Acute and delayed nephropathy due to methamphetamine abuse

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, inf lammation and fibrosis in kidney, thus promoting hypertension, atherosclerosis and chronic kidney disease.