sodium-bicarbonate and Hypoalbuminemia

Metabolic acidosis is a frequent complication of chronic kidney disease. Although it is known to appear at advanced stages, many studies suggest a state of "global protonic retention" starting at early stages of the disease, responsible of tissue damage, particularly musculoskeletal, alteration of protidic metabolism and endocrine disorders, promoting malnutrition and chronic inflammation, and finally increasing mortality. The majority of international recommandations suggest of supplementation by alkali, most of the time by sodium bicarbonate, to struggle against this complication. An interesting alternative to correct acidosis would consist on the modulation of the endogenous production of acid by playing with the alimentary incomes. In fact, it has been demonstrated that some different types of food produce or consume protons during their metabolism. Low protein diet and rich fresh fruits and vegetables diet would manage to correct at least as well as the supplementation by sodium bicarbonate the metabolic acidosis, and to struggle against its complications, noteworthy by slowing the decline of glomerular filtration rate by limiting the toxic adaptative fibrotic mechanisms, demonstrated by the decrease of urinary tubulo-interstitial suffering markers. Of the condition of being well led, those diets do not seem to expose patients to an over-risk of malnutrition or hyperkaliemia. They therefore appear to be an attractive alternative, efficiency and safe, to fight against chronic kidney disease metabolic acidosis and its complications.

Topics: Acidosis; Chronic Kidney Disease-Mineral and Bone Disorder; Combined Modality Therapy; Diet, Protein-Restricted; Dietary Proteins; Fruit; Humans; Hyperkalemia; Hypoalbuminemia; Inflammation; Malnutrition; Nutrition Policy; Protons; Renal Insufficiency, Chronic; Sarcopenia; Sodium Bicarbonate; Vegetables

Our objective was to study the risk factors and mechanisms of hypernatraemia in critically ill patients, a common and potentially serious problem.. In 2005, all patients admitted to the medical, surgical or neurological intensive care unit (ICU) of a university hospital were reviewed. A 1:2 matched case-control study was performed, defining cases as patients who developed a serum sodium >/=150 mmol/l in the ICU.. One hundred and thirty cases with ICU-acquired hypernatraemia (141 +/- 3 to 156 +/- 6 mmol/l) were compared to 260 controls. Sepsis (9% versus 2%), hypokalaemia (53% versus 34%), renal dysfunction (53% versus 13%), hypoalbuminaemia (91% versus 55%), the use of mannitol (10% versus 1%) and use of sodium bicarbonate (23% versus 0.4%) were more common in cases (P < 0.05 for all) and were independently associated with hypernatraemia. During the development of hypernatraemia, fluid balance was negative in 80 cases (-31 +/- 2 ml/kg/day), but positive in 50 cases (72 +/- 3 ml/kg/day). Cases with a positive fluid balance received more sodium plus potassium (148 +/- 2 versus 133 +/- 3 mmol/l, P < 0.001). On average, cases were polyuric (40 +/- 5 ml/kg). Mortality was higher in cases (48% versus 10%, P < 0.001), for which hypernatraemia was an independent predictor (odds ratio 4.3, 95% confidence interval 2.5 to 7.2).. Hypernatraemia seems to develop in the ICU because various factors promote renal water loss, which is then corrected with too little water or overcorrected with relatively hypertonic fluids. Therapy should therefore rely on adding electrolyte-free water and/or creating a negative sodium balance. Adjustments in intravenous fluid regimens may prevent hypernatraemia.

Topics: Adult; Aged; Case-Control Studies; Critical Illness; Female; Fluid Therapy; Humans; Hypernatremia; Hypoalbuminemia; Hypokalemia; Intensive Care Units; Kidney Diseases; Male; Mannitol; Middle Aged; Risk Factors; Sepsis; Sodium Bicarbonate; Water-Electrolyte Balance