“Ms. LK,” a 22-year-old Caucasian woman, was referred to our outpatient psychiatry clinic in January 2011 by Urology for help with her lithium therapy in the setting of new-onset renal tubular ectasia. She has a past medical history of childhood-onset bipolar disorder. Other pertinent medical history includes numerous E. coli urinary tract infections successfully treated with short courses of ciprofloxacin.
LK was referred to urology because of her report of “fragments in my urine.” She denied dysuria, hematuria, and polyuria. Her blood urea nitrogen (BUN) and serum creatinine (SCr) remained stable, at 11 mg/dL and 0.9 mg/dL. Her GFR was >60 ml/min/1.79 m2. Her lithium level at this time was 1.32 mmol/L. Previously, she had only one other elevated lithium level, 1.44 mmol/L, in 2006. Otherwise, her lithium levels consistently ranged from 0.3 mmol/L to 0.8 mmol/L. A pelvic exam, cystoscopy, and pelvic ultrasound were negative. A kidney ultrasound revealed increased echogenicity of the periphery of the medullary pyramids, of uncertain etiology, but thought to be most commonly seen in the setting of medullary nephrocalcinosis. However, an X-ray of the kidneys, ureters, and bladder (KUB) was negative for renal calcinosis. A computed tomography (CT) of the abdomen and pelvis revealed renal tubular ectasia. HIV test was negative. She was tapered off lithium, as nephrology thought this was the culprit for the renal ectasia. Two months after this incident, she had a follow-up outpatient visit with nephrology. LK presented to this visit with no urinary complaints. Nephrology ruled out HIV-induced nephropathy with negative HIV antibodies. Therefore, they maintained that lithium caused her renal ectasia and advised her to remain off lithium. Her bipolar disorder is stable and treated with lamotrigine 200 mg daily.