Kidney cells mounting

Maintenance of red cell volume is critical to having an adequate oxygen supply to the tissues [10]. Healthy individuals finely balance erythropoiesis and erythrocyte loss and maintain constant hematocrit. The glycoprotein hormone erythropoietin is the principal controller of the homeostatic mechanism that links tissue oxygen delivery to red cell production. While hypothesized as early as 1863, unequivocal evidence of erythropoietin was first published in 1953. A few years later, scientists showed that animals subjected to bilateral nephrectomy were unable to mount an erythropoietin response to hypoxia. Indeed, the kidneys produce about 90% of circulating erythropoietin. 

The vulnerability of the kidney to cisplatin is almost certainly linked to its primary role in the excretion of the drug. The P3 segment of the proximal tubule is particularly vulnerable to it. The cause of renal cell death induced by cisplatin is unknown, but mounting evidence points to its genotoxic effect. In cisplatin nephrotoxicity, as in other forms of nephrotoxic renal damage, reduced renal blood flow and diminished renal conservation of water are common physiologic derangements. 

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