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ACUTE RENAL FAILURE

Andrews and Bates (1986) reported that the response of rat kidney to a 45 minute period of ischemia was dramatically affected by prior protein intake. For example, 93 percent of rats fed a high-protein diet for the preceding 2 weeks died of renal ischemia within 3 days, compared with 12 percent of rats fed a low-protein diet. One hundred percent of rats fed a zero protein diet survived, and most of them exhibited normal serum creatinine levels by the fourth day after ischemia.

Instituting protein restriction after a period of ischemia provided no protection, nor did switching from a zero-protein diet to a high-protein diet immediately after the ischemic insult cause any increase in mortality. Approximately I week of prior protein restriction was required to produce this remarkable effect.

The authors suggested that patients who are to be subjected to surgical procedures with a high risk of acute renal failure might benefit from protein restriction in the pre-operative period.

It is not clear how these findings might be applicable to soldiers, since their risk of acute renal failure, even in combat, is low. It is clear, however, that at least with regard to the risk of morbidity from acute renal failure, dietary protein restriction is more likely to confer benefit than to increase risk.

PROTEIN INTAKE AND THE DEVELOPMENT OF GLOMERULOSCLEROSIS

Glomerular filtration rate (GFR) declines with age for people over 40 in approximately two-thirds of persons without frank kidney disease (Lindeman et al., 1985), especially if they are hypertensive (Lindeman et al., 1984); in the remaining one third, GFR remains constant or increases with age (Lindeman, 1990). According to Fliser et al. (1997), about two-thirds of elderly subjects who are not in heart failure and not on diuretics (even if hypertensive) have GFRs within the range of younger subjects (Figure 7-4). Kidneys examined at autopsy of persons dying of causes other than kidney disease show a progressive, though extremely variable, increase in the fraction of glomeruli that are sclerotic (Figure 7-5) (Kaplan et al., 1975). Circulatory impairment may be another factor, since there may be localized areas of reduced flow within the kidneys of older subjects (Friedman et al., 1972).

In rats, the development of chronic renal failure with age is nearly universal (Coleman et al., 1977; Hayashida et al., 1986). The predominant lesion is glomerulosclerosis. Because this process was apparently attenuated by protein restriction (see review by Masoro and Yu, 1989), Anderson and Brenner (1987) suggested that the high protein intake of Western societies plays a central role in



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