Samad Godrati
1,2 
, Aiyoub Pezeshgi
1,2 , Rohollah Valizadeh
3 , Steven James Kellner
4 , Seyed Ramin Radfar
5,6 1 Internal Medicine Department, Zanjan University of Medical Sciences, Zanjan, Iran
2 Zanjan Metabolic Diseases Research Center, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran
3 Department of Epidemiology, Student Research Committee, School of Public Health, Iran University of Medical science, Tehran, Iran
4 Head International Research and Development, Mesencell Biotech International Ltd, 20-22 Wenlock Road, London, N1 7GU, UK
5 University of California, Los Angeles, Integrated Substance Abuse Programs, 11075 Santa Monica Blvd., Suite 200, Los Angeles, CA, USA
6 Substance Abuse and Dependence Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran
Abstract
Methamphetamine is a highly addictive drug that acts as a stimulant for the central nervous system. It increases alertness and physical activity but can cause cardiac dysrhythmias, hypertension, hallucinations and violent behavior. The excretion rate of methamphetamine by the kidney can be seriously altered by urinary pH. Methamphetamine is a weak base, consequently, the proportion of the excreted amount of unchanged drug can vary from as little as 2% in alkaline (pH ≥8.0) to 76% in acidic urine (pH ≤5.0). Methamphetamine is metabolized by hepatic metabolism and renal excretion via cytochrome P450 2D6 (CYP2D6). The effects of methamphetamine on the kidneys can be divided into the following sub-groups: vascular effects, non-traumatic rhabdomyolysis and direct nephrotoxicity. Additionally, methamphetamine directly stimulates the release of ET-1, a potent vasoconstrictor. ET-1 stimulates vasoconstriction, inflammation and fibrosis in kidney, thus promoting hypertension, atherosclerosis and chronic kidney disease.
Implication for health policy/practice/research/medical education:
The effects of methamphetamine on kidneys could be divided into three sub-groups: vascular effects, non-traumatic rhabdomyolysis, and direct nephrotoxicity. Methamphetamine directly stimulates the release of endothelin 1 (ET-1) leading to vasoconstriction, inflammation and fibrosis, thus inducing hypertension, arterial sclerosis and chronic kidney disease. Acute kidney injury is also seen frequently with methamphetamine and is triggered indirectly via vascular (pre-renal) effects and rhabdomyolysis.
Please cite this paper as: Godrati S, Pezeshgi A, Valizadeh R, James Kellner S, Radfar SR. Acute and delayed nephropathy due to methamphetamine abuse. J Nephropathol. 2020;9(3):e22. DOI: 10.34172/jnp.2020.22.