011)
New insights into the mechanism of aminoglycoside nephrotoxicity: an integrative point of view 
Jose M. Lopez-Novoa, Yaremi Quiros, Laura Vicente, Ana I. Morales, Francisco J. Lopez-Hernandez 
Kidney International 
Volume 79, Issue 1, Pages (January 2011)
DOI: /ki
Copyright © 2011 International Society of Nephrology Terms and Conditions

2. Figure 1
Mechanisms and cell signaling pathways underlying the cytotoxic effect of gentamicin. ATP, adenosine triphosphate; CaSR, extracellular calcium-sensing receptor; Cyto c, cytochrome c; ER, endoplasmic reticulum; PPARα, peroxisome proliferator-activated receptor-α; ROS, reactive oxygen species; UPR, unfolded protein response; ?, The contribution of these mechanisms to cell death is not completely known.
Kidney International  , 33-45DOI: ( /ki )
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3. Figure 2
Glomerular effects of gentamicin. AP-1, activator protein 1; CaSR, extracellular calcium-sensing receptor; ET-1, endothelin-1; GBM, glomerular basement membrane; GFB, glomerular filtration barrier; GFR, glomerular filtration rate; HMW, high molecular weight; Kf, ultrafiltration coefficient; MMW, medium molecular weight; NO, nitric oxide; PAF, platelet activating factor; PGE2, prostaglandin E2; PLA2, phospholipase A2; RAS, renin–angiotensin system; ROS, reactive oxygen species; TXA2, thromboxane A2; ?, Unknown pathophysiological consequences.
Kidney International  , 33-45DOI: ( /ki )
Copyright © 2011 International Society of Nephrology Terms and Conditions

4. Figure 3
Vascular effects of gentamicin. Ade, adenosine; ANG-II, angiotensin-II; ET-1, endothelin-1; GFR, glomerular filtration rate; Kf, ultrafiltration coefficient; PAF, platelet-activating factor; PGs, prostaglandins; ROS, reactive oxygen species; TXA2, thromboxane A2.
Kidney International  , 33-45DOI: ( /ki )
Copyright © 2011 International Society of Nephrology Terms and Conditions

5. Figure 4
Integrative view of the mechanisms leading to gentamicin nephrotoxicity. It can be appreciated that, in the absence of a significant tubular obstruction, vascular and mesangial mechanisms are necessary to explain the reduction in glomerular filtration (GFR) and renal excretion, once the tubuloglomerular feedback adapts. ANG-II, angiotensin-II; ATP, adenosine triphosphate; ET-1, endothelin-1; GFR, glomerular filtration rate; Kf, ultrafiltration coefficient; ΔP, net ultrafiltration pressure; PAF, platelet-activating factor; Pt, intratubular pressure; RBF, renal blood flow.
Kidney International  , 33-45DOI: ( /ki )
Copyright © 2011 International Society of Nephrology Terms and Conditions

6. Figure 5
Comparative temporal evolution of the acute kidney injury (AKI), tubular necrosis, glomerular filtration, tubuloglomerular feedback, and vascular and mesangial contraction on treatment with gentamicin. Initially, tubuloglomerular feedback (TGF) controls glomerular filtration rate. As TGF adapts, increasing tubular obstruction (TO), and vascular and mesangial contraction (VC and MC) take over and make GFR progressively lower.
Kidney International  , 33-45DOI: ( /ki )
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7. Figure 6
Role of inflammation in the amplification of tubular, glomerular, and vascular effects of gentamicin. PAF, platelet-activating factor; RBF, renal blood flow; ROS, reactive oxygen species; TLRs, toll-like receptors.
Kidney International  , 33-45DOI: ( /ki )
Copyright © 2011 International Society of Nephrology Terms and Conditions