allopurinol and Hypokalemia

Fructose is a commonly used sweetener associated with diets that increase the prevalence of metabolic syndrome. Thiazide diuretics are frequently used in these patients for treatment of hypertension, but they also exacerbate metabolic syndrome. Rats on high-fructose diets that are given thiazides exhibit potassium depletion and hyperuricemia. Potassium supplementation improves their insulin resistance and hypertension, whereas allopurinol reduces serum levels of uric acid and ameliorates hypertension, hypertriglyceridemia, hyperglycemia, and insulin resistance. Both potassium supplementation and treatment with allopurinol also increase urinary nitric oxide excretion. We suggest that potassium depletion and hyperuricemia in rats exacerbates endothelial dysfunction and lowers the bioavailability of nitric oxide, which blocks insulin activity and causes insulin resistance during thiazide usage. Addition of potassium supplements and allopurinol with thiazides might be helpful in the management of metabolic syndrome.

Topics: Allopurinol; Animals; Blood Pressure; Body Weight; Diuretics; Fructose; Gout Suppressants; Hydrochlorothiazide; Hyperglycemia; Hypertension; Hypertriglyceridemia; Hyperuricemia; Hypokalemia; Insulin; Insulin Resistance; Kidney; Male; Metabolic Syndrome; Nitric Oxide; Potassium; Rats; Rats, Sprague-Dawley; Sodium; Uric Acid

Two patients with chronic sialoadenitis had features of Bartter's and Gitelman's syndrome, respectively. The main complaints were leg paraesthesiae and acute arthritis. A good response to oral K+ supplementation, allopurinol and low-dose prednisone was obtained. The features of Sjögren's-related renal diseases are reviewed.

Topics: Adult; Aged; Alkalosis; Allopurinol; Anti-Inflammatory Agents; Antimetabolites; Bartter Syndrome; Calcium; Chronic Disease; Dose-Response Relationship, Drug; Female; Humans; Hypokalemia; Magnesium; Potassium; Prednisone; Sialadenitis; Sjogren's Syndrome; Syndrome

Particle-free extracts prepared from kidney cortex of rat catalyze the formation of ammonia via the purine nucleotide cycle. The cycle generates ammonia and fumarate from aspartate, using catalytic amounts of inosine monophosphate, adenylosuccinate, and adenosine monophosphate. The specific activities of the enzymes of the cycle are 1.27+/-0.27 nmol/mg protein per min (SE) for adenoylosuccinate synthetase, 1.38+/-0.16 for adenylosuccinase, and 44.0+/-3.3 for AMP deaminase. Compared with controls, extracts prepared from kidneys of rats fed ammonium chloride for 2 days show a 60% increase in adenylosuccinate synthetase and a threefold increase in adenylosuccinase activity, and a greater and more rapid synthesis of ammonia and adenine nucleotide from aspartate and inosine monophosphate. Extracts prepared from kidneys of rats fed a potassium-deficient diet show a twofold increase in adenylosuccinate synthetase and a threefold increase in adenylosuccinase activity. In such extracts the rate of synthesis of ammonia and adenine nucleotide from aspartate and inosine monophosphate is also increased. These results show that the reactions of the purine nucleotide cycle are present and can operate in extracts of kidney cortex. The operational capacity of the cycle is accelerated by ammonium chloride feeding and potassium depletion, conditions known to increase renal ammonia excretion. Extracts of kidney cortex convert inosine monophosphate to uric acid. This is prevented by addition of allopurinol of 1-pyrophosphoryl ribose 5-phosphate to the reaction mixture.

Topics: Adenine Nucleotides; Allopurinol; Ammonia; Ammonium Chloride; AMP Deaminase; Animals; Aspartic Acid; Edetic Acid; Hypokalemia; In Vitro Techniques; Inosine Nucleotides; Kidney; Kidney Cortex; Male; Purine Nucleotides; Rats; Tissue Extracts; Uric Acid