The uremic patient has multiple nutritional problems including those associated with dietary protein intake, fluid and electrolyte balance, phosphate retention, and acid-base disturbances. In the last two decades, enormous strides have been made in the care of these patients. A better understanding of the nutritional needs of the uremic patient has developed, and problem areas have been better defined. I addition, the advent of dialysis has generated an entirely new area for nutritional investigation. This review will describe the present status of nutritional therapy in dialyzed and undialyzed renal failure patients, including some recent advances in our understanding of protein metabolism and their influence on dietary therapy.
PRINCIPLES OF PROTEIN METABOLISM
An understanding of protein metabolism is of critical importance in the dietary management of renal failure patients. Protein is composed of amino acids. The amino acids can bedevided into two types, essential and nonessential. The essential amino acids cannot be synthesized by the body and must be supplied by the diet. There are at least nine essential amino acids, including histidine, an amino acid that has only very recently been shown to be essential. They are found in predominance in eggs, milk, and meat. The nonessential amino acids can be synthesized by the body. They are found in predominance in vegetable protein. Proteins that are primarily composed of essential amino acids are called high biologic value protein and conversely, those composed primarily of nonessential amino acids are called low biologic value protein.
The kidney is the principal organ responsible for the elimination of the nitrogenous products of protein catabolism, with urinary loss of nitrogen accounting for approximately 70 percent of dietary nitrogen intake, fecal loss for about 10 to 20 percent, and skin loss for the remainder. There is an enterohepatic circulation of urea, the chief nitrogenous endproduct of protein catabolism. Urea is acted upon by bacterial ureases in the gastrointestinal tract to form ammonia. The ammonia is picked up by the portal circulation and carried to the liver, where it may be used to resynthesize urea. It was thought until very recently that the large pool of urea nitrogen found in renal failure patients could be utilized in significant amounts to resynthesize amino acids, thereby decreasing effective protein catabolism and improving nitrogen balance. However, it has been clearly demonstrated that this is not the case. Urea degradation is not substantially increased in renal failure. In addition, Varcoe found that even though utilization of urea nitrogen for albumin synthesis in the uremic is of minor nutritional significance. He also demonstrated an addition stimulus for urea reutilization of protein restriction, but even on a 30 gram per day protein diet, the contribution of urea nitrogen to albumin synthesis in the uremic was only 3.1 percent. Richards also demonstrated the stimulus of protein restriction and found that it was a more potent stimulus to urea reutilization than uremia.
Protein turnover appears to be an adaptive process with lower turnover rates in patients with low protein intakes. This is true of normals and renal failure patients alike. The mechanism for the adaptation to varying levels of protein intake has not been delineated. Efficient protein utilization also requires an adequate energy intake. People with inadequate caloric intakes will tend to utilize nitrogen sources for energy needs.
The toxins of renal failure appear to be primary by-products of protein catabolism. They are an ill-defined group, with molecular weights generally thought to be between 500 and 1500 daltons. These compounds accumulate in renal insufficiency and, depending upon the severity of the disease, may reach levels which produce symptoms. Thus, reduction in protein catabolism will decrease the quantity of toxins that must be eliminated.