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Go back to clinical information and images Diagnosis: Membranous Glomerulonephritis, Stage I, associated to mercury exposure Membranous glomerulonephritis (MGN) is a frequent cause of nephrotic syndrome in the adult population. In our case the subepithelial localization of the immnune deposits permits the diagnosis. On light microscopy there were no significant pathological alterations in mesangial cells, basement membranes, or the Bowman's space. This type of MGN is called Stage I. In the patient the urinary concentrations of mercury were 10 times higher than reference values for non-exposed population. The present case is relevant due to the fact that the patient was chronically exposed to mercury, and the fact that remission was achieved withdrawing the exposure (MGN secondary to mercury exposure) Mercury and its compounds can be absorbed into the human body by inhalation, ingestion, and through the skin. It is toxic when certain threshold values are exceeded. Acute toxicity is due to the inactivation of enzymes by the heavy metal, which leads to interstitial pneumonitis, ulcerative gastro-enteritis, or tubular necrosis, depending on the route of exposure. Long-term mercury poisoning affects mainly the central nervous system and the kidneys. In the latter case the nephrotoxicity is usually manifested as MGN with nephrotic syndrome. Since 1920, numerous cases of nephrotic syndrome due to long-term contact with mercury and mercury compounds have been reported. The nephrotoxicity associated with mercury may be manifested as either acute tubular necrosis or an immune complex glomerulonephritis, depending upon the conditions under which the patient is exposed to the metal. Withdrawal of exposure to the metal resulted in disappearance of mercury from body fluids and clinical remission. In humans, the pathomechanism of mercury-induced MGN has not been elucidated. Experimental studies in rats point to a genetic susceptibility and to polyclonal stimulation of the immune system in mercury-induced MGN. The underlying pathogenetic mechanism is characterized by a T-lymphocyte-dependent polyclonal B-cell activation, with subsequent production of autoantibodies against proteins of the glomerular basement membrane as laminin and fibronectin, and also against heparan sulphate proteoglycans. It is not known whether similar mechanisms operate in humans. The results of epidemiological studies in workers exposed to mercury are inconsistent concerning renal function and immune reaction (Hua J, et al. Toxicology. 1993;79:119-29. [PubMed link]; Aymaz S, et al. Nephrol Dial Transplant. 2001;16:2253-5. [PubMed link] [Free full text]). In the follow-up, one year after exposure withdrawal, mercury concentrations in blood and urine had fallen below reference values for non-exposed populations. The 24-h urine protein excretion decreased to 0.12 g and creatinine clearance was 98 ml/min. See the chapter Membranous glomerulonephritis (English version). Go back to clinical information and images Bibliography
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