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From http://www.arabmedmag.com/issue-31-05-2007/urology/main03.htm

MEDICAL MANAGEMENT

 

One factor that contributes to uric acid stone formation is the total amount of uric acid to be eliminated. Minimizing dietary animal protein intake will decrease exogenous sources and help patients whose primary cause for uric acid stone is purine gluttony. Endogenous purine production can oversaturate the kidney's elimination capacity in a patient with a myeloproliferative disorder or a malignancy, or who is undergoing chemotherapy, or who has experienced massive weight loss after gastric bypass surgery, or who is in a catabolic state. To prevent uric acid stone formation, manipulation of urinary volume, urinary acidity, and uric acid production are necessary.

 

 

Urinary volume. Increasing urinary volume makes intuitive sense since doubling urinary volume will double the amount of urate species that the kidneys can excrete. Clinically, this may be simple to achieve in compliant patients whose primary problem is low dietary fluid intake. For most, only modest increases in 24-hour urine output (500 mL/d) can be achieved in the outpatient setting. For inpatients undergoing chemotherapy where tumor lysis and high endogenous uric acid production are anticipated, aggressive intravenous hydration will help minimize risk of uric acid supersaturation. In patients with inflammatory bowel disease, chronic diarrhea, or ileostomy bowel diversion, dehydration continues to be a major problem.

 

 

Urinary acidity. The most important factor in the pathogenesis of uric acid stones is urinary acidity. Uric acid saturation is pH-dependent and, as such, patients with metabolic acidosis or any metabolic state leading to acidic urine will be at increased risk for stone formation.

 

Within the distal nephron, acid is primarily excreted in the form of ammonium: NH 3 + H + ↔NH 4 +

 

A defect in ammonium excretion may be a mechanism for acidic urine in patients with uric acid stones, obesity, insulin-resistance, or diabetes.11,14,18,19

 

 

Diets rich in animal proteins are not only high in purine but also high in organic acids. It has been shown that popular weight loss diets that are high in animal protein and low in carbohydrates (for example, Atkins or South Beach) are associated with marked acid loads to the kidneys, putting patients with uric acid stones at increased risk for recurrence.

 

 

The mainstay of medical management continues to be urinary alkalization. Unlike increasing urinary volume, where the uric acid solubility relationship is linear, uric acid saturation increases exponentially with increasing urinary pH. For example, increasing the urinary pH level from 5 to 7 can increase the amount of dissolvable urate species 24-fold.

 

The goal of urinary alkalization is to achieve a urinary pH level between 6 and 6.5. Higher pH levels should be avoided as calcium phosphate may precipitate.

 

 

Clinically, alkalization can be achieved with sodium bicarbonate (650 mg, 3 times a day) or with commercial baking soda (1 to 2 teaspoons, 3 times a day).22 Patients should check their urinary pH levels at home with pH test strips until a consistently alkaline pH is noted. For patients with congestive heart failure, cirrhosis, or hypertension, in whom a sodium load may not be tolerated, potassium citrate (10 to 20 mEq, 3 times a day) is effective.23 Use of oral alkalization for uric acid stone dissolution is effective, with success rates ranging from 70% to 80%. With optimal alkalization, uric acid stones will dissolve at a rate of approximately 1 cm per month as measured by plain radiography (IVP). The treating physician must remember that patient education and motivation are critical to success.24

 

 

In the postsurgical setting where small residual fragments remain after percutaneous nephrolithotomy, intravenous alkalization with one sixth molar sodium lactate and direct nephrostomy tube irrigation with alkaline fluid can be used. Similarly, alkalization after shock wave lithotripsy can be effective in dissolving stone fragments. Nevertheless, with advances in endourologic techniques, the practice of prolonged chemolysis is not cost effective.25

 

 

 

 

From http://www.scientificpsychic.com/health/gout.html

Why do alcoholic beverages trigger episodes of gout? One reason is that uric acid is insoluble in alcohol.[1] As the alcohol content of the blood increases, the blood is not able to dissolve as much uric acid, and the excess crystalizes. Gout problems are compounded because acute and chronic alcohol consumption impair the function of the kidneys. Alcohol increases purine catabolism in the liver and increases the formation of lactic acid which blocks urate secretion by the renal tubules. Excessive alcohol consumption can have severe negative effects in the ability of the kidneys to maintain the body's fluid, electrolyte, and acid-base balance.[7]

 

Niacin, also known as nicotinic acid or vitamin B3, has been used for many years to treat hyperlipidemia because it reduces total cholesterol, low density lipoprotein cholesterol (LDL) and triglycerides while it increases high density lipoprotein cholesterol (HDL). Elevated uric acid levels have occurred with niacin therapy, and the high dosages required for this treatment are associated with toxic side effects that include worsening of diabetes control and exacerbation of peptic ulcer disease and gout.[14]

 

A study of 46,393 men with no history of gout found that, during 12 years of follow-up, 755 eventually developed gout in direct proportion to the consumption of sugar-sweetened soft drinks.[16] The risk of gout was related to the amount of fructose consumed. Men who consumed two or more servings of sugary drinks per day had an 85% greater risk of developing gout. Fruit juices rich in fructose such as apple juice or orange juice were also associated with a higher risk of gout. Diet soft drinks were not associated with risk of gout.

 

Effect of Temperature and pH on Uric Acid Solubility
The solubility of monosodium urate is a function of temperature. At normal body temperature, 37°C (98.6°F), the maximum solubility of urate in physiologic saline is 6.8 mg per 100 ml, but at 30°C (86°F) it is only 4.5 mg per 100 ml.[2] Several studies have shown that gout attacks are more frequent in springtime.[12, 13] This may be due to the accumulation of monosodium urate crystals in the extremities during the cold winter months.

 

Uric acid also has higher solubility in solutions of alkali hydroxides and their carbonates than in acidic media. Acidity and alkalinity is measured using the pH (potential of Hydrogen) scale, which ranges from 0 for the most acidic solutions to 14 for the most alkaline solutions. The mid-point at pH 7 is neutral (neither acid, nor alkaline). In acid urine of pH less than 5.5, uric acid crystals precipitate and lead to stone formation. If the urine is neutral or alkaline, uric acid remains in solution and does not precipitate. At 37°C and pH 6.6, the solubility of uric acid is 6 mg per 100 ml, whereas at pH 7.0, uric acid is almost three times more soluble and forms stable solutions at concentrations of 16 mg per 100 ml.[15] Hydration with bicarbonate solutions has been effective in managing uric acid stones.[4]

 

Home Treatment for Gout
The elimination of uric acid from the body may be increased using a combined approach consisting of

Warming the joints may be accomplished with a foot bath or a heating pad. Hydration requires increasing the volume of drinking water to promote more frequent urination. The advice to drink eight glasses of water per day is based on the general recommendations of the Institute of Medicine which advises that men should consume roughly 3.0 liters (about 13 cups) and women should consume 2.2 liters (about 9 cups) of total water from all beverages and foods.

WIEL

 

 

 

 

This is a reply to # 1,627,980

 

Uric Acid, Fructose and Hypertension