Despite the progress made in treating bipolar and unipolar
affective disorders,
lithium carbonate is still a common
drug in psychiatric practice.
Lithium-related renal side effects include
nephrogenic diabetes insipidus,
chronic tubulointerstitial nephropathy, and
acute kidney injury (AKI).
Nephrotic syndrome (NS) is an uncommon but severe complication of
lithium treatment. We present a 49-year-old female treated with
lithium carbonate due to a recurrent
depressive disorder who developed NS during this
therapy. NS spontaneously remitted after the
drug withdrawal. Since her
lithium serum levels were within the recommended values, we performed a retrospective analysis of
lithium-induced NS cases trying to determine causes predisposing to the NS development, underlying histopathology, and preservation or irreversible loss of kidney function. This analysis revealed that in
lithium-induced NS with AKI,
lithium serum level was the key determinant of AKI development (the β coefficient = 0.8499 with a confidence interval ranging from 0.7452 to 0.9546 and p value < 0.0001). In these cases, the underlying pathology was mainly
minimal change disease (MCD), which was quickly reversible upon the
drug withdrawal. The development of
chronic kidney disease (CKD) seemed to be associated with
lithium therapy duration. However, the multiple regression analysis for CKD as the dependent variable showed that the decisive factor was
focal segmental glomerulosclerosis (FSGS) as the underlying pathology (the β coefficient = 0.7866 with a confidence interval ranging from 0.600 to 0.9704 and the p value < 0.0001). Thus, we conclude that in
lithium-induced NS/AKI, serum
lithium levels contribute to these complications, while FSGS lesions are responsible for CKD's
disease progression.