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Does Dietary Protein Restriction Slow the Rate of Progression of Chronic Renal Disease?

Chronic renal failure is characterized by a progressive and often irreversible decline in glomerular filtration rate (GFR). Three major mechanisms (1) have been invoked to explain the progressive course of renal failure: a) persistent injury due to the initial pathogenetic insult; b) secondary glomerular injury due to either adaptive changes in initially normal or minimally affected glomeruli or to intraglomerular coagulation; and c) secondary injury due to compensatory changes or to abnormalities in tubular and interstitial function. In general, GFR values are used to estimate the mass of functional renal tissue or the number of functioning nephrons. Exogenous markers can be used to measure GFR. These markers should be freely filterable across the glomerulus, not secreted, reabsorbed, catabolized, or synthesized by the kidney. Several exogenous compounds including inulin and iothalamate fulfill these requirements but are not widely used clinically to measure GFR. Instead, creatinine has been used extensively as an endogenous marker (2) even though it is not an ideal substance for this purpose. Although its clearance estimates GFR accurately in the normal range, it tends to overestimate it as renal failure progresses because it is also secreted into the urine (2). The observations by two groups (3, 4) that the reciprocal of serum creatinine tends to decline linearly with time as renal function decreases has had an immense impact on assessing the effect of therapeutic interventions in renal failure. Since serum creatinine is measured periodically in virtually every patient with renal disease, it seemed possible to establish the rate of progression of renal disease by plotting the slope of the inverse of serum creatinine versus time. In the past 15 years there has been much interest in the possible role of protein restriction on the progression of chronic renal disease. Low protein diets have been utilized since the beginning of this century, primarily for the relief of clinical symptoms of uremia; and in the 1960's it was suggested that they might actually prolong the life of patients with end-stage renal disease (5). Yet it was not until the mid-seventies that several Authors suggested limiting the intake of phosphorus and protein to prolong survival of the kidney and halt the deterioration of progressive renal disease (6-10). Restriction of dietary protein decreases renal plasma flow and glomerular filtration rate in normal animals and humans whereas increases in protein intake have the opposite effect (11). In addition, it has been demonstrated in animals (particularly the rat) with experimentally-induced renal disease that· protein restriction has a beneficial effect on the rate of progression of renal disease and on the degree of histological changes (12). Several mechanisms have been suggested by which protein restriction may influence the progression of renal disease. Protein restriction decreases intraglomerular pressure, single nephron GFR, and glomerular plasma flow in rats with experimental renal disease. It may thus have a beneficial effect by decreasing intraglomerular pressures and flows. Protein restriction may limit hypertrophy of remnant nephrons and prevent some of the adaptive changes that may lead to progressive renal disease. It also decreases proteinuria in humans and experimental animals. A link between the degree of proteinuria and the progression of renal disease has been suggested. Protein restriction may influence immune mechanisms, both immune-complex and cell mediated. Decreased protein intake may also ameliorate interstitial disease by reducing ammonia production and excretion (13). This decreased ammonia production may inhibit activation of the complement system with its inflammatory and cytotoxic consequences (14). Protein restriction may protect the kidney by lowering serum lipids, particularly cholesterol. It also may affect total caloric intake, another possible important factor in the progression of renal disease. Finally, it will decrease the excretion of phosphorus in the urine and may thus reduce kidney calcification by lowering the calcium-phosphorus product.