Mechanisms of Cisplatin Nephrotoxicity
Abstract
:1. Introduction
Acute kidney injury (20–30%) | [15,16] |
Hypomagnesemia (40–100%) | [17,18,19,20,21] |
Fanconi-like syndrome | [22,23,24,25,26] |
Distal renal tubular acidosis | [27] |
Hypocalcemia | [28,29] |
Renal salt wasting | [22,30,31,32,33,34,35,36] |
Renal concentrating defect | [22,34,37,38,39,40] |
Hyperuricemia | [41] |
Transient proteinuria | [42] |
Erythropoietin deficiency | [43] |
Thrombotic microangiopathy | [44] |
Chronic renal failure | [15,45,46] |
2. Clinical Characteristics of Cisplatin Nephrotoxicity
Increased risk |
Dose |
Frequency |
Cumulative dose |
Older age |
Female sex |
Smoking |
Hypoalbuminemia |
Pre-existing renal insufficiency (limited data in humans) |
Decreased risk |
Diabetes (uncertain in humans) |
OCT2 polymorphisms |
3. Mechanisms of Cisplatin Nephrotoxicity
3.1. Accumulation of Cisplatin in Kidney Cells
3.2. Biotransformation of Cisplatin in the Kidney
3.3. Cellular Targets of Cisplatin
3.4. Apoptotic Pathways of Cisplatin Cytotoxicity
4. Inflammation in Cisplatin Nephrotoxicity
4.1. Cytokines
4.2. TLR Receptors
4.3. Immune Cells
4.3.1. Neutrophils
4.3.2. Macrophages
4.3.3. T Cells
4.3.4. Treg Cells
4.3.5. Dendritic Cells
5. Prevention of Cisplatin Nephrotoxicity
Reduced renal cisplatin accumulation or activation | |
OCT2 inhibitors, e.g., cimetidine or metformin | [61,208] |
Ctr1 inhibitors, e.g., copper | [68] |
Micellar/liposomal cisplatin | [206,207] |
Gamma-glutamyl transpeptidase inhibitors | [76,210] |
Glutathione transferase inhibitors | [74] |
Anti-oxidants | |
Amifostine | [203] |
BNP7787 | [211] |
N-acetyl cysteine | [212] |
Superoxide dismutase | [23,146] |
Catalase | [149] |
Selenium and Vitamin E | [150] |
Heme oxygenase-1 induction | [96] |
Iron chelators, e.g., Desferoximine | [145] |
Allopurinol plus ebselen | [213] |
Milk thistle extract (silymarin) | [214] |
Cannabidiol | [215] |
Lycopene | [216] |
Anti-apoptosis | |
p53 inhibitors, e.g., pifithrin | [100,115,127,128,129] |
HDAC inhibitors | [137,138] |
Caspase inhibitors | [113] |
p21agonists/CDK2 inhibitors | [123,124] |
Anti-inflammation | |
TNF-α antagonists | [102] |
TLR4 antagonists | [162] |
p38 inhibitors | [142] |
JNK inhibitors | [141] |
Salicylates | [98] |
PPAR-α ligands, e.g., fibrates | [217] |
PPAR-γ ligands, e.g. rosiglitazone | [218] |
Alpha lipoic acid | [219] |
IL-10 | [152] |
6. Summary
Acknowledgements
References
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Miller, R.P.; Tadagavadi, R.K.; Ramesh, G.; Reeves, W.B. Mechanisms of Cisplatin Nephrotoxicity. Toxins 2010, 2, 2490-2518. https://doi.org/10.3390/toxins2112490
Miller RP, Tadagavadi RK, Ramesh G, Reeves WB. Mechanisms of Cisplatin Nephrotoxicity. Toxins. 2010; 2(11):2490-2518. https://doi.org/10.3390/toxins2112490
Chicago/Turabian StyleMiller, Ronald P., Raghu K. Tadagavadi, Ganesan Ramesh, and William Brian Reeves. 2010. "Mechanisms of Cisplatin Nephrotoxicity" Toxins 2, no. 11: 2490-2518. https://doi.org/10.3390/toxins2112490