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55 to 88 years (Figure 7-6). In both groups, there was a similar pronounced dependence of clearance on protein intake; in the older subjects, a lower intercept was seen, reflecting the effect of age on GFR. If protein intake is not controlled, the apparent decline in GFR with age will be exaggerated, because older subjects consume less protein than younger subjects (Kerr et al., 1982).

Third, Tobin and Spector (1986) measured creatinine clearance in 198 normal men on two occasions, 10 to 18 years apart, and correlated the decline in clearance during this interval with protein intake: no relationship was detected. They found no evidence that a high intake of protein caused a progressive reduction in renal function.

Fourth, high-protein feeding (60%) for 2 years in rats had no effect on the percentage of sclerotic glomeruli (Collins et al., 1990).

Fifth, the progressive decline in renal function seen in rats after partial nephrectomy (Brenner et al., 1982) may be unique to this species. In dogs with 75 percent nephrectomy, GFR does not decline progressively with time for the ensuing 4 years, whether protein intake is high or low (Bovée, 1991). In baboons followed for 5 years after subtotal nephrectomy and on either 8 percent protein or 25 percent protein diets, renal failure did not occur; GFR, measured as inulin clearance, increased sharply in baboons fed 25 percent protein, and this difference tended to disappear with time (curiously, creatinine clearances did not decrease with time in either group). Even in baboons fed 8 percent protein, a slow decline in GFR with time was seen (5% per year). Proteinuria did not differ between the two groups and did not progress (Bourgoignie et al., 1994). In human kidney donors, mild proteinuria (but not albuminuria) is often seen, and the incidence of hypertension may be increased, but progressive renal failure rarely if ever occurs, and there is no correlation between protein intake and proteinuria (Anderson et al., 1985; Hakim et al., 1984). Such individuals are not generally advised to restrict their protein intake (Rocher and Swartz, 1987), although some clinicians have recommended that these individuals do so until the question is settled (Bay and Hebert, 1987). Likewise, protein restriction is not advised for persons with a solitary normal kidney (Mitch, 1989).

From these observations, it is clear that protein restriction does not prevent the decline in renal function with age and, in fact, is the major cause of that decline. A better way to prevent the decline would be to increase protein intake. Indeed, protein malnutrition in the elderly is a far more prevalent problem (Morgan et al., 1956; Rudman et al., 1989) than is nitrogen retention as a consequence of an age-related decline in renal function.


Concerns about an adverse effect of high protein intake on renal function, and in particular on its decline with age, appear to be ill advised. Putting aside the potential adverse effects of protein intake on nephrolithiasis or on morbidity

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