Abstract: SA-PO0582
Bilateral Medullary Nephrocalcinosis in a Young Woman on Long-Term Lithium Therapy: An Underrecognized Imaging Phenotype
Session Information
- Bones, Stones, and Mineral Metabolism: Research and Cases
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 502 Bone and Mineral Metabolism: Clinical
Authors
- Pulusu, Vinay Krishna, UPMC, Pittsburgh, Pennsylvania, United States
- Gangadharan, Keerthana, UPMC, Pittsburgh, Pennsylvania, United States
- Thakkar, Jyotsana, UPMC, Pittsburgh, Pennsylvania, United States
Introduction
Chronic lithium use is a well-established cause of tubulointerstitial nephropathy with cortical and medullary microcysts and progressive chronic kidney disease (CKD). Bilateral medullary nephrocalcinosis is a comparatively under-recognized imaging finding in lithium nephropathy. We describe a young woman with 15 years of lithium exposure presenting with CKD and bilateral medullary nephrocalcinosis.
Case Description
A 40-year-old woman with bipolar disorder was referred for a rising creatinine. She had taken lithium for about 15 years, with a 1-year preconception pause; it was reintroduced in the second trimester for symptom recurrence, with dose reduction for elevated levels. She delivered an uncomplicated singleton in February 2024. Creatinine was 0.99 mg/dL pre-pregnancy, 0.7-0.9 mg/dL antepartum (gestational hyperfiltration), and rose to 1.02-1.13 mg/dL postpartum (eGFR 63 mL/min/1.73 m2). BP and exam were unremarkable. Renal ultrasound showed preserved kidney lengths (11.3 and 11.6 cm), bilateral cortical thinning, and bilateral medullary nephrocalcinosis without hydronephrosis or calculi. Metabolic evaluation for medullary nephrocalcinosis, including calcium-PTH-phosphate studies, were negative.
Discussion
Lithium nephrotoxicity classically produces interstitial fibrosis, tubular atrophy, and pathognomonic cortical/medullary microcysts. Medullary nephrocalcinosis is less commonly emphasized but mechanistically plausible: lithium antagonism of the calcium-sensing receptor drives hyperparathyroidism and hypercalciuria; distal tubular dysfunction with an incomplete distal RTA phenotype favors calcium phosphate precipitation; and AQP2 downregulation produces a urinary concentrating defect.
Recognition of medullary nephrocalcinosis may provide an important noninvasive clue to chronic lithium nephropathy, particularly when kidney function decline is subtle or masked by physiologic states such as pregnancy-related hyperfiltration. Long-term lithium therapy warrants serial monitoring of creatinine and the calcium-PTH axis, and renal ultrasound may identify microcysts or nephrocalcinosis early in the disease course.
In patients with prolonged lithium exposure, bilateral medullary nephrocalcinosis on renal imaging should prompt consideration of chronic lithium nephropathy even in the absence of nephrolithiasis or significant CKD.