Lithium-associated Kidney Microcysts

Chronic lithium ingestion in patients with bipolar (manic-depressive) illness has been associated with several different forms of renal injury. Nephrogenic diabetes insipidus (NDI) is the most common renal side effect of lithium therapy[1] Lithium is a univalent cation of the white metal series, closely related to both sodium and potassium, but having no known role in human physiology. Lithium is completely absorbed by the GI tract. The drug is not protein bound and is completely filtered at the glomerulus. Up to 90% of the filtered load is reabsorbed by the nephron, 60% in the proximal tubule, and the remainder in the thick ascending limb of the loop of Henle, the connecting tubule, and the cortical collecting duct. The predominant form of chronic renal disease associated with lithium therapy is a chronic tubulointerstitial nephropathy. The image findings of renal disease that distinguish patients treated with lithium from other renal cystic disorders are the presence of distal tubular dilatation and microcysts. These cysts are present in 33%–62% of patients undergoing lithium therapy [2][3]. They originate from distal and collecting tubules and probably stem from the proliferation of distal tubular cells. They are localized in both the cortex and the medulla. In general, they do not exceed 1–2 mm in diameter. However, the number of renal microcysts present in lithium nephropathy has yet to be clearly defined. Lithium-associated kidney microcysts are usually echogenic on ultrasound examination because these cysts are lined by cuboidal epithelial cells in a stroma, which has surrounding much fibrosis [4]. This surrounding fibrosis dominates the ultrasound image and appears as echogenic shadow. CT and MRI demonstrate usual appearance of a cyst except the size is usually in 1-2mm range and no contrast enahancement is present.