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Renal Tubular Acidosis Medscape

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

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management 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 >>

Acidosis, Cystinosis, Hyperchloremic Metabolic Acidosis, Corneal Deposit: Causes & Diagnoses | Symptoma.com

Acidosis, Cystinosis, Hyperchloremic Metabolic Acidosis, Corneal Deposit: Causes & Diagnoses | Symptoma.com

Disorder Subdivisions infantile nephropathic cystinosis intermediate cystinosis non-nephropathic cystinosis General Discussion Summary Cystinosis is a rare, multisystem genetic [webmd.com] As a result, a topical formulation of cysteamine was developed to target corneal cystine crystal deposition. [eyewiki.aao.org] (hyperchloremic, normal anion gap) and severity of hypokalemia, hyponatremia, hypophosphatemia, and low bicarbonate concentration Blood gases: To detect metabolic acidosis [emedicine.medscape.com] Patients usually present during the first year of life with polyuria, polydipsia, dehydration, metabolic acidosis (normal anion gap hyperchloremic acidosis), hypophosphatemic [emedicine.medscape.com] Steady-state pharmacokinetics and pharmacodynamics of cysteamine bitartrate in paediatric nephropathic cystinosis patients. [pedclerk.bsd.uchicago.edu] Metabolic acidosis in the critically ill: part 2. [lifeinthefastlane.com] II of Spain , who is speculated to have suffered with dRTA Hyperchloremic acidosis Hypokalemic acidosis References [ edit ] a b Laing CM, Toye AM, Capasso G, Unwin RJ (2005 [en.wikipedia.org] Laboratory testing is notable for hyperchloremic and normal anion gap metabolic acidosis and hypokalemia. [medbullets.com] Causes of type II RTA includes in further Cystinosis (body is unable to break down the substance cysteine) Drugs such as ifosfamide (a chemotherapy drug), certain antibiotics [medvin2u.net] "Proximal renal tubular acidosis. [ipfs.io] "Cystinosis" . [en.wikipedia.org] Laboratory studies revealed a hyperchloremic metabolic acidosis without aciduria, hypokalemia, hypouricemia with uricosuria, hypercalciuria, LMW proteinuria, phosphaturia, [link.springer.com] "Cystinosis" . [wikidoc.org] Diagnosis Hyperchloremic metabolic acidosis, normo or hy Continue reading >>

What Is Metabolic Acidosis?

What Is Metabolic Acidosis?

Metabolic acidosis happens when the chemical balance of acids and bases in your blood gets thrown off. Your body: Is making too much acid Isn't getting rid of enough acid Doesn't have enough base to offset a normal amount of acid When any of these happen, chemical reactions and processes in your body don't work right. Although severe episodes can be life-threatening, sometimes metabolic acidosis is a mild condition. You can treat it, but how depends on what's causing it. Causes of Metabolic Acidosis Different things can set up an acid-base imbalance in your blood. Ketoacidosis. When you have diabetes and don't get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes ketones. Lots of ketones in your blood turn it acidic. People who drink a lot of alcohol for a long time and don't eat enough also build up ketones. It can happen when you aren't eating at all, too. Lactic acidosis. The cells in your body make lactic acid when they don't have a lot of oxygen to use. This acid can build up, too. It might happen when you're exercising intensely. Big drops in blood pressure, heart failure, cardiac arrest, and an overwhelming infection can also cause it. Renal tubular acidosis. Healthy kidneys take acids out of your blood and get rid of them in your pee. Kidney diseases as well as some immune system and genetic disorders can damage kidneys so they leave too much acid in your blood. Hyperchloremic acidosis. Severe diarrhea, laxative abuse, and kidney problems can cause lower levels of bicarbonate, the base that helps neutralize acids in blood. Respiratory acidosis also results in blood that's too acidic. But it starts in a different way, when your body has too much carbon dioxide because of a problem with your lungs. Continue reading >>

Renal Tubular Acidosis (rta)

Renal Tubular Acidosis (rta)

About Symptoms and Signs, Complications Diagnosis and Treatment RTA Type 1 RTA Type 2 RTA Type 4 FAQs Latest Publications and Research Reference Renal tubular acidosis is a condition where the kidneys are unable to maintain the acid base balance in the body due to defect in secretion of acid, reabsorption of bicarbonate or both. This results in acid content of the blood being higher than normal and that of the urine lower than normal. The pH of the blood is normally maintained in a tight range between 7.35 to 7.45. Ions such as bicarbonate increase the pH and make the blood alkaline. On the other hand, hydrogen ions make it acidic. The kidneys play a very important role in controlling the pH. The kidneys produce urine by filtering waste products from the blood. They consist of a large number of small units called nephrons. Each nephon consists of a cup shaped structure called the glomerulus and a long tubule. The tubules end in the collecting ducts. These ducts ultimately lead to the funnel shaped collection area called pelvis. Finally the urine flows into the bladder through a 25 cms small diameter pipe called the ureters that connect the pelvis of the kidneys to the bladder. Filtration of blood takes place at the level of the glomerulus. The filtrate passes through the tubules that reabsorb a large amount and divert it back into the blood. The cells lining the first part of the tubules reabsorb bicarbonate from the urine. This process maintains the alkalinity of the blood and makes the urine more acidic. In the later or distal part, the tubules throw out hydrogen into the urine making it even more acidic. This process further reduces the acidity of the blood. A hormone aldosterone secreted by the adrenal glands also acts on the tubules at this level and plays a role 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 >>

Orphanet: Arthrogryposis Renal Dysfunction Cholestasis Syndrome

Orphanet: Arthrogryposis Renal Dysfunction Cholestasis Syndrome

The prevalence is unknown but less than 100 patients have been reported in the literature so far. The phenotype is variable, even within the same family and cases may go undiagnosed as not all the patients present with the three cardinal features. Renal tubular dysfunction ranges from isolated renal tubular acidosis to complete Fanconi syndrome (polyuria, aminoaciduria, glycosuria, phosphaturia and bicarbonate wasting). Hepatic anomalies include variable combinations of cholestasis, intrahepatic biliary duct hypoplasia and lipofuscin deposition. Additional features include severe failure to thrive, platelet dysfunction (which may be responsible for severe bleeding), facial dysmorphism (low set ears, lax skin, a high arched palate, beaked nose and small anterior fontanelle), diarrhea, recurrent febrile illness, cerebral malformations and sensorineural deafness. Mutations in the VPS33B gene (15q26.1), involved in intracellular protein trafficking and membrane fusion, have been found in 75% of ARC families, as well as mutations in the VIPAR gene (C14ORF133), encoding a protein that complexes with VPS33B. The differential diagnosis should include progressive familial intrahepatic cholestasis disorders, other forms of arthrogryposis multiplex congenita and congenital ichthyosiform dermatoses (see these terms). The syndrome is generally considered to be transmitted as an autosomal recessive trait. There is no specific treatment for the disease. Most patients die within the first year of life despite supportive care for metabolic acidosis and cholestasis and those surviving longer show cirrhosis and severe developmental delay. Expert reviewer(s): Dr Martine LE MERRER - Last update: June 2010 Continue reading >>

Medullary Sponge Kidney

Medullary Sponge Kidney

Medullary sponge kidney is a benign congenital disorder characterized by dilatation of collecting tubules in one or more renal papillae, affecting one or both kidneys (see the image below). The term medullary sponge kidney is misleading because the affected kidney does not resemble a sponge. Tubular ectasia and cystic dilatation of the collecting ducts have been suggested as alternative names for the disorder; however, medullary sponge kidney is the most commonly used name. Medullary sponge kidney is usually a benign condition, and patients can remain asymptomatic. Despite being a congenital disorder, medullary sponge kidney usually is not diagnosed until the second or third decade of life or later. [ 1 , 2 ] See Presentation and Epidemiology . IVU-like, volume-rendered (VR) computed tomography (CT) scan of both kidneys demonstrates brushlike densities throughout multiple papillae of both kidneys consistent with renal tubular ectasia. Correlation of the stone disease with the ectatic tubules is diagnostic of medullary sponge kidney. Image courtesy of Dr. Terri J. Vrtiska, Consultant, Department of Radiology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA. Treatment of medullary sponge kidney centers on management of complications, which include the following (see Treatment and Medication ): Distal renal tubular acidosis (RTA; type 1 RTA) For discussion of this disorder in children, see Pediatric Medullary Sponge Kidney. The most important abnormality in medullary sponge kidney is the spherical, oval, or irregular dilatation of the medullary and papillary portions of the collecting ducts. The underlying abnormality responsible for this developmental anomaly is unknown. The disease is bilateral in 70% of cases, and unilateral involvement of only one pyramid i Continue reading >>

Renal Tubular Acidosis

Renal Tubular Acidosis

Significant bilateral nephrocalcinosis (calcification of the kidneys) on a frontal X-ray (radiopacities (white) in the right upper and left upper quadrant of the image), as seen in distal renal tubular acidosis. Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine . [1] In renal physiology , when blood is filtered by the kidney, the filtrate passes through the tubules of the nephron , allowing for exchange of salts , acid equivalents, and other solutes before it drains into the bladder as urine . The metabolic acidosis that results from RTA may be caused either by failure to reabsorb sufficient bicarbonate ions (which are alkaline ) from the filtrate in the early portion of the nephron (the proximal tubule ) or by insufficient secretion of hydrogen ions (which are acidic) into the latter portions of the nephron (the distal tubule ). Although a metabolic acidosis also occurs in those with renal insufficiency , the term RTA is reserved for individuals with poor urinary acidification in otherwise well-functioning kidneys. Several different types of RTA exist, which all have different syndromes and different causes. The word acidosis refers to the tendency for RTA to cause an excess of acid , which lowers the blood's pH . When the blood pH is below normal (7.35), this is called acidemia . The metabolic acidosis caused by RTA is a normal anion gap acidosis . Failure of proximal tubular cells to reabsorb H C O 3 Deficiency of aldosterone , or a resistance to its effects, ( hypoaldosteronism or pseudohypoaldosteronism ) Main article: Distal renal tubular acidosis Radiograph of a child with rickets , a complication of both distal and proximal RTA. Distal RTA (dRT Continue reading >>

Renal Tubular Acidosis Type Ii Associated With Vitamin D Deficiency Presenting As Chronic Weakness

Renal Tubular Acidosis Type Ii Associated With Vitamin D Deficiency Presenting As Chronic Weakness

Renal tubular acidosis type II associated with vitamin D deficiency presenting as chronic weakness Yaseen Ali, Ohio University, 120 Chubb Hall, Athens, OH 45701, USA; Chronic vitamin D deficiency, though common in the elderly, is often under diagnosed and when progressing to renal tubular acidosis type II (RTA 2) can cause several simultaneous electrolyte imbalances that may present with weakness and pain as chief symptoms. We present such a case that after months of evaluation and symptomatic treatment did not lead to an effective establishment of the etiology causing chronic weakness and body pain in an elderly female patient. Eventually, after a careful review of the patients history, repeat physical examinations, laboratory data evaluation, and diagnostic testing led to the establishment of the diagnosis of proximal RTA 2 associated with vitamin D deficiency, which caused the patient to develop several remarkable secondary electrolyte imbalances such as hypokalemia, hypocalcemia, hypophosphatemia, acidemia, hyperparathyroidism, with weakness and body pain. Keywords: RTA type 2, Hypokalemia, Acidosis, Vitamin D deficiency, chronic weakness Weakness leading to falls is one of the most common reasons for outpatient clinic visits and inpatient hospitalizations among elderly patients, severely compromising their quality of life [ Moreland et al. 2004 ]. Weakness accompanied by chronic generalized pain can be attributed to several etiologies and can lead clinicians to expend excessive time and healthcare resources in diagnosis and treatment [ Bohl et al. 2012 ]. Even with all our advanced diagnostic capabilities, a single etiology is difficult to determine in some cases, and treatment can include the utilization of multiple therapeutic modalities [ Bohl et al. 2012 ]. In Continue reading >>

Hyporeninemic Hypoaldosteronism

Hyporeninemic Hypoaldosteronism

Author: James H Sondheimer, MD, FACP, FASN; Chief Editor: Vecihi Batuman, MD, FASN more... This article reviews some of the pathophysiologic aspects, the clinical picture, and the treatment strategies of hyporeninemic hypoaldosteronism from the standpoint of clinical presentation, evaluation, and treatment. In chronic kidney disease (CKD), the kidney retains a remarkable ability to compensate for nephron loss by increasing single-nephron excretion of various substances. This situation is particularly important in the renal adaptation to potassium handling. (For a detailed discussion of the regulation of acid-base balance, see Metabolic Acidosis .) When compensation is intact, hyperkalemia is uncommon until renal function (glomerular filtration rate [GFR]) decays to an advanced stage (ie, GFR or creatinine clearance 15 mL/min). At times, however, tubular adaptation is impaired, and hyperkalemia is observed much earlier in the course of CKD. This picture of hyperkalemia , often with mild acidosis, in the setting of mild-to-moderate CKD (stages 2-4) is quite common in clinical practice. Several pathophysiologic mechanisms are involved. However, the diagnostic workup does not always establish the precise mechanism, and, unfortunately, much confusion has arisen from the nomenclature employed. Strictly speaking, the term hyporeninemic hypoaldosteronism should be limited to cases in which testing reveals the cause of hyperkalemia to be a deficiency of renin and aldosterone. Similarly, the term type IV renal tubular acidosis (RTA)or hyperkalemic RTA or tubular hyperkalemiashould be employed for cases with normal renin and aldosterone production but impaired tubular responsiveness, usually caused by a distal tubular voltage defect. The term type IV RTA is in itself confusing be Continue reading >>

Renal Tubular Acidosis Medscape

Renal Tubular Acidosis Medscape

Medullary Nephrocalcinosis on X-ray Medullary Nephrocalcinosis on Ultrasound. Renal Tubular Acidosis Diagnosis Chronic metabolic acidosis (eg, uremia, renal tubular acidosis [RTA]) is associated with substantial bone disease from bone buffering of calcium carbonate. Renal tubular acidosis (RTA) type IV generally is asymptomatic unless severe hyperkalemia leads to muscle weakness or life-threatening arrhythmia (see Hyperkalemia). Hanip M, Cheong I, Chin G, Khalid B. Rhabdomyolysis associated with hypokalemic periodic paralysis of renal tubular acidosis. Singapore Med J. 1990; 31:15961. Uti In Babies Causes Remedies For Period Cramps While every ladys cycle differs, most women can attest from personal experience that menstrual cramps can make you want to curl up with a hot pad and movie. Natural home remedy for menstrual cramp is heat therapy, as it is very effective for relieving cramps caused by the menstrual cycle. Learn Renal tubular acidosis What is renal tubular acidosis? What are its symptoms and how can it be cured? Medical rx, no cure. Renal tubular acidosis (rta) involves. Continue reading >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP more... This article covers the pathophysiology and causes of hyperchloremic metabolic acidoses , in particular the renal tubular acidoses (RTAs). [ 1 , 2 ] It also addresses approaches to the diagnosis and management of these disorders. A low plasma bicarbonate (HCO3-) concentration represents, by definition, metabolic acidosis, which may be primary or secondary to a respiratory alkalosis. Loss of bicarbonate stores through diarrhea or renal tubular wasting leads to a metabolic acidosis state characterized by increased plasma chloride concentration and decreased plasma bicarbonate concentration. Primary metabolic acidoses that occur as a result of a marked increase in endogenous acid production (eg, lactic or keto acids) or progressive accumulation of endogenous acids when excretion is impaired by renal insufficiency are characterized by decreased plasma bicarbonate concentration and increased anion gap without hyperchloremia. The initial differentiation of metabolic acidosis should involve a determination of the anion gap (AG). This is usually defined as AG = (Na+) - [(HCO3- + Cl-)], in which Na+ is plasma sodium concentration, HCO3- is bicarbonate concentration, and Cl- is chloride concentration; all concentrations in this formula are in mmol/L (mM or mEq/L) (see also the Anion Gap calculator). The AG value represents the difference between unmeasured cations and anions, ie, the presence of anions in the plasma that are not routinely measured. An increased AG is associated with renal failure, ketoacidosis, lactic acidosis, and ingestion of certain toxins. It can usually be easily identified by evaluating routine plasma chemistry results and from the clinical picture. A normal AG Continue reading >>

Renal Tubular Disorders

Renal Tubular Disorders

Renal tubular disorders are a very heterogeneous group of hereditary and acquired diseases that involve singular or complex dysfunctions of transporters and channels in the renal tubular system. The disorders may lead to fluid loss and abnormalities in electrolyte and acid-base homeostasis. Renal tubular acidosis ( RTA ) refers to normal anion gap (hyperchloremic) metabolic acidosis in the presence of normal or almost normal renal function. The various types of RTA include proximal tubular bicarbonate wasting (type II), distal tubular acid secretion (type I), very rarely carbonic anhydrase deficiency (type III) , and aldosterone deficiency/resistance (type IV). X-linked hypophosphatemic rickets , the most common form of hereditary hypophosphatemic rickets , is caused by phosphate wasting and presents with hypophosphatemia and symptoms related to rickets . Bartter syndrome , Liddle, and Gitelman syndrome are inherited disorders of tubular function that are characterized by hypokalemia and metabolic alkalosis . Renal tubular disorders are suspected when characteristic clinical features and/or laboratory findings are present. The diagnosis of hereditary conditions is usually confirmed by genetic testing. Treatment options vary depending on nature of the renal tubular disorder. Treatment: lifelong oral potassium substitution with potassium-sparing diuretics that directly block ENaC in the collecting duct (e.g., amiloride , triamterene ) 1. Soriano JR. Renal Tubular Acidosis: The Clinical Entity. J Am Soc Nephrol. 2002; 13(8): pp.21602170. doi: 10.1097/01.ASN.0000023430.92674.E5 . 2. McMillan JI. Renal Tubular Acidosis. . Updated January 1, 2016. Accessed April 10, 2017. 3. Mattoo TK. Etiology and clinical manifestations of renal tubular acidosis in infants and children. In Continue reading >>

Acid-base Homeostasis: Overview For Infusion Nurses

Acid-base Homeostasis: Overview For Infusion Nurses

Acid-Base Homeostasis: Overview for Infusion Nurses September/October 2016, Volume 39 Number 5 , p 288 - 295 This article has an associated Continuing Education component. Expires October 31, 2018. Go to CE Details Acid-base homeostasis is essential to normal function of the human body. Even slight alterations can significantly alter physiologic processes at the tissue and cellular levels. To optimally care for patients, nurses must be able to recognize signs and symptoms that indicate deviations from normal. Nurses who provide infusions to patients-whether in acute care, home care, or infusion center settings-have a responsibility to be able to recognize the laboratory value changes that occur with the imbalance and appreciate the treatment options, including intravenous infusions. D.J., a 24-year-old male, presented to the hospital following a serious motor vehicle collision. He suffered a head injury and multiple internal injuries that required admission to the intensive care unit. D.J. developed acute kidney injury and received rapid-volume resuscitation with 0.9% sodium chloride. In the following days, he experienced multiple seizures requiring intubation for airway protection and large doses of intravenous (IV) lorazepam. He subsequently was placed on IV phenobarbital. Despite management of the kidney injury and seizures, the patient continued to demonstrate hyperkalemia and muscle twitching. Arterial blood gases obtained throughout this time showed alteration in acid-base balance. Acid-base homeostasis must be maintained in a narrow range for the body to function normally. Even slight changes can significantly alter physiologic processes at the tissue and cellular levels, as well as the pharmacokinetics of infused products. Nurses must be able to recognize possi 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 >>

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