Urinary alkalization

Urinary alkalinization- Urates tend to crystallize out of an acid urine therefore, a liberal fluid intake is recommended, as well as sufficient sodium bicarbonate (3 to 7.5 g/day) or potassium citrate (7.5 g/day) to maintain an alkaline urine continue alkalization until the serum uric acid level returns to normal limits and tophaceous deposits disappear. Thereafter, urinary alkalization and the restriction of purine-producing foods may be relaxed. 

Beard TC, Wilkinson SJ, Vial JH. Hazards of urinary alkalizing agents. MedJ Aust (1988) 149, 723. 

In both sexes, CCM-OJ provided an alkali load that significantly increased urinary pH compared to basal levels and versus milk consumption, and also increased urinary citrate excretion versus basal levels. An elevated urine pH and citrate level are generally considered to reduce Ca oxalate supersaturation and crystallization potential (Odvina, 2006). However, in this study the relative supersaturation measurement for Ca oxalate was not different between the CCM-OJ and milk treatment groups, or between either treatment and the basal levels. Although the alkalizing effect of milk was less than that of CCM-OJ, it also induced a higher urinary pH compared to basal levels (p <. 01 and p <. 05 in women and men, respectively). 

B. Proteus species produce urease (A) that produces ammonia and urea, alkalizing urine. Urine requires acidification for effective therapy. Hippuric (B), mandelic, or ascorbic acids or methionine are urinary acidifying agents. The normal acidic urinary environment is disturbed by recurrent Proteus in-... 

In the absence of allopurinol, the dominant urinary purine is uric acid. During allopurinol treatment, the urinary purines include hypoxanthine, xanthine, and uric acid. Since each has its independent solubility, the concentration of uric acid in plasma is reduced and purine excretion increased, without exposing the urinary tract to an excessive load of uric acid. Despite their increased concentrations during allopurinol therapy, hypoxanthine and xanthine are efficiently excreted, and tissue deposition does not occur. There is a small risk of xanthine stones in patients with a very high urate load before allopurinol therapy this can be minimized by liberal fluid intake and urine alkalization. 

Ketosis— The most common causes of this condition— which is characterized by an excess of ketones in the blood— are (1) diabetes (2) diets high in fat and protein, but low in carbohydrate (3) fevers and (4) starvation. A mild ketosis in normally healthy people is usually not dangerous, unless it occurs regularly over a long period of time, flien, it may lead to such problems as (1) excessive urinary loss of sodium and water (2) acidosis which provokes the loss of calcium from bone, and potassium from muscle and (3) the accumulation of uric acid (a waste product of protein metabolism) in the blood, and sometimes in the soft tissues where it causes damage and pain (the latter disorder is commonly called gout). Uric acid buildup is usually treated with alkalizers to prevent the formation of kidney stones. However, the alkalizers may cause other alterations in mineral metabolism. 

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