The Agony of Ecstasy

Campbell, G. Adam; Rosner, Mitchell H.

doi:10.2215/cjn.02080508

Cited by 108 publications

(92 citation statements)

References 78 publications

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“…The absolute incidence of this complication cannot be determined but is probably low. In most cases, AKI is associated with nontraumatic rhabdomyolysis in the setting of hyperthermia, extreme exertion, and volume depletion (51). Elevations of creatinine phosphokinase are usually pronounced (.100,000 U/L).…”

Section: Clinical Manifestations Of Ecstasy Use and Underlying Pathogmentioning

confidence: 99%

“…The most common renal complication of ecstasy use is symptomatic hyponatremia (51). In these cases, the sodium level at presentation is typically ,130 mEq/L and can be as low as 100 mEq/L.…”

Section: Clinical Manifestations Of Ecstasy Use and Underlying Pathogmentioning

confidence: 99%

“…In these cases, the sodium level at presentation is typically ,130 mEq/L and can be as low as 100 mEq/L. Of note, for public health concerns, most cases occurred in young women who ingested a single dose of ecstasy; in many cases this was the first use of the drug (51). Hyponatremia with ecstasy is dilutional in nature.…”

Section: Clinical Manifestations Of Ecstasy Use and Underlying Pathogmentioning

confidence: 99%

“…The effects of amphetamines, which increase the sensation of thirst as well as cause xerostomia, may increase the intake of water as well. However, merely the high intake of fluids is probably not enough to lead to hyponatremia because the kidney can usually excrete free water rapidly enough to match intake (51). Thus, impairment of renal free water excretion due to elevated AVP levels is the other major factor that ultimately leads to hyponatremia.…”

Section: Clinical Manifestations Of Ecstasy Use and Underlying Pathogmentioning

confidence: 99%

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Nephrotoxic Effects of Common and Emerging Drugs of Abuse

Pendergraft

Herlitz

Thornley‐Brown

et al. 2014

Clinical Journal of the American Society of Nephrology

112

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The kidneys can be injured in diverse ways by many drugs, both legal and illegal. Novel associations and descriptions of nephrotoxic effects of common and emerging drugs of abuse have appeared over the past several years. Anabolic androgenic steroids, illicitly used by athletes and others for decades to increase muscle mass and decrease body fat, are emerging as podocyte toxins given recent descriptions of severe forms of FSGS in long-term abusers. Synthetic cannabinoids, a new group of compounds with marijuana-like effects, recently became popular as recreational drugs and have been associated with an atypical form of AKI. 3,4-Methylenedioxymethamphetamine, commonly known as ecstasy, is a widely used synthetic recreational drug with mood-enhancing properties and a constellation of toxicities that can result in death. These toxic effects include hyperthermia, hypotonic hyponatremia due to its arginine vasopressin secretagogue-like effects, rhabdomyolysis, and cardiovascular collapse. Cocaine, a serotonin-norepinephrine-dopamine reuptake inhibitor that serves as an illegal stimulant, appetite suppressant, and anesthetic, also causes vasoconstriction and rhabdomyolysis. Recent adulteration of much of the world's supply of cocaine with levamisole, an antihelminthic agent with attributes similar to but distinct from those of cocaine, appears to have spawned a new type of ANCAassociated systemic vasculitis. This review discusses the nephrotoxic effects of these common and emerging drugs of abuse, of which both community and health care providers should become aware given their widespread abuse. Future investigation into pathogenetic mechanisms associated with these drugs is critical and may provide a window into ways to lessen and even prevent the nephrotoxic effects of these drugs of abuse and perhaps allow a deeper understanding of the nephrotoxicities themselves.

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Section: Clinical Manifestations Of Ecstasy Use and Underlying Pathogmentioning

confidence: 99%

Section: Clinical Manifestations Of Ecstasy Use and Underlying Pathogmentioning

confidence: 99%

Section: Clinical Manifestations Of Ecstasy Use and Underlying Pathogmentioning

confidence: 99%

Section: Clinical Manifestations Of Ecstasy Use and Underlying Pathogmentioning

confidence: 99%

See 2 more Smart Citations

Nephrotoxic Effects of Common and Emerging Drugs of Abuse

Pendergraft

Herlitz

Thornley‐Brown

et al. 2014

Clinical Journal of the American Society of Nephrology

112

View full text Add to dashboard Cite

show abstract

“…MA may cause hepatotoxicity, rhabdomyolysis, cardiotoxicity, nephrotoxicity, and neurotoxicity separately or sometimes together as multisystem toxicity, mostly as a serious condition requiring hospitalization. Nephrotoxicity generally presents as acute kidney injury, hyponatremia, and hypertension 1, 2, 3.…”

Section: Introductionmentioning

confidence: 99%

Multisystem toxicity after methamphetamine use

Gürel

2016

Clinical Case Reports

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Oxytocin and the Role of Fluid Restriction in MDMA-Induced Hyponatremia

Atila,

Straumann,

Vizeli

et al. 2024

JAMA Netw Open

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Importance3,4-Methylenedioxymethamphetamine (MDMA, or ecstasy) is a recreational drug being investigated for the treatment of posttraumatic stress disorder. Acute hyponatremia is a potentially serious complication after even a single dose of MDMA. The assumed etiology has been a vasopressin release inducing the syndrome of inappropriate antidiuresis combined with increased thirst, causing polydipsia and water intoxication.ObjectiveTo investigate the incidence and severity of hyponatremia after a single dose of MDMA, underlying neuroendocrine mechanisms of action, and the potential effect of fluid restriction on lowering the incidence of hyponatremia.Design, Setting, and ParticipantsThis ad hoc secondary analysis pooled data from 4 placebo-controlled crossover randomized clinical trials conducted at the University Hospital Basel, Basel, Switzerland. The 96 participants received experimental doses of MDMA between March 1, 2017, and August 31, 2022.InterventionA single oral 100- or 125-mg dose of MDMA. Fluid intake was not restricted in 81 participants; it was restricted in 15.Main Outcomes and MeasuresPlasma oxytocin, copeptin (marker of vasopressin), and sodium levels were measured repeatedly within 360 minutes after MDMA intake. The association of plasma oxytocin or copeptin levels with plasma sodium level at 180 minutes (peak concentration of MDMA) was determined.ResultsAmong the 96 participants, the mean (SD) age was 29 (7) years, and 62 (65%) were men. A total of 39 participants (41%) received a 100-mg dose of MDMA, and 57 (59%) received a 125-mg dose. At baseline, the mean (SD) plasma sodium level was 140 (3) mEq/L and decreased in response to MDMA by 3 (3) mEq/L. Hyponatremia occurred in 30 participants (31%) with a mean (SD) sodium level of 133 (2) mEq/L. In 15 participants with restricted fluid intake, no hyponatremia occurred, while in the 81 participants with unrestricted fluid intake, hyponatremia occurred in 30 (37%) (P = .002) with a difference in plasma sodium of 4 (95% CI, 2-5) mEq/L (P &lt; .001) between both groups, suggesting that fluid restriction may mitigate the risk of hyponatremia. At baseline, the mean (SD) plasma oxytocin level was 87 (45) pg/mL and increased in response to MDMA by 388 (297) pg/mL (ie, a mean [SD] 433% [431%] increase at 180 minutes), while the mean (SD) copeptin level was 4.9 (3.8) pmol/L and slightly decreased, by 0.8 (3.0) pmol/L. Change in plasma sodium level from baseline to 180 minutes demonstrated a negative correlation with the changes in oxytocin (R = −0.4; P &lt; .001) and MDMA (R = −0.4; P &lt; .001) levels while showing no correlation with the change in copeptin level.Conclusions and RelevanceIn this secondary analysis of 4 randomized clinical trials, a high incidence of acute hyponatremia was observed in response to MDMA, which may be mitigated by fluid restriction. Hyponatremia was associated with acute oxytocin but not copeptin release. This challenges the current hypothesis of direct vasopressin release and rather indicates that oxytocin mimics the effect of vasopressin in the kidneys due to structural homology.

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The Agony of Ecstasy

Cited by 108 publications

References 78 publications

Nephrotoxic Effects of Common and Emerging Drugs of Abuse

Nephrotoxic Effects of Common and Emerging Drugs of Abuse

Multisystem toxicity after methamphetamine use

Oxytocin and the Role of Fluid Restriction in MDMA-Induced Hyponatremia

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