Effects of Nutritional Treatment on Hormonal and Metabolic Derangements of the Uremic Syndrome

Abstract

Secondary hyperparathyroidism (HPTH) is common in patients with CRF and is constant in severe cases. A conventional low-nitrogen diet (CLND) (0.6 g/kg/day) can prevent HPTH only in early renal failure [1–2], but a very-low-phosphorus, low-PR vegan diet supplemented with CaCO3 and a mixture of essential amino acids (EAAs) and calcium salts of keto analogues (KAs) can reverse secondary HPTH, even in severe cases (figure 27–1) [3–6]. The fall of serum inorganic phosphorus (sPi) (causing an increase of ionized calcium) and an increase of total serum calcium are the most probable causes of the reversal of secondary HPTH, which is accompanied by a fall in serum alkaline phosphatase. This is known to indicate an improvement of uremic osteodystrophy [7]. It has been reported, however, that a mixture of EAAs and KAs can lower serum parathyroid hormone (PTH), even in chronic uremics on maintenance hemodialysis (MHD) and free diet [8], suggesting that the EAAs and KAs supplement acts directly, or through its calcium content, on PTH secretion. Dietary phosphorus restriction facilitates intestinal calcium absorption and also raises 1,25(OH)2D3 levels [9] but this is unlikely to occur in uremic patients.