Dear Editor,

We report the case of a 48-year-old female patient, treated with lithium for bipolar disorder for more than 20 years, without other special health issues. In December 2008, she was examined for a deteriorating renal function (Cr 2.7mg/dl and FG according to MDRD of 20ml/min/1.73m),2 her renal function of the previous year being Cr 1.4mg/dl. At the physical examination her blood pressure without any medical treatment was 170/95mmHg. The test carried out revealed Cr of 3.1mg/dl, Ur of 109mg/dl, K of 5.5mEq/l, P 4.7mg/dl, lithaemia of 0.9mEq/l and haemoglobin of 12.8g/dl; the rest of the biochemical parameters being normal. Her urine showed proteinuria of 5.7g/24 h, with 10-12 red blood cells/field in the sediment. The immunological test showed: negative ANA and ANCA, normal immunoglobulin levels and a normal complement system. The ultrasound revealed normal-sized hyperecogenic kidneys. Due to these findings, it was decided to carry out a renal biopsy which showed the following: 5 glomeruli, one with segmental hyalinosis and another with complete sclerosis. Mesangial thickening and diffuse interstitial fibrosis with tubular atrophy and dilation present in those not suffering from sclerosis. Mesangial deposits of IgA (+++) and C3 (+++). Anatomopathological diagnosis of IgA nephropathy with chronic tubulointerstitial nephritis. The patient began treatment with calcium antagonists with an improvement in the pressure figures; however, renal function continued to worsen, which is why it was necessary to prepare for the substitutive treatment.

Lithium salts are widely used in bipolar disorder. The treatment of the chronic form of the disorder with these salts is associated with different types of renal damage, including nephrogenic diabetes insipidus, metabolic acidosis, chronic nephritis and hypercalcaemia. The most important predisposing factor is the time of exposure to lithium, while other factors include age, episodes of lithium poisoning and comorbidity. The anatomopathological substrate of the toxicity from lithium is interstitial fibrosis, which can appear 5 years following treatment. At the same time, focal segmental glomerulosclerosis is associated with tubulointerstitial changes. Renal tubular cysts are a sign of tubular damage, which is manifested as dilation of the distal segment and the tubular collector. The progression of nephritis brought about by lithium is slow, considering a drop in the glomerular filtration rate of 2.2ml/min per year of exposure, with a very low rate of terminal chronic kidney disease in the various published studies. Interruption of the treatment with lithium salts does not achieve the recovery of the patient¿s baseline renal function. Instead, in some cases, the deterioration continues at a similar rate following its interruption. It is thought that a point of no return exists, after which renal fibrosis continues despite discontinuing the aggression that triggered it in the first place. This depends on the anatomopathological substrate at that moment, with better response of the illness to small changes. In this instance, the renal biopsy allowed us to position the clinical condition, and it was decided to continue with the lithium treatment. This could not fully justify the patient¿s progress in full view of the biopsy result that was compatible with IgA nephropathy, which justified the clinical condition described.