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研究显示慢性汞暴露时尿蛋白的早期变化乃低分子蛋白比例增加,提示肾小管功能障碍可能是慢性汞性肾损伤的早期特点。研究发现,尿汞除以低分子汞复合物形式存在外,还以蛋白结合汞形式存在,如低分子蛋白结合汞、白蛋白结合汞等,后者随染毒量的积累可增至尿汞总量90％,提示肾小球滤出亦可能是肾脏排汞的重要途径。研究认为汞性白蛋白尿并非一定是肾脏明显损伤结果,可能与白蛋白与Hg~(2+)结合后本身负电性下降而较易透过肾小球滤膜有关。
Studies have shown that early changes in urinary protein during chronic mercury exposure is an increase in the proportion of low-molecular-weight proteins, suggesting that renal tubular dysfunction may be an early feature of chronic mercury-induced kidney injury. The study found that urine mercury divided by the presence of low molecular weight mercury complexes, but also in the form of protein-bound mercury, such as low molecular weight protein-bound mercury, albumin-bound mercury, which increases with the accumulation of exposure to urine mercury 90% of the total, suggesting that glomerular filtration may also be an important way of renal excretion of mercury. Studies suggest that mercury is not necessarily a significant renal damage caused by albumin, may be associated with albumin and Hg ~ (2+) itself after the decrease of negative and more permeable through the glomerular filtration membrane.