Urinary acid excretion diets

In order to lower uric acid excretion, oral purine uptake must be reduced unless one administers allopuri-nol. In view of the known tendency of patients with gout to develop renal stones one of these two measures is indicated. For patients treated with a uricosuric drug a low purine diet is certainly advisable. In order to be effective, such a diet should be supervised by repeated 24 hour collections of urine and determination of urinary acid excretion, as explained above. 

In a study with 40 healthy men and women, average age 63.7 years, who were randomized to either an alkali diet (meat plus fruits and vegetables) or an acid diet (meat plus cereal grains) (Jajoo and others 2006), altering the renal net acid excretion over a period of 60 days affected several biochemical markers of bone turnover and calcium excretion. The acidity of the diet had a significant effect on increasing NTX, a urinary marker of bone breakdown, and increasing the amount of calcium excreted in the urine. 

Prophylactic treatment can be withheld if the first episode of acute gouty arthritis was mild and responded promptly to treatment, the patient s serum urate concentration was only minimally elevated, and the 24-hour urinary uric acid excretion was not excessive (less than 1,000 mg/24 hours on a regular diet). 

Such acid and calcium excretion may be important in development of osteoporosis. To test diets of meat and vegetable protein upon urinary acid and calcium, nine human adults, aged 22 to 69 years, were fed isonitrogenous diets of chicken or soy beans in seven-day feeding periods. Diets provided daily ... 

The meat diet resulted in markedly greater titratable acid and calcium excretion compared with the soy diet (P<0.02). This occurred despite the fact that each diet contained the same amounts of protein, calcium, phosphorus, and sulfur. Increased urinary calcium excretion in subjects accompanied this increased output of TTA (P<0.02) ... 

Since this increased calcium loss, the quality of dietary protein may be important in conserving body calcium in the bone reservoir via the kidney. Human renal studies have corroborated animal data in-so-far as calcium excretion as influenced by urinary acidity is concerned. This was emphasized by Marone et al. (15) who reported increased excretion of calcium in the acidotic dog and by Zemel, et al. (27) who studied calcium filtration by the kidney. They fed subjects low or high-protein (50 or 150 g/d) diets, then compared... 

This phenomenon also had been reported in human subjects fed acid ash foods. Farquharson, et al. (33) fed a high-protein (200 g) diet to human subjects who promptly excreted more urinary acid and calcium. This occurred whether the protein level was raised to 200 g, or an equivalent amount of ammonium chloride was fed. If, on the other hand, the acid ash in the protein were neutralized with sodium bicarbonate, the hypercalciuria did not occur. 

Zinc and Ascorbic Acid Metabolism and Excretion. Iron has an oxidizing effect on ascorbic acid, reducing its urinary excretion therefore, Keltz et al. (61) questioned whether zinc would show a similar effect. Human subjects were fed a diet containing either 11.5 or 19.5 mg of zinc/d for 7-d balance periods. Daily ascorbic acid intake was 100 mg. Consistent with the findings from iron-loaded Africans, the higher zinc intake caused a significant 30% decrease in urinary ascorbate excretion. No explanation for the zinc-related reduction in ascorbic acid beyond the analogy with the iron-loaded individuals is readily available. 

After the first attack of acute gouty arthritis or after the passage of the first renal stone, a decision to institute prophylactic therapy must be entertained. If the first episode was mild and responded promptly to treatment, the patient s serum urate concentration was elevated only minimally, and the 24-hour urinary uric acid excretion was not excessive (<1000 mg/24 hours on a regular diet), then prophylactic treatment can be withheld. Some patients never have a second attack or a second stone. Others may not experience a second gouty episode for 5 to 10 years. Therefore a wait-and-see attitude seems justified in patients who meet these conditions. ... 

Stone formation appeared to depend on a deficiency of sulfur-containing amino acids. Increasing the protein content of the diet to 27 % or adding 1 % taurine to the diet increased urinary taurine excretion, increased con-... 

Table 2 Urinary uric acid excretion and concentration in Ca oxalate stone formers and healthy controls on individual diet. 

Classical orotic aciduria is a rare autosomal recessive disorder which is characterized by retarded growth and excretion of large quantities of orotic acid in the urine [221,222]. The disease was described in 1959 as an inborn error of pyrimidine biosynthesis in patients with crystals of orotic acid in the urine [223]. The urinary excretion of orotic acid by these patients was 1.34 g per day in contrast to approximately 0.014 g per day excreted by normal individuals [222,224]. When the diet of patients was supplemented with uridine, clinical remission and a remarkable reduction in orotic acid excretion took place [221,225,226]. 

The increased urinary PBG produced by rats after AIA administration was found to be enhanced by fasting and decreased by a carbohydrate diet [Rose et al.. 111]. DeMatteis [77] later found that the porphyria induced by AIA in rats could be completely suppressed by feeding glucose frequently, at a high level. The induced porphyria also caused a marked increase in ascorbic acid excretion, which, however, was not overcome by glucose. Actinomycin blocked the synthesis of ALA in rats treated with AIA but did not affect ascorbic acid production. 

The different responses to the administration of RNA and DNA demonstrate that not all dietary purines have the same effect on purine metabolism. Therefore, the values for total purines in conventional food tables are of restricted usefulness for dietary purposes. If further experiments should extend the finding that purines from different nucleic acids exert quantitatively different effects on plasma uric acid and uric acid excretion, a new and more detailed set of food tables would have to be constructed. Until then, the success of dietary prescriptions must be controlled by repeated determinations of plasma uric acid and urinary uric acid excretion, even if there is no doubt about adherence to diet. 

Pig. 1 Response of plasma uric acid level and urinary uric acid excretion to loads of RNA and DNA added to a purine free liquid fonnula diet. In the experiments with RNA the basal uric acid excretion on the purine free formula diet was larger than is generally our experience. 

Fig. 3 Correlation of plasma uric acid levels and urinary uric acid excretion during administration of RNA (00) and DNA (a a) in persons, who were normouricemic (filled symbols) or hyperuricemic(plasma uric acid above 6.5 mg/lOOml)(open symbols) on conventional diets.

All studies were conducted in the morning following an overnight fast. Medication known to effect the level of serum uric acid or urinary uric acid excretion was withdrawn at least 4 days prior to the studies. All subjects were maintained on a purine-free, low protein, isocaloric diet for at least 3 days prior to and throughout the studies. 

Reduced activities of carboxylase enzymes can cause a metabolic block of certain substrates and a use of alternative pathways for catabolism. Therefore, 3-hydroxyisovaleric acid and 3-methylcrotonyl glycine are formed consequently to a shunt of 3-methylcrotonyl carboxylase counterbalancing its activity decrease. Marginal biotin deficiency experimentally induced by 20 days of free biotin diets in human increased 3-hydroxyisovaleric acid excretion in urine above the upper limit of normal. The normal urinary excretion of 3-hydroxyisovaleric acid in healthy adults is 112 38 pmol per 24 hours (Mock et al. 1997). This suggests that 3-hydroxyisovaleric acid urinary excretion is a good indicator of marginal biotin deficiency. 

The administration of polychlorinated biphenyl (PCB) isomers increases hepatic tissue content of ascorbic acid as well as urinary excretion of ascorbic acid in the rat (Horio et al., 1986) and similarly increases the content of the major cytochrome P-450 enzymes induced by both phenobarbital and 3-methylcholanthrene (De-nomme et aL, 1983 Parkinson et ai, 1983). Guinea pigs fed an ascorbic acid-deficient diet have lower content of cytochrome P-450. A trend has been observed toward a higher cytochrome P-450 content with increasing dietary ascorbic acid, suggesting that ascorbic acid also influences drug metabolism (Peterson et al., 1983). 

---