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Why Does Acute Kidney Injury Cause Metabolic Acidosis?

Pathogenesis, Consequences, And Treatment Of Metabolic Acidosis In Chronic Kidney Disease

Pathogenesis, Consequences, And Treatment Of Metabolic Acidosis In Chronic Kidney Disease

The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2018 UpToDate, Inc. All topics are updated as new evidence becomes available and our peer review process is complete. INTRODUCTION — Most individuals produce approximately 15,000 mmol (considerably more with exercise) of carbon dioxide and 50 to 100 meq of nonvolatile acid each day. Acid-base balance is maintained by normal elimination of carbon dioxide by the lungs (which affects the partial pressure of carbon dioxide [PCO2]) and normal excretion of nonvolatile acid by the kidneys (which affects the plasma bicarbonate concentration). The hydrogen ion concentration of the blood is determined by the ratio of the PCO2 and plasma bicarbonate concentration. (See "Simple and mixed acid-base disorders", section on 'Introduction'.) Acidosis associated with chronic kidney disease (CKD) will be discussed in this topic. An overview of simple acid-base disorders and renal tubular acidosis, as well as the approach to patients with metabolic acidosis, are presented elsewhere. (See "Simple and mixed acid-base disorders" and "Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance" and "Approach to the adult with metabolic acidosis" and "Approach to the child with metabolic acidosis".) ACID-BASE BALANCE IN CHRONIC KIDNEY DISEASE — Acid-base balance is normally maintained by the renal excretion of the daily acid load (about 1 meq/kg per day, derived mostly from the generation of sulfuric acid during the metabolism of sulf Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Causes Of Metabolic Acidosis

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Causes Of Metabolic Acidosis

Recommendations for the treatment of acute metabolic acidosis Gunnerson, K. J., Saul, M., He, S. & Kellum, J. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit. Care Med. 10, R22-R32 (2006). Eustace, J. A., Astor, B., Muntner, P M., Ikizler, T. A. & Coresh, J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int. 65, 1031-1040 (2004). Kraut, J. A. & Kurtz, I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am. J. Kidney Dis. 45, 978-993 (2005). Kalantar-Zadeh, K., Mehrotra, R., Fouque, D. & Kopple, J. D. Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure. Semin. Dial. 17, 455-465 (2004). Kraut, J. A. & Kurtz, I. Controversies in the treatment of acute metabolic acidosis. NephSAP 5, 1-9 (2006). Cohen, R. M., Feldman, G. M. & Fernandez, P C. The balance of acid base and charge in health and disease. Kidney Int. 52, 287-293 (1997). Rodriguez-Soriano, J. & Vallo, A. Renal tubular acidosis. Pediatr. Nephrol. 4, 268-275 (1990). Wagner, C. A., Devuyst, O., Bourgeois, S. & Mohebbi, N. Regulated acid-base transport in the collecting duct. Pflugers Arch. 458, 137-156 (2009). Boron, W. F. Acid base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368-2382 (2006). Igarashi, T., Sekine, T. & Watanabe, H. Molecular basis of proximal renal tubular acidosis. J. Nephrol. 15, S135-S141 (2002). Sly, W. S., Sato, S. & Zhu, X. L. Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis. Clin. Biochem. 24, 311-318 (1991). Dinour, D. et al. A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1/ SLC4A4) Continue reading >>

Ethylene Glycol Toxicity A Rare Cause Of High Anion Gap Metabolic Acidosis In Australia

Ethylene Glycol Toxicity A Rare Cause Of High Anion Gap Metabolic Acidosis In Australia

ETHYLENE GLYCOL TOXICITY A RARE CAUSE OF HIGH ANION GAP METABOLIC ACIDOSIS IN AUSTRALIA ETHYLENE GLYCOL TOXICITY A RARE CAUSE OF HIGH ANION GAP METABOLIC ACIDOSIS IN AUSTRALIA GJ WILSON1,2, J ROWLAND1, MR DOWLING1, L FRANCIS3, GT JOHN1,2,AL KARK1,2 1Department of Renal Medicine, Royal Brisbane and Womens Hospital, Herston, Queensland;2School of Clinical Medicine, University of Queensland, Herston, Queensland;3Department of Pathology, Royal Brisbane and Womens Hospital, Herston, Queensland Background: Ethylene glycol toxicity is a well-known cause of acute kidney injury (AKI) and high anion gap metabolic acidosis. However, it is a rare presentation in Australia with only 22 cases reported in 2014. The diagnosis of ethylene glycol toxicity is challenging in the absence of a history of ingestion and can be misdiagnosed as lactic acidosis which, due to structural similarities with glycolate, causes falsely elevated lactate levels on some instruments. Case Report: A 36 year-old female presented to the emergency department with an altered level of consciousness and tachypnoea requiring urgent intubation. She was anuric and had an AKI (creatinine 182 umol/L). An iSTAT venous blood gas demonstrated a high anion gap metabolic acidosis (pH 7.08, HCO3 6, CO2 19, anion gap 34) and an elevated serum lactate (9.4 mmol/L). She was provisionally diagnosed with type B lactic acidosis and transferred to ICU for ventilation and continuous veno-venous haemodiafiltration. Upon extubation, the patient denied any toxic ingestions and renal biopsy was performed demonstrating crystalloid material birefringent under polarised light consistent with oxalate nephropathy. Urinary organic acids were requested and urinary glycolate and oxalate levels were elevated (2200 mmol/mol Cr and 520 mmol/mol C Continue reading >>

Metabolic Acidosis Aggravates Experimental Acute Kidney Injury

Metabolic Acidosis Aggravates Experimental Acute Kidney Injury

Volume 146 , 1 February 2016, Pages 58-65 Metabolic acidosis aggravates experimental acute kidney injury Ischemia/reperfusion (I/R) injury and metabolic acidosis (MA) are two critical conditions that may simultaneously occur in clinical practice. The result of this combination can be harmful to the kidneys, but this issue has not been thoroughly investigated. The present study evaluated the influence of low systemic pH on various parameters of kidney function in rats that were subjected to an experimental model of renal I/R injury. Metabolic acidosis was induced in male Wistar rats by ingesting ammonium chloride (NH4Cl) in tap water, beginning 2days before ischemic insult and maintained during the entire study. Ischemia/reperfusion was induced by clamping both renal arteries for 45min, followed by 48h of reperfusion. Four groups were studied: control (subjected to sham surgery, n=8), I/R (n=8), metabolic acidosis (MA; 0.28M NH4Cl solution and sham surgery, n=6), and MA+I/R (0.28M NH4Cl solution plus I/R, n=9). Compared with I/R rats, MA+I/R rats exhibited higher mortality (50 vs. 11%, p=0.03), significant reductions of blood pH, plasma bicarbonate (pBic), and standard base excess (SBE), with a severe decline in the glomerular filtration rate and tubular function. Microscopic tubular injury signals were detected. Immunofluorescence revealed that the combination of MA and I/R markedly increased nuclear factor B (NF-B) and heme-oxygenase 1 (HO-1), but it did not interfere with the decrease in endothelial nitric oxide synthase (eNOS) expression that was caused by I/R injury. Acute ischemic kidney injury is exacerbated by acidic conditions. Continue reading >>

Acid/base Disorders: Metabolic Acidosis

Acid/base Disorders: Metabolic Acidosis

Are there clinical practice guidelines to inform decision-making? Does this patient have metabolic acidosis? Metabolic acidosis is generally defined by the presence of a low serum bicarbonate concentration (normal range 22-28 mEq/L), although occasionally states can exist where the serum bicarbonate is normal with an elevated anion gap (e.g., patients with a lactic acidosis who have received a bicarbonate infusion or patients on hemodialysis). In general, a metabolic acidosis is associated with a low urine pH but depending on the presence or absence of a respiratory alkalosis, this may also be normal or elevated. Thus, a patient can have an acidosis but not be acidemic. Metabolic acidoses occur when there is excess acid in the plasma. In the basal state, the body generates about 12,000 to 13,000 mmol of carbon dioxide (CO2), and 1-1.5 mmol per kilogram body weight of nonvolatile acid. The body has a large buffering capacity, with CO2-HCO3 as the major buffer system. The two major routes of acid excretion are the lungs (for CO2) and the kidneys (for nonvolatile acids) A metabolic acidosis can be caused by three major mechanisms: 1) increased acid production; 2) bicarbonate loss; and 3) decreased renal acid excretion Increased acid production leads to anion-gap (AG) metabolic acidosis, and involves a variety of different clinical processes, see An anion gap acidosis may also result for ingestion of an acid load. Both bicarbonate loss and decreased renal acid excretion lead to normal-anion gap (NG) metabolic acidosis. When there is HCO3 loss, chloride is retained to maintain electrical neutrality. The different clinical processes are summarized in Toxic ingestions are common causes of AG metabolic acidosis. The commonest causes are methanol and ethylene glycol intoxicatio Continue reading >>

Metabolic Acidosis And The Progression Of Chronic Kidney Disease

Metabolic Acidosis And The Progression Of Chronic Kidney Disease

Metabolic acidosis and the progression of chronic kidney disease 1Division of Nephrology, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA 2Department of Epidemiology & Population Health, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Ullmann 615, Bronx, NY 10461, USA 1Division of Nephrology, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA 2Department of Epidemiology & Population Health, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Ullmann 615, Bronx, NY 10461, USA Received 2014 Jan 8; Accepted 2014 Mar 31. Copyright 2014 Chen and Abramowitz; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( ) applies to the data made available in this article, unless otherwise stated. This article has been cited by other articles in PMC. Metabolic acidosis is a common complication of chronic kidney disease. Accumulating evidence identifies acidosis not only as a consequence of, but as a contributor to, kidney disease progression. Several mechanistic pathways have been identified in this regard. The dietary acid load, even in the absence of overt acidosis, may have deleterious effects. Several small trials now suggest that the treatment of acidosis with oral alkali can slow the progression of kidney disease. Keywords: Bicarbonate, Dietary acid, Net endogenous acid production, Sodium bicarbonate, Alkali, Ammonia, Complement, Endothelin, Aldosterone Metabolic acidosis is a common complication of chronic kidney disease (CKD). Based on a cr Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

What is metabolic acidosis? The buildup of acid in the body due to kidney disease or kidney failure is called metabolic acidosis. When your body fluids contain too much acid, it means that your body is either not getting rid of enough acid, is making too much acid, or cannot balance the acid in your body. What causes metabolic acidosis? Healthy kidneys have many jobs. One of these jobs is to keep the right balance of acids in the body. The kidneys do this by removing acid from the body through urine. Metabolic acidosis is caused by a build-up of too many acids in the blood. This happens when your kidneys are unable to adequately remove the acid from your blood. What are the signs and symptoms? Not everyone will have signs or symptoms. However, you may experience: Long and deep breaths Fast heartbeat Headache and/or confusion Weakness Feeling very tired Vomiting and/or feeling sick to your stomach (nausea) Loss of appetite If you experience any of these, it is important to let your healthcare provider know immediately. What are the complications of metabolic acidosis if I have kidney disease or kidney failure? Increased bone loss (osteoporosis): Metabolic acidosis can lead to a loss of bone in your body. This can lead to a higher chance of fractures in important bones like your hips or backbone. Progression of kidney disease: Metabolic acidosis can make your kidney disease worse. Exactly how this happens is not clear. As acid builds up, kidney function lowers; and as kidney function lowers, acid builds up. This can lead to the progression of kidney disease. Muscle loss: Albumin is an important protein in your body that helps build and keep muscles healthy. Metabolic acidosis lowers the amount of albumin created in your body, and leads to muscle loss, or what is called Continue reading >>

Acute Kidney Injury - Wikipedia

Acute Kidney Injury - Wikipedia

Pathologic kidney specimen showing marked pallor of the cortex, contrasting to the darker areas of surviving medullary tissue. The patient died with acute kidney injury. Acute kidney injury (AKI), previously called acute renal failure (ARF), [1] [2] is an abrupt loss of kidney function that develops within 7 days. [3] Its causes are numerous. Generally it occurs because of damage to the kidney tissue caused by decreased kidney blood flow (kidney ischemia ) from any cause (e.g., low blood pressure ), exposure to substances harmful to the kidney , an inflammatory process in the kidney, or an obstruction of the urinary tract that impedes the flow of urine. AKI is diagnosed on the basis of characteristic laboratory findings, such as elevated blood urea nitrogen and creatinine , or inability of the kidneys to produce sufficient amounts of urine . AKI may lead to a number of complications, including metabolic acidosis , high potassium levels , uremia , changes in body fluid balance , and effects on other organ systems , including death. People who have experienced AKI may have an increased risk of chronic kidney disease in the future. Management includes treatment of the underlying cause and supportive care, such as renal replacement therapy . The clinical picture is often dominated by the underlying cause.The symptoms of acute kidney injury result from the various disturbances of kidney function that are associated with the disease. Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms, such as fatigue , loss of appetite , headache , nausea and vomiting . [4] Marked increases in the potassium level can lead to abnormal heart rhythms , which can be severe and life-threatening. [5] Fluid balance is frequently affected, t Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Practice Essentials Metabolic acidosis is a clinical disturbance characterized by an increase in plasma acidity. Metabolic acidosis should be considered a sign of an underlying disease process. Identification of this underlying condition is essential to initiate appropriate therapy. (See Etiology, DDx, Workup, and Treatment.) Understanding the regulation of acid-base balance requires appreciation of the fundamental definitions and principles underlying this complex physiologic process. Go to Pediatric Metabolic Acidosis and Emergent Management of Metabolic Acidosis for complete information on those topics. Continue reading >>

Acute Kidney Injury: Complications Associated With Acute Kidney Injury

Acute Kidney Injury: Complications Associated With Acute Kidney Injury

Acute Kidney Injury: Complications associated with Acute Kidney Injury Acute Kidney Injury: Complications associated with Acute Kidney Injury Does this patient have complications associated with acute kidney injury? Acute kidney injury (AKI) is often associated with systemic complications including volume overload; electrolyte and acid-base disturbances, particularly hyponatremia, hyperkalemia and metabolic acidosis; nutritional and gastrointestinal disturbances; anemia and bleeding diatheses, and increased risk of infection. It is often difficult, however, to differentiate complications related to the AKI per se from those related to the underlying cause of AKI. See reviews of specific conditions below for appropriate tests, if any. How should patients with complications associated with AKI be managed? Disturbances of volume homeostasis are extremely common in the setting of AKI. Although effective intravascular volume depletion is a common contributing factor in the development of AKI it is an uncommon complication of AKI. Volume depletion as a result of renal salt and water wasting occasionally develops in patients with non-oliguric AKI; more commonly it may develop during recovery from acute tubular necrosis (ATN), when patients may become polyuric, or following relief of urinary obstruction, when a post-obstructive diuresis may occur. In contrast to volume depletion, volume overload is a common complication of AKI, particularly in patients with oliguric or anuric AKI. Volume overload may develop as a consequence of volume resuscitation in patients with hypotension or may be related to underlying cardiac or hepatic disease. Volume overload often develops as a consequence of obligate intravenous infusions (eg, antibiotics, vasopressors or other medications) required Continue reading >>

Metabolic Acidosis As A Risk Factor For The Development Of Acute Kidney Injury And Hospital Mortality

Metabolic Acidosis As A Risk Factor For The Development Of Acute Kidney Injury And Hospital Mortality

Metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality 1Division of Nephrology, Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai 200032, P.R. China 2Shanghai Institute of Kidney and Dialysis, Shanghai 200032, P.R. China 3Shanghai Key Laboratory for Kidney and Blood Purification, Shanghai 200032, P.R. China 1Division of Nephrology, Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai 200032, P.R. China 2Shanghai Institute of Kidney and Dialysis, Shanghai 200032, P.R. China 3Shanghai Key Laboratory for Kidney and Blood Purification, Shanghai 200032, P.R. China 1Division of Nephrology, Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai 200032, P.R. China 2Shanghai Institute of Kidney and Dialysis, Shanghai 200032, P.R. China 3Shanghai Key Laboratory for Kidney and Blood Purification, Shanghai 200032, P.R. China 1Division of Nephrology, Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai 200032, P.R. China 2Shanghai Institute of Kidney and Dialysis, Shanghai 200032, P.R. China 3Shanghai Key Laboratory for Kidney and Blood Purification, Shanghai 200032, P.R. China 1Division of Nephrology, Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai 200032, P.R. China 2Shanghai Institute of Kidney and Dialysis, Shanghai 200032, P.R. China 3Shanghai Key Laboratory for Kidney and Blood Purification, Shanghai 200032, P.R. China 1Division of Nephrology, Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai 200032, P.R. China 2Shanghai Institute of Kidney and Dialysis, Shanghai 200032, P.R. China 3Shanghai Key Laboratory for Kidney and Blood Purification, Shanghai 200032, P.R. China 1Division of Nephrology, Zhongshan Continue reading >>

8.3 Acidosis And Renal Failure

8.3 Acidosis And Renal Failure

Metabolic acidosis occurs with both acute and chronic renal failure and with other types of renal damage. The anion gap may be normal or may be elevated. If the renal damage affects both glomeruli and tubules, the acidosis is a high-anion gap acidosis. It is due to failure of adequate excretion of various acid anions due to the greatly reduced number of functioning nephrons. If the renal damage predominantly affects the tubules with minimal glomerular damage, a different type of acidosis may occur. This is called Renal Tubular Acidosis (RTA) and this is a normal anion gap or hyperchloraemic type of acidosis. The GFR may be normal or only minimally affected. The acidosis occurring in uraemic patients 1 is due to failure of excretion of acid anions (particularly phosphate and sulphate) because of the decreased number of nephrons. There is a major decrease in the number of tubule cells which can produce ammonia and this contributes to uraemic acidosis. Serious acidosis does not occur until the GFR has decreased to about 20 mls/min. This corresponds to a creatinine level of about 0.30-0.35 mmols/l. The plasma bicarbonate in renal failure with acidosis is typically between 12 & 20 mmols/l. Intracellular buffering and bone buffering are important in limiting the fall in bicarbonate. This bone buffering will cause loss of bone mineral (osteomalacia). Most other forms of metabolic acidosis are of relatively short duration as the patient is either treated with resolution of the disorder or the patient dies. Uraemic acidosis is a major exception as these patients survive with significant acidosis for many years. This long duration is the reason why loss of bone mineral (and bone buffering ) is significant in uraemic acidosis but is not a feature of other causes of metabolic acid Continue reading >>

Acute Kidney Injury (aki)

Acute Kidney Injury (aki)

By Anna Malkina, MD, Assistant Clinical Professor of Medicine, Division of Nephrology, University of California, San Francisco Acute kidney injury is a rapid decrease in renal function over days to weeks, causing an accumulation of nitrogenous products in the blood (azotemia) with or without reduction in amount of urine output. It often results from inadequate renal perfusion due to severe trauma, illness, or surgery but is sometimes caused by a rapidly progressive, intrinsic renal disease. Symptoms may include anorexia, nausea, and vomiting. Seizures and coma may occur if the condition is untreated. Fluid, electrolyte, and acid-base disorders develop quickly. Diagnosis is based on laboratory tests of renal function, including serum creatinine. Urinary indices, urinary sediment examination, and often imaging and other tests (including sometimes a kidney biopsy) are needed to determine the cause. Treatment is directed at the cause but also includes fluid and electrolyte management and sometimes dialysis. In all cases of acute kidney injury (AKI), creatinine and urea build up in the blood over several days, and fluid and electrolyte disorders develop. The most serious of these disorders are hyperkalemia and fluid overload (possibly causing pulmonary edema). Phosphate retention leads to hyperphosphatemia. Hypocalcemia is thought to occur because the impaired kidney no longer produces calcitriol and because hyperphosphatemia causes calcium phosphate precipitation in the tissues. Acidosis develops because hydrogen ions cannot be excreted. With significant uremia, coagulation may be impaired, and pericarditis may develop. Urine output varies with the type and cause of AKI. Hemodialysis or hemofiltration is initiated when Severe electrolyte abnormalities cannot otherwise be c Continue reading >>

Serum Bicarbonate May Independently Predict Acute Kidney Injury In Critically Ill Patients: An Observational Study

Serum Bicarbonate May Independently Predict Acute Kidney Injury In Critically Ill Patients: An Observational Study

Serum bicarbonate may independently predict acute kidney injury in critically ill patients: An observational study Anuksha Gujadhur , Ravindranath Tiruvoipati , Elizabeth Cole , Saada Malouf , Erum Sahid Ansari , and Kim Wong Anuksha Gujadhur, Kim Wong, Department of Renal Medicine, Frankston Hospital, Frankston VIC 3199, Australia Ravindranath Tiruvoipati, School of Public Health, Faculty of Medicine, Nursing and Health Sciences, Monash University, Victoria 3800, Australia Ravindranath Tiruvoipati, Elizabeth Cole, Saada Malouf, Erum Sahid Ansari, Department of Intensive Care Medicine, Frankston Hospital, Frankston VIC 3199, Australia Author contributions: Gujadhur A, Cole E, Malouf S, Ansari ES and Wong K contributed to conception and design, acquisition of data, interpretation of data, drafting the manuscript and revising it critically for important intellectual content and have given final approval of the version to be published; Tiruvoipati R contributed to conception and design, acquisition of data, or analysis and interpretation of data; Tiruvoipati R had been involved in drafting the manuscript or revising it critically for important intellectual content; Tiruvoipati R had given final approval of the version to be published; all authors read and approved the final manuscript. Correspondence to: Dr. Ravindranath Tiruvoipati, Department of Intensive Care Medicine, Frankston Hospital, 2 Hastings Road Frankston, Victoria 3199, Australia. [email protected] Telephone: +61-431-279347 Fax: +61-3978-47398 Received 2014 May 10; Revised 2014 Dec 27; Accepted 2015 Jan 9. Copyright The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved. This article has been cited by other articles in PMC. AIM: To explore whether serum bicarbonate at ad 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?

Nephrol Dial Transplant. 2012 Aug;27(8):3056-62. doi: 10.1093/ndt/gfs291. Metabolic acidosis and kidney disease: does bicarbonate therapy slow the progression of CKD? Division of Nephrology, Salem Veterans Affairs Medical Center, Salem, VA, USA. [email protected] Metabolic acidosis is a common complication associated with progressive loss of kidney function. The diminishing ability of the kidneys to maintain acid-base 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 acid-base 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 acid-base 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. Continue reading >>

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