Many organophosphates, besides inhibiting acetylcholinesterase, can also permanently inhibit the enzyme neuropathy target esterase, leading to nerve damage. NTE also happens to be found in the kidneys, and is involved in osmolyte production. Have organophosphates been known to affect kidney function through the inhibition of NTE in the kidneys? If so, how?


Gallazzini, M., & Burg, M. B. (2009). What’s New About Osmotic Regulation of Glycerophosphocholine. Physiology, 24(4), 245–249. doi:10.1152/physiol.00009.2009


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One article suggests that NTEs in kidneys are important for regulating NaCl concentrations, whereby if increasing concentrations of NaCl are sensed in inner medullary collecting duct cells transcription of the building blocks of NTEs are increased to decrease this NaCl. If NTEs are inhibited due to being irreversibly bonded with moieties of organophosphates at their active sites then this would mean that the kidneys would lose their mechanism for controlling how much salt is excreted from the body.

Gallazzini, M., Ferraris, J. D., Kunin, M., Morris, R. G., & Burg, M. B. (2006). Neuropathy target esterase catalyzes osmoprotective renal synthesis of glycerophosphocholine in response to high NaCl. Proceedings of the National Academy of Sciences, 103(41), 15260 LP – 15265. https://doi.org/10.1073/pnas.0607133103

This loss of chloride and sodium, I posit, would then have a knock-on effect on the concentration gradients maintained in the kidney as necessary for effective absorption and excretion of other ions. My guess is that hyponatraemia would be one of the direct results of the presence of organophosphates in the kidneys.


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