sodium-bicarbonate and Metabolic-Diseases

Mineral and bone disorder (MBD) in chronic kidney disease (CKD) is associated with increased cardiovascular calcification and mortality. Pharmacological interventions for MBD in CKD are characterized by inconsistent data and a wide spectrum of (sometimes costly) treatment options. The objective of this article is a guideline-oriented overview of the differential indications for pharmacotherapy considering cost-effectiveness.. The serum phosphate concentration in patients with CKD stages 3-5 with a glomerular filtration rate (GFR) of < 45 ml/min should be kept within the normal range. Currently, under consideration of cost-effectiveness, calcium-containing phosphate binders and combinations of calcium acetate with magnesium carbonate are the preferred treatment options. Phosphate binders free of calcium are indicated in patients with high normal or elevated serum calcium levels. Low vitamin D concentrations in CKD stages 3-5 should be treated under consideration of serum calcium and parathyroid hormone (PTH) with calcidiol (25-cholecalciferol) and in dialysis patients (CKD 5D) with calcitriol (1,25 dihydroxycholecalciferol, activated vitamin D). In CKD the PTH levels should be kept in the range of 2-9-times the upper limit of normal levels. This is achieved by administration of phosphate binding drugs, activated vitamin D, calcimimetic compounds and parathyroidectomy. In CKD stages 3-5 patients metabolic acidosis with < 22 mmol/l serum bicarbonate should be treated with oral sodium bicarbonate.. In MBD of CKD patients an individualized pharmacotherapy which is closely guideline-oriented is required in order to achieve cost-effectiveness.

Topics: Bone Density Conservation Agents; Bone Diseases; Calcification, Physiologic; Calcimimetic Agents; Calcium; Germany; Humans; Metabolic Diseases; Practice Guidelines as Topic; Renal Insufficiency, Chronic; Sodium Bicarbonate; Vitamin D

There are no controlled trials on the efficacy of oral bicarbonate therapy in patients with mild to moderate chronic kidney disease (CKD). This prospective randomized controlled study was done to evaluate the effects of correction of metabolic acidosis on renal functions and bone metabolism in this group of patients.. Forty patients were randomized to treatment with oral bicarbonate or placebo for a period of 3 months. Investigations at baseline included venous pH, bicarbonate, renal functions, serum iPTH, and bone radiology. The treatment group (Group B) received daily oral sodium bicarbonate therapy at a dose of 1.2 mEq/kg of body weight. Their venous blood pH and bicarbonate levels were estimated weekly to keep blood pH near 7.36 and bicarbonate at 22-26 mEq/L by adjusting the dose of sodium bicarbonate. At the end of 3 months, all the tests were repeated in both groups.. After oral bicarbonate therapy (OBT), there was a significant decline in the rise of blood urea level in Group B associated with a sense of well-being in 50% patients. The rise in parathormone (PTH) was six times the baseline value in Group A and only 1.5 times baseline value in Group B, although not statistically significant. There was no significant change in total calcium, phosphorus, alkaline phosphatase, creatinine, total protein, or albumin levels.. Correction of metabolic acidosis in patients with moderate CKD attenuates the rise in blood urea and PTH, which might prevent the deleterious long-term consequences of secondary hyperparathyroidism.

Topics: Acidosis; Adult; Aged; Bone and Bones; Chronic Disease; Female; Humans; Kidney Diseases; Male; Metabolic Diseases; Middle Aged; Prospective Studies; Severity of Illness Index; Single-Blind Method; Sodium Bicarbonate; Urea

Acid hydrolysis of components from the diet in the stomach require the presence of an acid and a hydrolysing agent. The acid involved is hydrochloric acid. The present mechanism of hydrochloric acid production in the stomach is demonstrated to be incompatible with measured intracellular or intercellular concentrations of the relevant ions. An alternative set of chemical reactions whereby hydrochloric acid is formed in the stomach is presented. The hydrolysing agent is identified and a mechanism of transfer of chemical compounds into the metabolism is described. The hypothesis demonstrates that some of chemical compounds produced in the stomach can induce conditions such as asthma and that the conditions of osteoporosis and hemochromatosis can be linked to the function of the stomach. Possible treatments for these and other conditions such as stomach acidity and anaemia are proposed.

Topics: Adult; Ammonia; Antacids; Asthma; Bicarbonates; Calcium Chloride; Calcium Phosphates; Chlorides; Digestion; Ferric Compounds; Ferrous Compounds; Gastric Acid; Gastric Juice; Gastric Mucosa; Gastritis; Gastrointestinal Contents; Helicobacter Infections; Helicobacter pylori; Hemochromatosis; Humans; Hydrolysis; Ion Transport; Metabolic Diseases; Models, Biological; Models, Chemical; Nitrous Oxide; Osteoporosis; Parietal Cells, Gastric; Sodium Bicarbonate; Stomach

Topics: Absorption; Adrenal Cortex Hormones; Aluminum Hydroxide; Antacids; Bicarbonates; Biological Availability; Calcium Carbonate; Dicumarol; Drug Interactions; Humans; Metabolic Diseases; Quinidine; Salicylates; Sodium Bicarbonate; Tetracyclines; Warfarin

Sixteen patients with asymptomatic hyperuricaemia were treated with "Citro-Soda', an urinary alkanlinizing agent, in a dose of 4 g four times daily for one month. Ten of the sixteen patients exhibited a meaningful reduction in serum uric acid (greater than 15%). No adverse effects were noted and various haematological and urinary tests were all normal. 'Citro-Soda' could, therefore, be considered a useful and well-tolerated adjunct in the treatment of hyperuricaemia.

Topics: Bicarbonates; Citrates; Citric Acid; Drug Combinations; Female; Humans; Male; Metabolic Diseases; Sodium Bicarbonate; Tartrates; Uric Acid