Case Presentation: A 56-year-old man with PMH chronic kidney disease (CKD) stage II, adjustment disorder, methamphetamine (meth) abuse, last use 2 days before admission, presented with decreased urine output, “coffee-colored” urine, diffuse muscle pain, severe back pain, and fatigue for 1 day. Urine was positive for amphetamines, CPK 218,000 mcg/L, AST, and ALT were 1254 U/L and 2610 U/L, respectively. WBC 17 x 10^9 mEq/L, C02 14.5 mEq/L . UA showed large blood, >182 RBC/HPF, glucose 150 mg/dL, pH 5, protein 100 mg, and >100 HPF hyaline casts. Urine Na 70, Urine Cr 236, BUN 34 mg/dL, Cr 3.68 mg/dL, Fena = 0.8%. CT scan of the abdomen and pelvis showed no obstruction or hydronephrosis. Renal ultrasound showed increased echogenicity consistent with renal medical disease. The patient’s admission was for acute oliguric kidney injury due to severe rhabdomyolysis complicated by metabolic acidosis, hyperphosphatemia, and transaminitis. He received 3 L of IV fluids. During the following ten days, urine output varied from 350 ml to 1L/day. On day ten, he became anuric, and Bun and creatinine peaked at 116 mg/dL and 18.89 mg/dL, respectively, and CPK decreased to 900 mcg/L. Hemodialysis was started due to anuria and continued for three total sessions. Post-dialysis output improved to >1 L/day, and creatinine plateaued at 9 mg/dL. Two months after discharge, creatinine was the baseline, however, progressed to CKD stage III over the two following years with continued meth use.
Discussion: Meth is the second most-used drug of abuse worldwide. Meth abuse can cause neuropsychosis, systemic and pulmonary hypertension, cardiomyopathy, liver failure, rhabdomyolysis, and renal failure. Meth effects on kidneys include vascular effects, non-traumatic rhabdomyolysis, and direct nephrotoxicity. Rhabdomyolysis-induced AKI is triggered by myoglobin causing renal vasoconstriction, formation of intratubular casts, and direct toxicity to tubular cells. In the largest to date prospective series of AKI in meth-intoxicated patients, AKI with meth use is relatively mild, short-lived, and resolved in all cases with simple crystalloid hydration (1). Only a few cases of severe kidney injury including ESRD due to meth use reported. Profound meth-induced rhabdomyolysis caused severe AKI requiring temporary hemodialysis, which led to the recovery of kidney function in our case. However later, kidney function progressed to CKD stage III. CPK measurement is the biochemical gold standard for diagnosis and is required in any instance of meth use.
Conclusions: Meth use is correlated with renal failure. Meth-associated rhabdomyolysis can cause recurrent episodes of AKI, which increases the risk of CKD and its progression. Clinicians should recognize the potential of AKI in meth users, aim to treat the substance use disorder, and provide education about the inevitable progression to CKD if usage continues and the opportunity to prevent this progression if meth usage stops.