the remaining 1,330,000 nephrons (assuming a normal total of 2,000,000) hypertrophied so that their filtration rate increased by 50%. Such fine adjustment rarely occurs; the presence of a substantial amount of structural and functional damage might be impossible to determine precisely with standard tests of renal function.
Finally, there are almost no epidemiologic data on the number of people who develop ESRD as a result of acute or chronic exposure to environmental nephrotoxicants. All the estimates depend on inferences drawn from inconclusive sources, such as surveys of patients entering dialysis and transplantation programs. The results of several of the surveys indicate that substantial gaps exist in the ability to identify the primary abnormality leading to ESRD (Burton and Hirschman, 1979; Easterling, 1977; Evans et al., 1981; NIH, 1990; Rostand et al., 1982). For example, data compiled by the U.S. Renal Data System (USRDS) for the years 1987–1990 indicate that disease of unknown cause made up 6.6% of the cases of ESRD (NIH, 1993). Patients with interstitial nephritis not due to analgesics abuse were 3.4% of the total. Because those groups of patients include some who have been exposed to xenobiotics, such as heavy metals, it is possible that for 10.0% of the patients with ESRD, environmental and occupational nephrotoxicants might be of primary importance in the etiology of the disease. Even in other persons with ESRD, exposure to environmental pollutants might have been a factor in the onset or progression of the disease. Information on occupational history or other factors that would implicate a patient's environment in his or her potentially catastrophic illness is rarely available.
On the basis of the available social and demographic data, several notable groupings might be relevant to the incidence of renal diseases. ESRD is found in a disproportionately high percentage of minority, ethnic, and racial groups in the United States. Native Americans, blacks, and Hispanics, especially Mexican Americans, have overall ESRD rates about 3–4 times greater than the rate in whites (USRDS, 1991). Although the reasons for the increased susceptibility of minority groups to developing ESRD are unknown (Rostand, 1992), several possibilities have been suggested (Feldman et al., 1992). They can be separated into two broad categories: differences in the access to preventive health care and renal-replacement therapy, and physiologic heterogeneity among racial groups that might increase renal sensitivity to toxic exposures.
A study of 9,390 black and white New York state residents who began treatment between 1982 and 1988 sought to determine whether the incidence of ESRD due to the three most frequent causes (diabetic glomerulosclerosis, hypertensive nephrosclerosis, and glomerulonephritis) was related to socioeconomic status (Byrne et al., 1994). A clear effect of socioeconomic status on the incidence of ESRD due to diabetes or hypertension was demonstrated in whites, but, perhaps because of overriding factors, no such effect was seen in