In 1963 it was first demonstrated that long-term lithium administration exerts a mood-stabilising effect, preventing recurrences of mania and depression in bipolar affective disorder. Despite the introduction of many other drugs having mood-stabilising effect, lithium still remains the first choice drug for the prophylaxis of affective episodes in mood disorder. Lithium is eliminated nearly exclusively by the kidneys: lithium clearance is proportional to creatininc clearance and is influenced by natriuretic and antinatriuretic factors. Nowadays, nearly 40-year experience with long-term lithium treatment point to a possibility of nephrotoxic effects of this ion. Impaired urinary concentrating ability, which, in a few patients can reach an intensity of diabetes insipidus, can occur after several weeks of lithium administration. Favourable results in the treatment of diabetes insipidus have been obtained with amiloride, the drug which block epithelial sodium channel. However, after 10-20 years of treatment, lithium-induced interstitial nephropathy may be demonstrated in some patients, which, in small proportion of the latter may lead to end-stage renal disease. Lithium-induced hipercalcemia and nephrotic syndrome are rare complications of lithium therapy. In patients on long-term lithium therapy periodic monitoring of kidney function by measuring serum creatinine concentration and glomerular filtration rate is necessary. In case of detecting nephropathy, a discontinuation of lithium should be considered. The patient in whom lithium was discontinued due to nephropathy should remain in nephrological treatment.