Glycosuria lead nephropathy

The functional changes in chronic lead nephropathy appear to be less specific than those observed in acute poisoning. As in other forms of interstitial nephritis, proteinuria and glycosuria are initially absent. In contrast to cadmium nephropathy, the excretion of a large array of urinary marker proteins such as retinal binding protein, lysozyme, and iriicroglobulin [33, 34] is not increased in the absence of a reduced GFR. 

Early kidney disease is difficult to detect. The urinalysis is normal in early lead nephropathy and the blood urea nitrogen and serum creatinine increase only when two-thirds of kidney function is lost. Measurement of creatinine clearance can often detect earlier disease as can other methods of measurement of glomerular filtration rate. An abnormal Ca-EDTA mobilization test has been used to differentiate between lead-induced and other nephropathies, but this procedure is not widely accepted. A form of Fanconi syndrome with aminoaciduria, glycosuria, and hyperphosphaturia indicating severe injury to the proximal renal tubules is occasionally seen in children. 

Acute exposure to inorganic lead can cause reversible damage to the kidneys, manifested as tubular dysfunction. Chronic exposure to lead, however, causes permanent interstitial nephropathy, which involves tubular cell atrophy, pathological changes in the vasculature, and fibrosis. The most pronounced changes occur in the proximal tubules. Indeed, lead-protein complexes are seen as inclusion bodies in tubular cells, and the mitochondria in such cells have been shown to be altered with impaired oxidative phosphorylation. Clearly, this will influence the function of the proximal tubular cells in reabsorption and secretion of solutes and metabolites. Consequently, one indication of renal dysfunction is amino aciduria, glycosuria, and impairment of sodium reabsorption. 

Lead-induced nephropathy was first reported more than a century ago. However, the condition remains to be clearly defined. A study from Queensland, Australia, described 34 patients with a chronic nephropathy who had suffered from lead palsy in childhood following exposure to lead paints (Nye, 1933). Interstitial fibrosis, tubular atrophy and dilation have been observed in workers with heavy long-term exposure to lead. Renal tubular dysfunction characterized by glycosuria and aminoaciduria has been observed in lead-exposed children (Chisholm and Leahy, 1962). Lead exposure should be considered in the differential diagnosis of glycosuria occurring in childhood. 

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