Abstract: PUB328
Lithium-Induced Renal Microcysts in a Young Woman: A Case of Delayed Cystic Sequelae Years After Discontinuation
Session Information
Category: Pharmacology (PharmacoKinetics, -Dynamics, -Genomics)
- 2000 Pharmacology (PharmacoKinetics, -Dynamics, -Genomics)
Authors
- Hasan, Irtiza, University of Florida College of Medicine, Jacksonville, Florida, United States
- Khan, Hafiz Sarfraz Ahmad, University of Florida College of Medicine, Jacksonville, Florida, United States
- Jaikaransingh, Vishal, University of Florida College of Medicine, Jacksonville, Florida, United States
Introduction
Chronic lithium therapy is a recognized cause of structural renal abnormalities, including microcyst formation. However, delayed development of renal microcysts years after drug cessation is uncommon and may mimic autosomal dominant polycystic kidney disease (ADPKD). We present a case of bilateral renal microcysts in a young woman with remote lithium exposure and no confirmed family history of ADPKD.
Case Description
A 33-year-old woman presented with intermittent bilateral flank pain. She had received lithium therapy from age 8 to 15, discontinued 15 years ago. Per patient, her psychiatrist monitored for lithium-related renal damage with imaging during treatment, none of which showed cystic changes. No known family history of ADPKD, although her mother has hypertension & some distant relatives had unspecified renal disease. She denies any history of hepatic cysts, mitral valve prolapse, or cerebral aneurysms. She has a remote history of childhood seizures but is not on antiepileptic medications. A renal ultrasound (US) five years earlier showed normal-sized kidneys with preserved corticomedullary differentiation & no cysts, confirming absence of cystic disease. A contrast-enhanced CT abdomen performed for flank pain revealed innumerable tiny microcysts diffusely involving both kidneys. A follow-up US three months later showed bilaterally increased cortical echogenicity & multiple small cysts—findings consistent with medical renal disease but not meeting US criteria for ADPKD. Despite these structural changes, renal function remains preserved (creatinine 0.7 mg/dL; eGFR >100 mL/min/1.73 m2). She has no proteinuria. Intermittent microscopic hematuria was previously noted but resolved on repeat testing. She has never had gross hematuria.
Discussion
This case illustrates delayed manifestation of lithium-induced renal microcysts despite long-term discontinuation and prior normal imaging. Lithium-associated nephropathy may evolve subclinically and become apparent years later. While imaging suggested cystic kidney disease, features typical of ADPKD and extrarenal involvement were absent. Lithium-induced microcysts can mimic hereditary cystic disease. Awareness of this delayed presentation is key to avoiding misdiagnosis and unnecessary genetic testing in patients with stable renal function and no other ADPKD features.