There are three ways in which protein intake may play a role in the development of renal disease: promotion of nephrolithiasis, enhancement of the morbidity of acute renal failure, and acceleration of glomerulosclerosis.
During recent decades, nephrolithiasis has been increasing in frequency in developed countries in association with improved nutrition (Goldfarb, 1988; Robertson et al., 1979a). In Japan, for example, the incidence of renal stone disease has increased threefold since the period preceding World War II (Iguchi et al., 1990). Estimates of the prevalence of nephrolithiasis in the general population range from I percent to 15 percent (Johnson et al., 1979). Approximately 12 percent of the U.S. population will have a kidney stone at some time (Johnson et al., 1979; Sierakowski et al., 1978). One contributory factor is rising intake of protein-rich foods, which may promote urolithiasis (uric acid stone formation) in several ways (Robertson et al., 1979b).
Calcific nephrolithiasis occurs when the activity product2 of free calcium times free oxalate or phosphate exceeds a certain level, which is in turn modified by crystallization inhibitory factors. Hence, a reduction in urinary calcium excretion might be expected to reduce the occurrence of calcific nephrolithiasis. Indeed, restriction of calcium intake has been a mainstay of dietary advice for the prevention of recurrent nephrolithiasis. However, as pointed out by Goldfarb (1988), this approach is inappropriate and even potentially dangerous for several reasons: first, negative calcium balance may ensue because gastrointestinal calcium losses continue, with resultant osteoporosis during long-term application (Lalau et al., 1992); second, retrospective data indicate that the incidence of stone recurrence is negatively correlated with spontaneous calcium intake, probably because ingested calcium precipitates oxalate in the gut (Curhan et al., 1993; Lemann et al., 1996). Whatever the explanation, it is clear that attempts to reduce renal clearance of calcium will be more fruitful than reducing calcium intake. In this respect the high calcium intake typically associated with a high protein intake may be protective against calcific nephrolithiasis.