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Interstitial nephritis 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. [Pg.777]

The increase in urinary N-acetyl- -D-glucosamini-dase (NAG) with increasing blood lead concentrations reflects the proximal tubule dysfunction seen in acute lead nephropathy rather than the chronic interstitial nephritis associated with occupational lead exposure [35, 36]. NAG excretion correlates positively with the blood lead concentration but not with the bone lead concentration [37]. Eicosanoid excretion in lead workers is similar to that in patients with essential... [Pg.777]

Lead nephropathy is important because it is one of the few renal diseases that is preventable. Moreover, lead-induced acute renal dysfunction can sometimes be reversed by chelation therapy [19, 28, 63]. The salutary effect of chelation therapy appears to be on the acute reduction in GFR and the acute elevation of blood pressure associated with elevated blood lead concentration rather than on the long-term effects of cumulative exposure associated with endothelial dysfunction, hypertension, and interstitial nephritis. There is no evidence that such therapy reverses established interstitial nephritis. The partial remission achieved among moonshiners and lead workers appears to represent reversal of the physiologic effects of acute poisoning superimposed on chronic lead nephropathy. No improvement in renal function has been observed once advanced interstitial nephritis is present and the steady-state serum creatinine concentration exceeds about 3 mg/ dL [64]. [Pg.780]

Solvents have been implicated as inducers of glomerulonephritis [72], while the association between chronic interstitial nephritis and analgesic abuse is acknowledged [73] and the association between hypertensive renal disease (nephrosclerosis) and lead nephropathy continues to be explored [74, 75]. According... [Pg.10]

Although chelation therapy effectively reverses acute lead nephropathy and the preclinical renal dysfunction of occupational lead nephropathy, there is no evidence that such therapy reverses established interstitial nephritis due to lead. The partial remissions achieved among moonshiners and symptomatic lead workers may represent reversal of acute poisoning superimposed on chronic lead nephropathy. No improvement in renal function can be expected once ad-... [Pg.503]

C. Aoyolovir orystal deposition in the tubular lumen leading to an obstructive nephropathy may cause acute renal failure. Indinavir is poorly water soluble and oan preoipitate in the kidney, causing kidney stones and interstitial nephritis. [Pg.111]

Lead worker nephropathy has comprised a sizeable hterature, at least in quantitative terms, within the earlier toxic nephropathy database. Illustrative smdies are summarized in Table 15.3. Such nephropathy has typically, but not always, presented histopathologicaUy as a focal interstitial nephritis and functionally as reduced GFR. Lead nephropathy has been documented in many countries, including the United States (Baker et al., 1979 Wedeen et al., 1975, 1979), Romania (LUis et al., 1968), Brazil (Pinto de Almeida et al., 1987), Japan (Omae et al., 1990), Singapore (Chia et al., 1995a), and Belgium (Buchet et al., 1980). [Pg.574]

U.S. male lead workers (N= 140) Workplace exposures Chronic nephropathy EDTA results for symptomatic Pb poisoning Reduced GFR (N = 21) in 57 workers with positive EDTA Pb mobilization 50% of a subset of workers with reduced GFR had focal interstitial nephritis Wedeen etal. (1975, 1979)... [Pg.575]

Balkan nephropathy is non-destructive and noninflammatory tubulointerstitial renal disease [69]. The changes are non-specific and in the chronic, sclerotic phase they may be quite similar to changes observed in other chronic interstitial diseases such as analgesic nephropathy [70], vascular nephrosclerosis [69] cyclosporine-induced nephropathy [71], radiation nephritis [72,73] and aging [72], intoxication with silicate, cadmium, lead, uranium [74], mycotoxin ochratoxin... [Pg.848]


See other pages where Interstitial nephritis lead nephropathy is mentioned: [Pg.16]    [Pg.95]    [Pg.773]    [Pg.775]    [Pg.776]    [Pg.271]    [Pg.885]    [Pg.501]    [Pg.502]    [Pg.891]    [Pg.80]   
See also in sourсe #XX -- [ Pg.773 ]

See also in sourсe #XX -- [ Pg.501 , Pg.503 ]




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