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An Overlooked Link between IgA Nephropathy and Lithium Toxicity: A Case Report
Sushil K Mehandru1, Supreet Kaur1, Aisha Ghias1
1Division of Nephrology & Hypertension, Department of Medicine, Jersey Shore University Medical Center, Hackensack Meridian School of Medicine, Neptune, New Jersey, USA.
Case Reports in Nephrology and Dialysis
|November 1, 2021
Summary
Lithium treatment for bipolar disorder can cause kidney damage, especially in patients with IgA nephropathy. High sodium-lithium transporter activity in IgA nephropathy may increase lithium accumulation and toxicity.
Area of Science:
- Nephrology
- Pharmacology
- Genetics
Background:
- Lithium is a first-line treatment for bipolar disorder but carries a risk of renal toxicity.
- Sodium-lithium counter-transporter (SLC-T) activity influences lithium metabolism and renal clearance.
- Enhanced SLC-T activity is associated with IgA nephropathy (IgA-N) and other renal conditions.
Observation:
- Patients with IgA-N may have reduced lithium clearance due to high SLC-T activity.
- This can lead to lithium accumulation in renal tubular cells, causing nephrotoxicity even at therapeutic serum levels.
- A case report details lithium-induced tubulointerstitial nephritis coexisting with IgA-N in a long-term lithium user.
Findings:
- The coexistence of IgA-N and lithium nephrotoxicity is rarely reported.
- High SLC-T activity in IgA-N likely contributes to reduced urinary lithium clearance and subsequent nephrotoxicity.
- Lithium accumulation in distal renal tubular cells exacerbates kidney damage.
Implications:
- Patients with bipolar disorder and IgA-N require careful lithium monitoring.
- Frequent renal function assessments and potential dose adjustments are crucial.
- Understanding SLC-T's role may help prevent severe lithium-induced nephropathy.
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