Kidney Week

Abstract: PUB247

Silent Legacy: Lithium-Associated Cystic Kidney Disease Decades After Discontinuation

Session Information

• Publication Only

Category: CKD (Non-Dialysis)

• 2201 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention

Authors

• Arwani, Suneel, The University of Mississippi Medical Center, Jackson, Mississippi, United States

Suneel Arwani, MD, MBBS

• Parkash, Om, Montefiore Einstein Medical Center, New York, New York, United States

Om Parkash, MD

• Jaradat, Raghad, The University of Mississippi Medical Center, Jackson, Mississippi, United States

Raghad Jaradat, MD

• Arwani, Sanjana, Ningxia Medical University, Yinchuan, Ningxia, China

Sanjana Arwani, MBBS

• ., Bhawna, Ningxia Medical University, Yinchuan, Ningxia, China

Bhawna ., MBBS

• Shahid, Shahzad, The University of Mississippi Medical Center, Jackson, Mississippi, United States

Shahzad Shahid, MD, MBBS

• Kumari, Kiran, Isra University Faculty of Medicine and Allied Medical Sciences, Hyderabad, Sindh, Pakistan

Kiran Kumari, MPH

• Somi, Shamima A., The University of Mississippi Medical Center, Jackson, Mississippi, United States

Shamima A. Somi, MD

• Atari, Mohammad, The University of Mississippi Medical Center, Jackson, Mississippi, United States

Mohammad Atari, MD, FASN

Introduction

Long-term lithium therapy is a well-recognized cause of chronic kidneydisease (CKD), often progressing silently over decades. Renal manifestations include tubular fibrosis, CKD, nephrogenic diabetes insipidus, and sometimes renal cysts development. We present a case illustrating lithium-induced CKD with incidental renal cysts, highlighting the importance of longitudinal nephrology follow-up even years after therapy cessation.

Case Description

A 72-year-old woman with well-controlled HTN, hypothyroidism, HLD, and bipolar I disorder presented for evaluation of elevated creatinine first noted in 2022 1.7 mg/dL, eGFR 29 with prior and subsequent creatinine values ranging 1.4–1.7 mg/dL. Current medications included acetaminophen, amlodipine, cariprazine, cholecalciferol, levothyroxine, losartan, pantoprazole, and rosuvastatin. She denied DM, NSAID exposure, or family history of kidney disease. UA remained bland without hematuria or proteinuria, with stable electrolytes and bicarbonate 25 mmol/L. Imaging demonstrated normal-sized kidneys with increased echogenicity and bilateral cysts, while CT revealed innumerable small bilateral simple cysts without enlargement. She confirmed a 25-year history of lithium use for bipolar disorder, discontinued nearly 30 years ago.

Discussion

The patient's presentation and clinical findings are most consistent with lithium associated chronic tubulo interstitial fibrosis, supported by cystic changes, absence of diabetes, stable blood pressure, bland urine sediment, no proteinuria, and relatively stable kidney function over time. Renal cysts are a recognized but often under appreciated feature of chronic lithium exposure, reflecting structural remodeling that may persist long after discontinuation. This case highlights how lithium related CKD can remain clinically silent for years with preserved electrolytes and minimal albumin uria yet reflect irreversible tubular injury and long term lithium use can leave lasting changes in the kidneys, even many years after the medication is stopped. This case shows how chronic tubulo interstitial injury and small renal cysts may appear decades later and contribute to CKD.This case highlight the importance of careful history taking and medications review, even investigating prior discontinued medications, which saved the patient unnecessary procedures and expenses