A 47-year-old man, who quit smoking ten years ago, smoked between 10-20 cigarettes/day for 15 years and was diagnosed 8 years ago with IgA mesangial glomerulonephritis. He had been working for 12 years as a welder in a company manufacturing steel discs with inserted cobalt and tungsten carbide "teeth" used to cut marble and granite. The welder used an autogenous welding system in which they used, as filler metal, metal rods based on: silver (39%), cadmium (25%), copper (22%) and zinc (14%). He consumed 1 kg/week; he did not use respiratory protective equipment and his workplace did not have a localised fume extraction system. Cadmium concentrations at her workplace were 52 μg/m3 (Environmental Limit Value (ELV) is 10 μg/m3). During the twelve years she had been working, she had undergone an initial examination and two periodic non-specific examinations without monitoring exposure to cadmium and other chemical pollutants; the laboratory results were within normal limits (complete blood count, blood glucose, cholesterol, liver transaminases, serum creatinine and urine cytochemistry). In a general blood test carried out by your family doctor, microhaematuria and proteinuria were detected. When his doctor took his medical history he detected exposure to cadmium fumes and was referred to the Toxicology Unit of our hospital. On admission, the patient was asymptomatic, had no personal or family history of nephrological problems, no obesity or diabetes (blood glucose levels were normal), did not take any type of medication regularly and his blood pressure was 105/65 mm/Hg. Laboratory tests showed proteinuria of 2 g/24 h, microhaematuria of 150 red blood cells/field, blood cadmium of 20 μg/l (Biological Limit Value [BLV]: 5μg/l) and urine cadmium of 85 μg/g creatinine (BLV: 5 μg/g creatinine). Since the renal involvement was of the glomerular type, and cadmium causes mainly tubular lesions, a renal biopsy was recommended. Light microscopy showed five glomeruli, one of which was completely sclerosed; the rest showed slight segmental hypercellularity; in two glomeruli there was an extracapillary segmental proliferation and foci of interstitial fibrosis with tubular atrophy. Immunofluorescence was positive for C3 (+++) and IgA (++) with mesangial pattern. The diagnosis was mesangial IgA focal glomerulonephritis and treatment with enalapril 10 mg/day was started. Due to the high concentrations of cadmium in biological fluids (blood and urine), which eight years after cessation of exposure are still above the maximum values allowed in Spain for workers exposed to cadmium, the patient was taken off work; in addition, he was considered a worker particularly sensitive to exposure to nephrotoxic substances and we advised him to avoid exposure in order to minimise the possibility of the patient progressing to chronic kidney disease as much as possible. He was followed up for 8 years (serum creatinine, glomerular filtration rate, proteinuria and urinary sediment values are shown in table 1) and repeated beta2-globulin and N-acetylglucosaminidase (NAG) controls were found to be within the normal range. At present, blood cadmium concentrations are 7 μg/l (VLB: 5 μg/l) and urine cadmium is 18 μg/g (VLB: 5 μg/g).

