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Renal Tubular Acidosis Workup

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

Renal Tubular Acidosis

Each time our internal organs do something, such as digesting food or healing damaged tissue, chemical reactions take place in the body's cells. These reactions cause acid to go into the bloodstream. Normally, the kidneys remove excess acid from blood, but certain diseases, genetic defects, or drugs can damage a kidney's ability to do this important job. This can allow too much acid to build up in the blood and cause problems. When this happens, it's called renal tubular acidosis (RTA). Without treatment, RTA can affect a child's growth and cause kidney stones , fatigue, muscle weakness, and other symptoms. Over time, untreated acidosis can lead to long-term problems like bone disease, kidney disease , and kidney failure. Fortunately, such complications are rare, since most cases of RTA can be effectively treated with medicines or by treating the condition that's causing the acid to build up. The kidneys are a pair of bean-shaped organs located toward the back of the abdominal cavity, just above the waist. The kidneys remove waste products and extra water from the food a person eats, returning chemicals the body needs (such as sodium, phosphorus, and potassium) back into the bloodstream. The extra water combines with other waste to become urine (pee). The main functional units of the kidneys, where the blood filtering happens, are tiny structures called nephrons. Each kidney has about a million nephrons, and each nephron has a renal tubule, a tube where the acid and waste products filtered from the blood are secreted into urine. Having a disease or defect can interfere with how the renal tubules function, which can lead to RTA. There are a few different kinds of RTA. The first two types are named for the part of the renal tubule in which the damage or defect is found. Continue reading >>

Renal Tubular Acidosis

Renal Tubular Acidosis

Please donate! Funds go solely to hosting and development costs that allow medical practitioners around the globe to freely access WikEM. Hyperchloremic metabolic acidosis , non-anion gap Diagnostic classification starts with low, normal, or high serum potassium Differentiate from uremia in which acidosis is anion gap Plasma aldosterone and cortisol for type IV RTA Note that when hyperkalemia is present, aldosterone should be elevated, so a "normal" aldosterone level may be relatively low Primary metabolic (cystinosis, von Gierke's) Familial (decreased H+/K+-ATPase, Na+/K+-ATPase activity) Mild acidosis in adults with bicarb > 20 mEq/L may not require treatment Children should be treated due to impaired growth For type I and II RTA, treat all children and infants Generally, 5-15 mEq/kg/day oral bicarbonate May require IV bicarbonate for severe acidosis Urine pH > 5.5 if undergoing alkali therapy Normokalemia may be seen in chronic interstitial renal disease Urinary anion gap > 50 mEq/L = Na + K - Cl Nephrolithiasis , calcium stones from chronic acidosis causing bone resorption and hypercalciuria Mild acidosis, with bicarb generally > 17 mEq/L Serum aldosterone and cortisol levels to determine between: Adrenal insufficiency, Addison's (low aldosterone, low cortisol) Selective aldosterone deficiency (low aldosterone, normal cortisol) Aldosterone resistance (nl to high aldosterone, nl to high cortisol) Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock. Renal Tubular Acidosis Syndromes. South Med J. 2000;93(11). . UCSF Education. Renal Tubular Acidosis. Nov 2002. . Continue reading >>

Diabetes Mellitus And Hyperkalemic Renal Tubular Acidosis: Case Reports And Literature Review

Diabetes Mellitus And Hyperkalemic Renal Tubular Acidosis: Case Reports And Literature Review

Diabetes mellitus and hyperkalemic renal tubular acidosis: case reports and literature review Diabetes mellitus e acidose tubular renal hipercalmica: relatos de caso e reviso da literatura Carlos Henrique Pires Ratto Tavares Bello; Joo Sequeira Duarte; Carlos Vasconcelos Hyporeninemic hypoaldosteronism, despite being common, remains an underdiagnosed entity that is more prevalent in patients with diabetes mellitus. It presents with asymptomatic hyperkalemia along with hyperchloraemic metabolic acidosis without significant renal function impairment. The underlying pathophysiological mechanism is not fully understood, but it is postulated that either aldosterone deficiency (hyporeninemic hypoaldosteronism) and/or target organ aldosterone resistance (pseudohypoaldosteronism) may be responsible. Diagnosis is based on laboratory parameters. Treatment strategy varies according to the underlying pathophysiological mechanism and etiology and aims to normalize serum potassium. Two clnical cases are reported and the relevant literature is revisited. Keywords: acidosis; acidosis, renal tubular; diabetes mellitus; hyperkalemia; hypoaldosteronism. Apesar de comum, o hipoaldosteronismo hiporeninmico continua a ser uma entidade sub-diagnosticada, com maior prevalncia em pacientes com diabetes mellitus. A doena cursa com hipercalemia assintomtica acompanhada de acidose metablica hiperclormica sem disfuno renal significativa. O mecanismo fisiopatolgico subjacente no entendido em sua totalidade, mas postula-se que a deficincia de aldosterona (hipoaldosteronismo hiporeninmico) e/ou a resistncia aldosterona no rgo-alvo (pseudo-hipoaldosteronismo) possam ser responsveis. O diagnstico fundamentado em parmetros laboratoriais. A estratgia teraputica varia de acordo com o mecanismo fisiopatolg Continue reading >>

Renal Tubular Acidosis And Uraemic Acidosis

Renal Tubular Acidosis And Uraemic Acidosis

Metabolic acidosis can occur in both acute and chronic renal disorders the anion gap may be elevated, due to uraemic acidosis the anion gap may be normal, due to renal tubular acidosis (RTA) Uraemic acidosis results from the loss of functional nephrons decreased glomerular filtration rate (GFR) (e.g. <20 mL/min) accumulation of acidic anions such as phosphate and sulfate occurs causes high anion gap metabolic acidosis (HAGMA) patients manifest as renal failure, often have prolonged survival and develop chronic complications such as bone demineralisation Renal tubular acidosis (RTA) involves defects isolated to the renal tubules only GFR may be normal or only minimally affected primary problem is defective renal acid-base regulation due to impaired ability to acidify the urine and excrete acid results in net acid retention and hyperchloremic normal anion gap metabolic acidosis (NAGMA) may be incomplete and only develop in the presence of an acid load occurs despite a normal or only mildly reduced glomerular filtration rate (GFR) RTA is often detected incidentally through an abnormal blood workup, but some patients present with clinical features such as poor growth, dehydration, or altered mental state COMPARISON OF TYPES OF RENAL TUBULAR ACIDOSIS (RTA) urine pH remains >5.5 despite severe acidaemia (HCO3 < 15mmol/L) HCO3loading test leads to increased urinary HCO3 may require an acid load test to see whether urinary pH remains > 5.5 hyperchloraemic acidosis, alkaline urine, and renal stone formation secondary hyperaldosteronism results in increased K+ loss in urine NaHCO3 (corrects Na+ deficit, ECF volume and corrects hypokalaemia) sodium and potassium citrate solutions can be useful if hypokalaemia persistent citrate also binds Ca2+ in the urine and can help to prevent Continue reading >>

Adult-onset Distal Renal Tubular Acidosis With Hypokalemic Quadriparesis In A Patient With Autoimmune Hypothyroidism Naveen L, Malkarnekar S - J Integr Nephrol Androl

Adult-onset Distal Renal Tubular Acidosis With Hypokalemic Quadriparesis In A Patient With Autoimmune Hypothyroidism Naveen L, Malkarnekar S - J Integr Nephrol Androl

A 40-year-old lady, a known case of hypothyroidism, presented with 1-day history of progressive weakness in all four limbs and reported a history of similar episodes since 3 years. Clinical examination revealed grade 2 hyporeflexic quadriparesis without any bulbar involvement. Workup revealed hypokalemia, non-anion gap hyperchloremic metabolic acidosis and alkaline urine suggestive of distal renal tubular acidosis (RTA). Antiperoxidase and antithyroglobulin antibodies were positive, suggestive of an autoimmune basis for hypothyroidism. She was managed with intravenous potassium chloride, thyroid replacement and bicarbonate therapy, following which remarkable recovery was noted. One week later, she was discharged on oral thyroxine and oral sodium bicarbonate and she remained weakness-free for a follow-up period of over 1 year. RTA presenting in a setting of autoimmune hypothyroidism is a rare occurrence and the possible role of immunological mechanisms and thyroxine deficiency in the pathogenesis of acidification defect seems most likely. Keywords:Autoimmune, distal renal tubular acidosis, hypothyroidism, hypokalemic quadriparesis Key Messages: This case study emphasizes the fact that recurrent hypokalemic paralysis warrants the search for an underlying cause, which must be adequately addressed to prevent the persistence or recurrence of paralysis. Naveen L, Malkarnekar S. Adult-Onset Distal Renal Tubular Acidosis with Hypokalemic Quadriparesis in a Patient with Autoimmune Hypothyroidism. J Integr Nephrol Androl 2014;1:82-4 Naveen L, Malkarnekar S. Adult-Onset Distal Renal Tubular Acidosis with Hypokalemic Quadriparesis in a Patient with Autoimmune Hypothyroidism. J Integr Nephrol Androl [serial online] 2014 [cited2018 Apr 25];1:82-4. Available from: Renal tubular acido Continue reading >>

Renal Tubular Acidosis An Adverse Effect Of Pd-1 Inhibitor Immunotherapy

Renal Tubular Acidosis An Adverse Effect Of Pd-1 Inhibitor Immunotherapy

Renal Tubular Acidosis an Adverse Effect of PD-1 Inhibitor Immunotherapy 1Department of Internal Medicine, Northwell Health Staten Island University Hospital, Staten Island, NY, USA 2Department of Hematology and Oncology, Northwell Health Staten Island University Hospital, Staten Island, NY, USA 3Department of Nephrology, Northwell Health Staten Island University Hospital, Staten Island, NY, USA Correspondence should be addressed to Sandy El Bitar ; [email protected] Received 26 October 2017; Accepted 18 January 2018; Published 31 January 2018 Copyright 2018 Sandy El Bitar 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. Immune checkpoint blockade therapy is gaining popularity among oncologists for treatment of solid and hematologic malignancies. The widespread use of these agents resulted in increasing incidence of renal immune-related adverse events. Reported renal toxicity described so far includes acute interstitial nephritis, minimal change disease, and immune complex glomerulonephritis. We report the case of a 79-year-old female with metastatic non-small cell lung cancer on anti-PD-1 therapy nivolumab. After the 4th administration of nivolumab, the treatment course was complicated with normal anion gap metabolic acidosis. Urine and blood studies were in favor of distal renal tubular acidosis (RTA). Following a negative workup for an underlying etiology, immunotherapy-induced RTA was suspected. Withholding of the offending agent and initiation of steroid therapy resulted in adequate response. The present report provides the first presentation of RTA as a renal immune-related adverse event Continue reading >>

Workup For Mild Hyperkalemia

Workup For Mild Hyperkalemia

A 63-year-old asymptomatic man has had mild hyperkalemia (5.6-6.0 mEq/L) for the past six months. His physical examination and lab work are remarkable only for an elevated cholesterol level. He is a heavy smoker. Does this patient require workup for Addisons disease? How would you proceed? Embedded within this complex question are two separate but potentially interrelated issues: persistent hyperkalemia and the specter of adrenal insufficiency. First, hyperkalemia is rare in normal subjects. Your history should include a thorough search for medication use, both OTC and prescription (e.g., nonsteroidal anti-inflammatory drugs and diuretics). A set of normal laboratory values in this case should, at a minimum, exclude renal dysfunction, diabetes, and metabolic acidosis. In the absence of these abnormalities or rarer causes of hyperkalemia, such as selective defects in renal potassium handling and type I renal tubular acidosis, hypoaldosteronism should be considered. Hypoaldosteronism in the context of Addisons disease results from primary failure of the adrenal glands. While we most often consider this diagnosis with more dramatic presentations of hypotension and/or shock (adrenal crisis), it is worth noting that early symptoms may be mild and include fatigue, weakness, anorexia, and weight loss. Hyperkalemia is, in fact, relatively common, occurring in approximately 60% of cases of adrenal insufficiency. Even if your patient is presently asymptomatic, his condition may evolve over time. I would, therefore, proceed with testing of morning cortisol levels, followed by an adrenocorticotropic stimulation test if needed. Should you discover adrenal insufficiency in this patient, it would be important to rule out adrenal metastatic disease in the context of heavy tobacco use. Continue reading >>

Metabolic Acidosis Workup: Approach Considerations, Laboratory Evaluation, Complete Blood Count

Metabolic Acidosis Workup: Approach Considerations, Laboratory Evaluation, Complete Blood Count

Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN more... Often the first clue to metabolic acidosis is a decreased serum HCO3- concentration observed when serum electrolytes are measured. Remember, however, that a decreased serum [HCO3-] level can be observed as a compensatory response to respiratory alkalosis. An [HCO3-] level of less than 15 mEq/L, however, almost always is due, at least in part, to metabolic acidosis. The only definitive way to diagnose metabolic acidosis is by simultaneous measurement of serum electrolytes and arterial blood gases (ABGs) , which shows pH and PaCO2 to be low; calculated HCO3- also is low. (For more information, see Metabolic Alkalosis .) A low serum HCO3- and a pH of less than 7.40 upon ABG analysis confirm metabolic acidosis. Go to Pediatric Metabolic Acidosis and Emergent Management of Metabolic Acidosis for complete information on these topics. The diagnosis is made by evaluating serum electrolytes and ABGs. A low serum HCO3- and a pH of less than 7.40 upon ABG analysis confirm metabolic acidosis. The anion gap (AG) should be calculated to help with the differential diagnosis of the metabolic acidosis and to diagnose mixed disorders. In general, a high-AG acidosis is present if the AG is greater than 10-12 mEq/L, and a non-AG acidosis is present if the AG is less than or equal to 10-12 mEq/L. It is important to note that the AG decreases by 2.5 mEq for every 1 g/dL decrease in serum albumin. If the AG is elevated, the osmolar gap should be calculated by subtracting the calculated serum osmolality from the measured serum osmolality. Ethylene glycol and methanol poisoning increase the AG and the osmolar gap. Acetone, produced by decarboxylation of acetoacetate, can also raise serum osmolalit Continue reading >>

Renal Tubular Acidosis: Diagnostic Work-up, Treatment And Mechanisms Of Growth Retardation

Renal Tubular Acidosis: Diagnostic Work-up, Treatment And Mechanisms Of Growth Retardation

, Volume 55, Issue4 , pp 552558 | Cite as Renal tubular acidosis: diagnostic work-up, treatment and mechanisms of growth retardation Astute clinical observations, careful evaluation of laboratory results, together with research aimed at understanding the mechanisms of growth failure in children with the various types of renal tubular acidosis, have led to a more cogent approach to the management of children with renal tubular acidosis. This review examines the different clinical presentations of renal tubular acidosis, the diagnostic workup, the recent advances in our understanding of the mechanisms of growth failure and current therapeutic modalities. Fractional ExcretionGrowth FailureNephrocalcinosisRenal Tubular AcidosisCystinosis These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in to check access. Unable to display preview. Download preview PDF. McSherry E, Kaplan JS, Grumbach MM. The effect of acidosis on human growth hormone (hGH) release with non-azotemic renal tubular acidosis (RTA).Clin Res 1980;28:535A Google Scholar McSherry E. Renal tubular acidosis in childhood.Kidney Int 1981;20: 799809 PubMed CrossRef Google Scholar Chan JCM. Urinary sulfate excretion in childhood with classic renal tubular acidosis.Nutr Metab 1978;22: 257261 PubMed CrossRef Google Scholar Chesney RW, Kaplan BS, Phelps M, etal. Renal tubular acidosis does not alter circulating values of calcitriol.J Pediatr 1984;104: 5155 PubMed CrossRef Google Scholar Kraut JF, Gordon EM, Random JC, et al. Effect of chronic metabolic acidosis on vitamin D metabolism in humans.Kidney Int 1983;24: 644648 PubMed CrossRef Google Scholar Kitagawa T, Akuts Continue reading >>

Renal Tubular Acidosis

Renal Tubular Acidosis

Renal tubular acidosis (RTA) is a disorder in which a defect in secretion of protons by the proximal and/or distal nephron of the kidney results in bicarbonate wasting (proximal) or reduced acid secretion (distal). George J. Schwartz MD, in Pediatric Clinical Advisor (Second Edition) , 2007 Renal tubular acidosis (RTA) is a disorder in which a defect in secretion of protons by the proximal and/or distal nephron of the kidney results in bicarbonate wasting (proximal) or reduced acid secretion (distal). As a consequence, a persistent nonanion gap (hyperchloremic) metabolic acidosis develops. The serum anion gap, [Na] ([Cl] + [HCO3]), is normally 8 to 12mEq/L in adults and 20% to 30% higher in infants. Type 1 or classic RTA (i.e., distal renal tubular acidosis [DRTA]) Type 2 RTA (i.e., proximal renal tubular acidosis [PRTA]) Type 3 RTA (i.e., no longer considered a distinct entity) Type 4 RTA (i.e., hyperkalemic distal renal tubular acidosis) 588.89Acidosis, renal, tubular (distal or proximal) (Other specified disorders resulting from impaired renal function) Incidence of DRTA is 1 in 10,000 people; PRTA is less common. Although primary RTA is recognized to be a rare disease, referrals to exclude RTA are much more common than the incidence of the disease. As a referring diagnosis, primary RTA accounted for 6% of renal consultations in children of Venezuela. There is no sex predominance in DRTA or in Type 4 RTA. DRTA may be inherited as an autosomal dominant or recessive trait. Autosomal recessive DRTA often presents in infancy, whereas autosomal dominant DRTA may not present until adolescence or young adulthood. Mutations in the genes encoding carbonic anhydrase II, kidney anion exchanger 1 (kAE1), and subunits of the renal proton pump (H+ATPase) have been identified in p Continue reading >>

Should Blood Gas Analysis Be Part Of The Diagnostic Workup Of Short Children? Auxological Data And Blood Gas Analysis In Children With Renal Tubular Acidosis

Should Blood Gas Analysis Be Part Of The Diagnostic Workup Of Short Children? Auxological Data And Blood Gas Analysis In Children With Renal Tubular Acidosis

Should Blood Gas Analysis Be Part of the Diagnostic Workup of Short Children? Auxological Data and Blood Gas Analysis in Children with Renal Tubular Acidosis Mul D.a Grote F.K.a Goudriaan J.R.a de Muinck Keizer-Schrama S.M.P.F.b Wit J.M.a Oostdijk W.a I have read the Karger Terms and Conditions and agree. I have read the Karger Terms and Conditions and agree. Buy a Karger Article Bundle (KAB) and profit from a discount! If you would like to redeem your KAB credit, please log in . Save over 20% compared to the individual article price. Buy Cloud Access for unlimited viewing via different devices Access to all articles of the subscribed year(s) guaranteed for 5 years Unlimited re-access via Subscriber Login or MyKarger Unrestricted printing, no saving restrictions for personal use * The final prices may differ from the prices shown due to specifics of VAT rules. For additional information: Background: Renal tubular acidosis (RTA) is a rare cause of growth failure, therefore it is uncertain whether routine screening with blood gas analysis of short infants and children is cost-effective. Objective: To investigate the clinical, growth and laboratory parameters in children with RTA to estimate the possible value of laboratory screening for this disorder in infants and children referred for short stature according to a recent guideline. Method: Retrospective chart analysis of 30 children diagnosed between 1978 and 2005 in The Netherlands and 3 centers in Belgium. Results: The current guideline for short stature detected 33% of children with RTA. Assuming a pre-test probability of RTA of 0.6 per 100,000 births, the likelihood ratio of poor growth was 58 and 17 below and above 3 years, respectively. Sensitivity was 17/30 and 12/24 for a 2.0 SDS cutoff for weight and body mass Continue reading >>

Renal Tubular Acidosis

Renal Tubular Acidosis

Renal tubular acidosis (RTA) is acidosis and electrolyte disturbances due to impaired renal hydrogen ion excretion (type 1), impaired bicarbonate resorption (type 2), or abnormal aldosterone production or response (type 4). (Type 3 is extremely rare and is not discussed.) Patients may be asymptomatic, display symptoms and signs of electrolyte derangements, or progress to chronic kidney disease. Diagnosis is based on characteristic changes in urine pH and electrolytes in response to provocative testing. Treatment corrects pH and electrolyte imbalances using alkaline agents, electrolytes, and, rarely, drugs. RTA defines a class of disorders in which excretion of hydrogen ions or reabsorption of filtered bicarbonate is impaired, leading to a chronic metabolic acidosis with a normal anion gap. Hyperchloremia is usually present, and secondary derangements may involve other electrolytes, such as potassium (frequently) and calcium (rarelysee Table: Some Features of Different Types of Renal Tubular Acidosis* ). Chronic RTA is often associated with structural damage to renal tubules and may progress to chronic kidney disease . Some Features of Different Types of Renal Tubular Acidosis* Treatment of concomitant abnormalities related to potassium, calcium, and phosphate metabolism Treatment consists of correction of pH and electrolyte balance with alkali therapy. Failure to treat RTA in children slows growth. Alkaline agents such as sodium bicarbonate, potassium bicarbonate, or sodium citrate help achieve a relatively normal plasma bicarbonate concentration (22 to 24 mEq/L). Potassium citrate can be substituted when persistent hypokalemia is present or, because sodium increases calcium excretion, when calcium calculi are present. Vitamin D (eg, ergocalciferol 800 IU po once/day) Continue reading >>

Renal Tubular Acidosis

Renal Tubular Acidosis

Proximal RTA, defect in HCO3- reabsorption, mild hypokalemia results, Fanconi syndrome Mild hypokalemia comes from secondary aldosterone response to HCO3- loss Urine pH in acute vs. clinical presentation of Type II RTA Acute pH > 6.5 because of bicarbonate wasting Clinical pH < 5.5 because all of filtered HCO3- is removed and serum HCO3- is lower Multiple myeloma, heavy metals, carbonic anhydrase inhibitors, hereditary Weakness, bone pain, fractures due to osteomalacia (decreased synthesis of active vitamin D and phosphate wasting), imparied growth Hypokalemic distal RTA, inability to lower urine pH < 5.5. Decreased H+ secretion causes negative CCD and increased K+ secretion Alpha intercolated cell blockade: mutations in H+/K+ ATPase, carbonic anhydrase and AE1 bicarbonate/chloride antiport Calcium phosphate kidney stones, low urine citrate excretion Aldosterone deficient hyperkalemic RTA, ENaC expression decreases, decreased K+ and H+ secretion, usually mild/asymptomatic, urine pH < 5.5 b/c hyperkalemia supresses ammoniagenesis Aldosterone blockade: ACE inhibitors, ARBs, K+ sparing diuretics, abnormal aldosterone receptor. Also heparin ENaC deficiency or severe hypovolemia causes greater lumen positive charge than Type IV, urine pH > 6 Voltage-dependent hyperkalemic RTA etiologies Continue reading >>

Review Of The Diagnostic Evaluation Of Renal Tubular Acidosis

Review Of The Diagnostic Evaluation Of Renal Tubular Acidosis

Review of the Diagnostic Evaluation of Renal Tubular Acidosis 1Department of Internal Medicine, Redcliffe Hospital, Redcliffe, Queensland, Australia 2Department of Anaesthesia and Intensive Care Medicine, Caboolture Hospital, Caboolture, Queensland, Australia Address correspondence to Julian Yaxley, MBBS, Department of Internal Medicine, Redcliffe Hospital, Anzac Avenue, Redcliffe, Queensland, 4020, Australia. Tel: +61-4-2080-8049. Email: [email protected] Copyright Academic Division of Ochsner Clinic Foundation This article has been cited by other articles in PMC. The term renal tubular acidosis (RTA) describes a group of uncommon kidney disorders characterized by defective acid-base regulation. Reaching the diagnosis of RTA is complex and often delayed, resulting in suboptimal treatment. This article provides an overview of the clinical features of RTA and diagnostic approaches in a format accessible to physicians for everyday use. The 3 major forms of disease are classified by their respective tubular transport defects, each of which produces persistent hyperchloremic metabolic acidosis. Distal RTA is characterized by limited urinary acid secretion, proximal RTA by restricted urinary bicarbonate reabsorption, and hyperkalemic RTA by absolute or relative hypoaldosteronism. RTA is often detected incidentally as a biochemical diagnosis in asymptomatic individuals. When present, clinical features may range from mild nonspecific complaints to life-threatening physiologic disturbances. RTA is a complex condition that requires thoughtful investigation. Physicians should be aware of the presentation of RTA and the investigative options available to confirm the diagnosis. Keywords: Acid-base equilibrium, acidosis, acidosisrenal tubular Renal tubular acidosis (RTA) re Continue reading >>

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