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Sodium Bicarbonate Infusion In Metabolic Acidosis

Review Article Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

Review Article Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

Correspondence should be addressed to Mar Received July ; Revised September ; Accepted September ; Published October a M. Adeva-Andany et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no denite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is benecial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this eect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buer used in dialysis uids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suering a transient metabolic alkalosis of variable severity. Side eects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. e potential impact of regular sodium bicarbonate therapy on worsening vascular calcications in patients with chronic kidney disease has been insuciently i Continue reading >>

Sodium Bicarbonate Use

Sodium Bicarbonate Use

metabolic acidosis leads to adverse cardiovascular effects bicarbonate must be administered in a solution as sodium bicarbonate 8.4% solution contains 1mmol of HCO3-/mL and is very hypertonic (2,000mOsm/kg) goal of NaHCO3 administration in severe metabolic acidosis to counteract the negative cardiovascular effects of acidaemia alternatives to NaHCO3 include carbicarb, dichloroacetate, Tris/THAM Treatment of sodium channel blocker overdose (e.g. tricyclic overdose) Urinary alkalinisation (salicylate poisoning) Metabolic acidosis (NAGMA) due to HCO3 loss (RTA, fistula losses) Cardiac arrest (in prolonged resuscitation + documented severe metabolic acidosis) Diabetic ketoacidosis (very rarely, perhaps if shocked and pH < 6.8) Severe pulmonary hypertension with RVF to optimize RV function Severe ischemic heart disease where lactic acidosis is thought to be an arrhythmogenic risk hypernatraemia (1mmol of Na+ for every 1mmol of HCO3-) hyperosmolality (cause arterial vasodilation and hypotension) impaired oxygen unloading due to left shift of the oxyhaemoglobin dissociation curve removal of acidotic inhibition of glycolysis by increased activity of PFK hypercapnia (CO2 readily passes intracellularly and worsens intracellular acidosis) severe tissue necrosis if extravasation takes place bicarbonate increases lactate production by: increasing the activity of the rate limiting enzyme phosphofructokinase and removal of acidotic inhibition of glycolysis shifts Hb-O2 dissociation curve, increased oxygen affinity of haemoglobin and thereby decreases oxygen delivery to tissues POINTS TO REMEMBER WHEN USING BICARBONATE it is generally better to correct underlying cause of acidosis and give supportive care than to give sodium bicarbonate ensure adequate ventilation to eliminate CO2 pro Continue reading >>

Sodium Bicarbonate (sodium Bicarbonate 5% Injection): Side Effects, Interactions, Warning, Dosage & Uses

Sodium Bicarbonate (sodium Bicarbonate 5% Injection): Side Effects, Interactions, Warning, Dosage & Uses

Sodium Bicarbonate (sodium bicarbonate 5% injection) Injection may be indicated in the treatment of metabolic acidosis which can occur in severe renal disease, uncontrolled diabetes , circulatory insufficiency due to shock , anoxia or severe dehydration, extracorporeal circulation of blood and severe primary lactic acidosis . Sodium Bicarbonate (sodium bicarbonate 5% injection) Injection is further indicated in the treatment of certain drug intoxications, including barbiturates, in poisoning by salicylates or methyl alcohol, and in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of blood pigments. Sodium Bicarbonate (sodium bicarbonate 5% injection) Injection may also be indicated in severe diarrhea which is often accompanied by a significant loss of bicarbonate. As directed by a physician. Dosage is dependent upon the age, weight and clinical condition of the patient as well as laboratory determinations. For mild acidosis, the usual dosage is 1 to 2 mEq per kg of body weight, administered slowly. For more severe acidosis, 2 to 5 mEq per kg of body weight may be administered over a 4 to 8 hour period. Subsequent therapy is dependent on the clinical response of the patient. In emergencies, 300 to 500 mL of the 5% Sodium Bicarbonate (sodium bicarbonate 5% injection) Injection should or administered as rapidly as is possible without overalkalinizing the patient. Generally, to avoid overalkalinizing a patient whose own body mechanisms for correcting metabolic acidosis may be maximally stimulated, only 1/3 to 1/2 of the calculated dose is administered as rapidly as indicated by the patient's cardiovascular and fluid balance status. The serum pH and bicarbonate concentration should then be redetermined. Parenteral drug products should be Continue reading >>

8.7 Use Of Bicarbonate In Metabolic Acidosis

8.7 Use Of Bicarbonate In Metabolic Acidosis

8.7 Use of Bicarbonate in Metabolic Acidosis Metabolic acidosis causes adverse metabolic effects (see Section 5.4 ). In particular the adverse effects on the cardiovascular system may cause serious clinical problems. Bicarbonate is an anion and cannot be given alone. Its therapeutic use is as a solution of sodium bicarbonate. An 8.4% solution is a molar solution (ie it contains 1mmol of HCO3- per ml) and is the concentration clinically available in Australia. This solution is very hypertonic (osmolality is 2,000 mOsm/kg). The main goal of alkali therapy is to counteract the extracellular acidaemia with the aim of reversing or avoiding the adverse clinical effects of the acidosis (esp the adverse cardiovascular effects). Other reasons for use of bicarbonate in some cases of acidosis are: to promote alkaline diuresis (eg to hasten salicylate excretion) 8.7.2 Undesirable effects of bicarbonate administration In general, the severity of these effects are related to the amount of bicarbonate used. These undesirable effects include: 8.7.3 Important points about bicarbonate 1. Ventilation must be adequate to eliminate the CO2 produced from bicarbonate Bicarbonate decreases H+ by reacting with it to to produce CO2 and water. For this reaction to continue the product (CO2) must be removed. So bicarbonate therapy can increase extracellular pH only if ventilation is adequate to remove the CO2. Indeed if hypercapnia occurs then as CO2 crosses cell membranes easily, intracellular pH may decrease even further with further deterioration of cellular function. 2. Bicarbonate may cause clinical deterioration if tissue hypoxia is present If tissue hypoxia is present, then the use of bicarbonate may be particularly disadvantageous due to increased lactate production (removal of acidotic i Continue reading >>

Sodium Bicarbonate Dosage

Sodium Bicarbonate Dosage

If acid-base status is available, dosages should be calculated as follows: 0.2 x weight (kg) x base deficit. HCO3 (mEq) required = 0.5 x weight (kg) x [24 - serum HCO3 (mEq/L)]. Moderate metabolic acidosis: 50 to 150 mEq sodium bicarbonate diluted in 1 L of D5W to be intravenously infused at a rate of 1 to 1.5 L/hour during the first hour. Severe metabolic acidosis: 90 to 180 mEq sodium bicarbonate diluted in 1 L of D5W to be intravenously infused at a rate of 1 to 1.5 L/hour during the first hour. If acid-base status is not available, dosages should be calculated as follows: 2 to 5 mEq/kg IV infusion over 4 to 8 hours; subsequent doses should be based on patient's acid-base status. Moderate metabolic acidosis: 325 to 2000 mg orally 1 to 4 times a day. One gram provides 11.9 mEq (mmoL) each of sodium and bicarbonate. Usual Adult Dose for Diabetic Ketoacidosis Although sodium bicarbonate is approved for the treatment of metabolic acidosis, data have shown that the use of this drug may be harmful in certain clinical settings such as lactic acidosis, acidosis with tissue hypoxia, uremia, severe cardiac dysfunction or arrest, and diabetic ketoacidosis. Most experts only allow for its use when tissue perfusion and ventilation are maximized and the arterial pH is 7.1 or lower. If sodium bicarbonate is used to treat diabetic ketoacidosis, the initial dosage is 50 mEq sodium bicarbonate in 1 L of appropriate IV solution to be given once. Insulin therapy may obviate the need for bicarbonate therapy since it will promote glucose utilization and decrease the production of ketoacids. Usual Adult Dose for Urinary Alkalinization 50 to 150 mEq sodium bicarbonate diluted in 1 L of D5W to be intravenously infused at a rate of 1 to 1.5 L/hour. 325 to 2000 mg orally 1 to 4 times a day. O Continue reading >>

Intravenous Sodium Bicarbonate

Intravenous Sodium Bicarbonate

Robin Gross, William Peruzzi, in Critical Care Medicine (Third Edition) , 2008 Intravenous sodium bicarbonate (NaHCO3) solution is an appropriate intervention for reversing metabolic acidemia, provided that lung and cardiac function are adequate. NaHCO3 solution adds HCO3 to the blood only after the CO2 load inherent in the NaHCO3 solution is eliminated by the lungs. When NaHCO3 solution is administered to a patient with acute ventilatory failure (respiratory acidosis), the Paco2 usually increases, and pH decreases because the CO2 load cannot be eliminated. As illustrated in Figure 14-8, low cardiac output may be a limiting factor in CO2 excretion. When NaHCO3 solution is administered to a patient with very poor cardiac output, the venous blood shows a paradoxical respiratory acidosis. When NaHCO3 is administered intravenously to correct severe metabolic acidemia, it is essential to quantify the abnormality as a guide to therapy. A simple way to calculate the amount of bicarbonate to administer is: mmol HCO3 = base deficit (mmol/L) ideal weight (kg) 0.25 (L/kg) where 0.25 represents the volume of distribution of the bicarbonate. It is generally prudent to administer one half to one third of the calculated deficit, obtain another ABG sample in 5 minutes, and re-evaluate. In Pocket Companion to Brenner and Rector's The Kidney (Eighth Edition) , 2011 In cases of intractable shock, metabolic acidosis may persist despite volume expansion and improved oxygen delivery. Intravenous bicarbonate is often used in this setting in an attempt to improve cardiac function. However, decreased cardiac contractility in the setting of lactic acidosis may be partially due to hypoxemia, hypoperfusion, or sepsis, and establishing the direct effects of the low pH is difficult. Many patients t Continue reading >>

Therapy Of Lactic Acidosis: Alternatives To Sodium Bicarbonate

Therapy Of Lactic Acidosis: Alternatives To Sodium Bicarbonate

Therapy of Lactic Acidosis: Alternatives to Sodium Bicarbonate Part of the Clinical Physiology Series book series (CLINPHY) Lactic acidosis is the most common form of metabolic acidosis, and the current mortality from this condition is in excess of 50%. Because of its diverse pathophysiology, the clinical management of lactic acidosis is difficult. The mainstay of therapy has traditionally been the intravenous administration of sodium bicarbonate (NaHCO3), but recent clinical and experimental evidence strongly suggests that such therapy may in fact be detrimental. Lactic acidosis is generally defined as a metabolic acidosis due to the accumulation of lactic acid in the blood in excess of 5 mM, with an accompanying blood pH of less than 7.25. However, the mechanisms by which lactic acid accumulation occurs vary and include both the stimulation of lactate production and reductions of lactate metabolism. Clinically, the disorders of lactate metabolism are conveniently divided as either anaerobic (type A) or aerobic (type B) (16). The hallmark of type A lactic acidosis is tissue hypoxia, resulting in anaerobic lactic acid production. The most common causes of type A lactic acidosis are cardiopulmonary arrest and other states characterized by impaired cardiac performance, reduced tissue perfusion, and arterial hypoxemia. In these states, the hypoxia and circulatory insufficiency combine to reduce tissue oxygen availability, resulting in anaerobic metabolism and stimulation of lactic acid production. In type B lactic acidosis, on the other hand, tissue hypoxia appears not to be present, and lactic acid production is metabolically enhanced for other reasons in what is apparently an aerobic state. Examples of type B lactic acidosis include diabetes mellitus, certain malignanci Continue reading >>

Intravenous Sodium Bicarbonate

Intravenous Sodium Bicarbonate

Intravenous sodium bicarbonate, also known as sodium hydrogen carbonate, is a medication primarily used to treat severe metabolic acidosis . [1] For this purpose it is generally only used when the pH is less than 7.1 and when the underlying cause is either diarrhea , vomiting , or the kidneys . [2] Other uses include high blood potassium , tricyclic antidepressant overdose , and cocaine toxicity as well as a number of other poisonings . [1] [3] [4] It is given by injection into a vein . [2] Side effects may include low blood potassium , high blood sodium , and swelling . [1] [4] It is not recommended in people with low blood calcium . [5] Sodium bicarbonate is in the alkalinizing family of medication. [5] It works by increasing blood bicarbonate , which buffers excess hydrogen ion and raises blood pH . [5] Commercial production of sodium bicarbonate began between 1791 and 1823. [6] Intravenous medical use began around the 1950s. [4] It is on the World Health Organization's List of Essential Medicines , the most effective and safe medicines needed in a health system . [7] Sodium bicarbonate is available as a generic medication . [5] The wholesale cost in the developing world is about 0.09 to 2.58 USD per 10 ml of 8.4% solution. [8] In the United Kingdom this amount costs the NHS about 11.10 pounds. [2] Intravenous sodium bicarbonate is indicated in the treatment of metabolic acidosis , such as can occur in severe kidney disease , diabetic ketoacidosis , circulatory insufficiency , extracorporeal circulation of blood, in hemolysis requiring alkalinization of the urine to avoid nephrotoxicity of blood pigments, and certain drug intoxications , such as by barbiturate overdose , salicylate poisoning , tricyclic antidepressant overdose or methanol poisoning . [9] In addition Continue reading >>

Sodium Bicarbonate In The Critically Ill Patient With Metabolic Acidosis

Sodium Bicarbonate In The Critically Ill Patient With Metabolic Acidosis

Sodium bicarbonate in the critically Ill patient with metabolic acidosis Uso de bicarbonato de sdio na acidose metablica do paciente gravemente enfermo Lactic acidosis is an acid-base imbalance frequently found in critically ill patients. It is associated with a poor prognosis. Despite the substantial body of evidence that critical levels of acidemia have several adverse effects on cell function, the use of sodium bicarbonate to treat lactic acidosis in critically ill patients remains highly controversial. This article aimed at: 1) analyzing the main differences between hyperchloremic and organic acidoses, with high anion gap; 2) comparing the risks associated with critical levels of acidemia with those associated with the use of sodium bicarbonate; 3) critically analyzing the literature evidence about the use of sodium bicarbonate for the treatment of lactic acidosis in critically ill patients, with an emphasis on randomized control trials in human beings; and 4) providing a rationale for the judicious use of sodium bicarbonate in that situation. Descriptors: lactic acidosis, diabetic ketoacidosis, sodium bicarbonate, septic shock. A acidose ltica um distrbio do equilbrio cido-base muito frequente em pacientes internados em unidades de terapia intensiva e est associado a um mau prognstico. Embora exista um acmulo substancial de evidncias de que nveis crticos de acidemia provocam inmeros efeitos adversos sobre o funcionamento celular, a utilizao de bicarbonato de sdio para o tratamento da acidose ltica em pacientes gravemente enfermos permanece alvo de controvrsias. Neste artigo, pretendemos: 1) analisar as principais diferenas entre as acidoses hiperclormicas e as acidoses orgnicas, com nion gap (AG) elevado, visando embasar a discusso sobre os fundamentos da terapia Continue reading >>

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

The Scientific World Journal Volume 2014 (2014), Article ID 627673, 13 pages Nephrology Division, Hospital General Juan Cardona, Avenida Pardo Bazán, s/n, Ferrol, 15406 A Coruña, Spain Academic Editor: Biagio R. Di Iorio Copyright © 2014 María M. Adeva-Andany et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc inter Continue reading >>

Bicarbonate Therapy In Severe Metabolic Acidosis

Bicarbonate Therapy In Severe Metabolic Acidosis

Abstract The utility of bicarbonate administration to patients with severe metabolic acidosis remains controversial. Chronic bicarbonate replacement is obviously indicated for patients who continue to lose bicarbonate in the ambulatory setting, particularly patients with renal tubular acidosis syndromes or diarrhea. In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted back to bicarbonate if the clinical situation improves. For these patients, therapy must be individualized. In general, bicarbonate should be given at an arterial blood pH of ≤7.0. The amount given should be what is calculated to bring the pH up to 7.2. The urge to give bicarbonate to a patient with severe acidemia is apt to be all but irresistible. Intervention should be restrained, however, unless the clinical situation clearly suggests benefit. Here we discuss the pros and cons of bicarbonate therapy for patients with severe metabolic acidosis. Metabolic acidosis is an acid-base disorder characterized by a primary consumption of body buffers including a fall in blood bicarbonate concentration. There are many causes (Table 1), and there are multiple mechanisms that minimize the fall in arterial pH. A patient with metabolic acidosis may have a normal or even high pH if there is another primary, contravening event that raises the bicarbonate concentration (vomiting) or lowers the arterial Pco2 (respiratory alkalosis). Metabolic acidosis differs from “acidemia” in that the latter refers solely to a fall in blood pH and not the process. A recent online survey by Kraut and Kurtz1 highlighted the uncertainty over when to give bicarbonate to patients with metabolic acidosis. They reported that nephrologists will prescribe therapy at a higher pH compared with Continue reading >>

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic AcidosisTreatment & Management Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN more... Treatment of acute metabolic acidosis by alkali therapy is usually indicated to raise and maintain the plasma pH to greater than 7.20. In the following two circumstances this is particularly important. When the serum pH is below 7.20, a continued fall in the serum HCO3- level may result in a significant drop in pH. This is especially true when the PCO2 is close to the lower limit of compensation, which in an otherwise healthy young individual is approximately 15 mm Hg. With increasing age and other complicating illnesses, the limit of compensation is likely to be less. A further small drop in HCO3- at this point thus is not matched by a corresponding fall in PaCO2, and rapid decompensation can occur. For example, in a patient with metabolic acidosis with a serum HCO3- level of 9 mEq/L and a maximally compensated PCO2 of 20 mm Hg, a drop in the serum HCO3- level to 7 mEq/L results in a change in pH from 7.28 to 7.16. A second situation in which HCO3- correction should be considered is in well-compensated metabolic acidosis with impending respiratory failure. As metabolic acidosis continues in some patients, the increased ventilatory drive to lower the PaCO2 may not be sustainable because of respiratory muscle fatigue. In this situation, a PaCO2 that starts to rise may change the plasma pH dramatically even without a significant further fall in HCO3-. For example, in a patient with metabolic acidosis with a serum HCO3- level of 15 and a compensated PaCO2 of 27 mm Hg, a rise in PaCO2 to 37 mm Hg results in a change in pH from 7.33 to 7.20. A further rise of the PaCO2 to 43 mm Hg drops the pH to 7.14. All of this would have occurred whi Continue reading >>

Nw Newborn Drug Protocol - Sodium Bicarbonate Pharmacology

Nw Newborn Drug Protocol - Sodium Bicarbonate Pharmacology

0.25-0.50 mmol/kg/hour. Continuous IV infusion. Doses needs to be individualised and titrated according to response and to adverse effects (e.g. hypernatraemia) Not recommended for hypercapnia or hypernatraemic states. Caution in infants with renal impairment. Caution in preterm infants. Rapid infusion of hypertonic NaHCO3 has been incriminated in the pathogenesis of intraventricular haemorrhage in preterm infants. Sodium bicarbonate is the alkali most frequently employed for correction of metabolic acidosis. The drug is well absorbed from the gastrointestinal tract. Between 20-50% of an orally administered dose can be recovered in the form of expired carbon dioxide. The apparent bicarbonate space has been estimated to be 74% of body weight (range of 37-134%). Thus calculations of bicarbonate dosage are based on an apparent volume of distribution of 0.3 to 0.6 L/kg. Bicarbonate is rapidly metabolised to carbonic acid which rapidly dissociates into water and carbon dioxide. The carbon dioxide is excreted via the lungs. Venous irritation, soft tissue injury at the site of IV injection. Increased vascular volume, serum osmolarity, serum sodium. Continue reading >>

Sodium Bicarbonate In Severe Metabolic Acidosis

Sodium Bicarbonate In Severe Metabolic Acidosis

Sodium Bicarbonate in Severe Metabolic Acidosis Sodium Bicarbonate in Severe Metabolic Acidosis Aka: Sodium Bicarbonate in Severe Metabolic Acidosis No evidence that Sodium Bicarbonate improves outcomes Treat acidosis with ventilation and perfusion Documented severe Metabolic Acidosis associated with: Diabetic Ketoacidosis with Arterial pH <6.9 Adequate ventilation and perfusion are critical V. Dosing: Adults (if arterial pH <6.9 to 7.0) Sodium Bicarbonate 1 amp (50 meq or 100 mmol) Dose full bag or 400 cc of 50 meq if pH <6.9 Dose half bag or 200 cc of 25 meq if pH 6.9 - 7.0 If arterial pH <6.9 on recheck in 2 hours Solution should contain <0.5 meq/ml bicarbonate Sodium should be <155 meq/L (NS concentration) Every bicarb ampule contains 2000 meq/L Sodium Limit infusion rate to <1 meq/kg/hour bicarbonate Example: 20 kg child with arterial pH <6.9 Maximum replacement is 40 meq bicarbonate Contains 40 meq Na + 38 meq Na = 78 meq Na Sodium concentration is 156 meq/L (same as NS) Limit this 20 kg child's rate to 20 meq/hour Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Sodium Bicarbonate in Severe Metabolic Acidosis." Click on the image (or right click) to open the source website in a new browser window. Search Bing for all related images Related Studies (from Trip Database) Open in New Window Continue reading >>

Metabolic Acidosis And Kidney Disease: Does Bicarbonate Therapy Slow The Progression Of Ckd?

Metabolic Acidosis And Kidney Disease: Does Bicarbonate Therapy Slow The Progression Of Ckd?

Metabolic acidosis and kidney disease: does bicarbonate therapy slow the progression of CKD? Correspondence and offprint requests to: Csaba P. Kovesdy; E-mail: [email protected] Search for other works by this author on: Nephrology Dialysis Transplantation, Volume 27, Issue 8, 1 August 2012, Pages 30563062, Csaba P. Kovesdy; Metabolic acidosis and kidney disease: does bicarbonate therapy slow the progression of CKD?, Nephrology Dialysis Transplantation, Volume 27, Issue 8, 1 August 2012, Pages 30563062, Metabolic acidosis is a common complication associated with progressive loss of kidney function. The diminishing ability of the kidneys to maintain acidbase homeostasis results in acid accumulation, leading to various complications such as impairment in nutritional status, worsened uremic bone disease and an association with increased mortality. In addition to these adverse effects which are related to acid retention, metabolic acidosis may also cause kidney damage, possibly through the stimulation of adaptive mechanisms aimed at maintaining acidbase homeostasis in the face of decreasing kidney function. Recent clinical trials have suggested that correction or prevention of metabolic acidosis by alkali administration is able to attenuate kidney damage and to slow progression of chronic kidney disease (CKD), and may hence offer an effective, safe and affordable renoprotective strategy. We review the physiology and pathophysiology of acidbase homeostasis in CKD, the mechanisms whereby metabolic acidosis may be deleterious to kidney function, and the results of clinical trials suggesting a benefit of alkali therapy, with special attention to details related to the practical implementation of the results of these trials. bicarbonate , chronic kidney disease , metabolic ac Continue reading >>

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