Kwon C, Zaritsky A, Dharnidharka VR (2003) Transient proximal tubular renal injury following Ecstasy ingestion. Pediatr Nephrol 18: 820-822.
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This report describes a case of hyponatremia and signs of renal injury in an 18-year old woman admitted to hospital after having general (grand-mal, clonic-tonic) seizures subsequent to Ecstasy use. The seizures occurred "in the early morning" after she and her friends had attended a nightclub (time elapsed from attending nightclub to occurrence of seizures not reported). Her friends denied any alcohol or drug use at the time of admission, but results of an extensive toxicological screening performed on the day of admission detected Ecstasy. However, the patient’s friends reported that she consumed excessive quantities of water (polydipsia) prior to admission. No information is provided as to whether this was a blood or urine screen, or whether "Ecstasy" refers only to MDMA or to related compounds, such as MDA or MDE). No information is provided concerning number of tablets taken. The screen was negative for heavy metals (e.g. lead, mercury, cadmium), benzodiazepines, cocaine or opiates. Initial observation and testing indicated hyponatremia (sodium at 117mEqL), blood hypo-osmality, and, in the few hours after admission, polyuria (large urine output). Detection of renal glycosuria and inappropriate phosphate levels in urine without any changes in potassium gradient suggested proximal tubular injury (part of kidneys). The patient’s hyponatremia was corrected over the 24 h after admission, and on the third day after admission, the patient was fully recovered, with all electrolyte values normalized. The authors state that hyponatremia with polyuria is not usually seen after the syndrome of inappropriate anti-diuretic hormone. (This may be relevant, as MDMA may induce arginine vasopressin, or anti-diuretic hormone, release (Forsling et al. 2001). The authors propose that proximal tubular injury might have arisen from cytotoxic injury, but since the only findings of MDMA-associated damage to renal cells involved high drug concentrations in an in-vitro study (Carvalho et al. 2002), not enough evidence exists in support of this claim.

 
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