The Role of Lithium Carbonate and Lithium Citrate in Regulating Urinary Citrate Level and Preventing Nephrolit

摘要

Background and purpose: Urinary Citrate is an inhibitor of Calcium oxalate stone formation. It is reab-sorbed in the proximal kidney through sodium dicarboxylate co-transporters (NaDC-1, NaDC-3) present in therenal tubular epithelium. Lithium (Li) is a known potent inhibitor of these transporters. We investigated theeffect of lithium carbonate (LiC) and lithium citrate (LiCit) in regulating urinary citrate levels and preventingnephrolithiasis (NL) in the rat model. Experimental approach: We took 220 Wistar rats and induced neph-rolithiasis in 130 of them by administering high doses of 5% ammonium oxalate (AmOx) for seven days andlabeled them as Group B. Rest were labeled as Group A. Each group was then divided into 3 subgroups. Firstsub-group acted as control while other two were treated with either lithium carbonate (LiC) or lithium citrate(LiCit) for 21 days. Ten rats from each of the six sub-groups were randomly selected for sacrifice on 3rd, 7th and14th day and additional 10th and 21~(st)day from Li treated groups. Blood and urine samples were collected andanalyzed on these days. The kidneys of the sacrificed rats were dissected and studied under light microscopy forcrystal deposition (left kidney) and histological changes (right kidney). Key results: Urinary citrate levels weresignificantly increased in response to either LiC (p<0.001) or LiCit (p<0.001). Increased urinary citrate levelsresulted in the reduction of calcium oxalate (CaOx) crystal deposition, kidney tubular dilatation and infiltra-tion of inflammatory cell in the tubulo-interstitium. Conclusions and implications: Use of lithium salts might bea potentially useful approach in the prevention of recurrent NL. (Int J Biomed Sci 2009; 5(3):215-222)