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Renal Tubular Acidosis Type 1

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 >>

Type 3 Renal Tubular Acidosis

Type 3 Renal Tubular Acidosis

Aka: Type 3 Renal Tubular Acidosis, Type III Renal Tubular Acidosis, Type III RTA Variant of Type I RTA ( Distal RTA ) affecting children May precipitously fall to lethal levels (<3 meq/L) Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Type 3 Renal Tubular 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 Related Topics in Acid and Base Disorders FPnotebook.com is a rapid access, point-of-care medical reference for primary care and emergency clinicians. Started in 1995, this collection now contains 6557 interlinked topic pages divided into a tree of 31 specialty books and 722 chapters. Content is updated monthly with systematic literature reviews and conferences. Although access to this website is not restricted, the information found here is intended for use by medical providers. Patients should address specific medical concerns with their physicians. This page was written by Scott Moses, MD , last revised on 10/21/2007 and last published on 4/22/2018. 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 >>

8.5 Renal Tubular Acidosis

8.5 Renal Tubular Acidosis

Renal Tubular Acidosis (RTA) is a syndrome due to either a defect in proximal tubule bicarbonate reabsorption, or a defect in distal tubule hydrogen ion secretion, or both. This results in a hyperchloraemic metabolic acidosis with normal to moderately decreased GFR. Anion gap is normal. A typical situation where RTA would be suspected is if urine pH is greater than 7.0 despite the presence of a metabolic acidosis. In contrast, the acidosis that occurs with acute, chronic, or acute on chronic renal failure is a high anion gap metabolic acidosis. As a general overview to help understand why renal disease can give different types of acidosis consider the following:Acidosis due to renal disease is considered in 2 categories depending on whether the predominant site of renal damage is in the glomeruli or in the tubules. Renal tubular acidosis is a form of hyperchloraemic metabolic acidosis which occurs when the renal damage primarily affects tubular function without much effect on glomerular function. The result is a decrease in H+ excretion which is greater than can be explained by any change in GFR. In contrast, if glomerular function (ie GFR) is significantly depressed (hence 'renal failure'), the retention of fixed acids results in a high anion gap acidosis. Predominantly tubular damage ---> Normal anion gap acidosis (Renal tubular acidosis - RTA) Predominantly glomerular damage ---> High anion gap acidosis Three main clinical categories or 'types' of renal tubular acidosis (RTA) are now recognised but the number of possible causes is large. The mechanism causing the defect in ability to acidify the urine and excrete acid is different in the three types. 1,2 8.5.2 Distal (Type 1) Renal Tubular Acidosis This is also referred to as classic RTA or distal RTA. The problem h 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 >>

Renal Tubular Disease

Renal Tubular Disease

Zhuo JL, Li XC ; Proximal nephron. Compr Physiol. 2013 Jul3(3):1079-123. doi: 10.1002/cphy.c110061. Fiseha T, Gebreweld A ; Urinary Markers of Tubular Injury in HIV-Infected Patients. Biochem Res Int. 20162016:1501785. doi: 10.1155/2016/1501785. Epub 2016 Jul 17. Bagga A et al ; Approach to Renal Tubular Disorders Indian Journal of Pediatrics Volume 72-September, 2005. Distal renal tubular acidosis ; Orphanet, 2014 Rehman HU ; A woman with generalised weakness, hypokalaemia, and metabolic acidosis. BMJ. 2012 Apr 12344:e2545. doi: 10.1136/bmj.e2545. Both T, Zietse R, Hoorn EJ, et al ; Everything you need to know about distal renal tubular acidosis in autoimmune disease. Rheumatol Int. 2014 Aug34(8):1037-45. doi: 10.1007/s00296-014-2993-3. Epub 2014 Mar 29. Renal tubular acidosis ; BMJ Best Practice, 2016. Walsh SB, Unwin RJ ; Renal tubular disorders. Clin Med October 1, 2012 vol. 12 no. 5 476-479. Goswami RP, Mondal S, Karmakar PS, et al ; Type 3 renal tubular acidosis. Indian J Nephrol. 2012 Nov22(6):466-8. doi: 10.4103/0971-4065.106058. Haas CS, Pohlenz I, Lindner U, et al ; Renal tubular acidosis type IV in hyperkalaemic patients--a fairy tale or reality? Clin Endocrinol (Oxf). 2013 May78(5):706-11. doi: 10.1111/j.1365-2265.2012.04446.x. Karunarathne S, Udayakumara Y, Govindapala D, et al ; Type IV renal tubular acidosis following resolution of acute kidney injury and disseminated intravascular coagulation due to hump-nosed viper bite. Indian J Nephrol. 2013 Jul23(4):294-6. doi: 10.4103/0971-4065.114476. Prasad N, Bhadauria D ; Renal phosphate handling: Physiology. Indian J Endocrinol Metab. 2013 Jul17(4):620-7. doi: 10.4103/2230-8210.113752. Moutzouri E, Liberopoulos EN, Elisaf M ; Life-threatening hypophosphataemia in a cirrhotic patient with jaundice. Arch Med Sci Continue reading >>

Successful Management Of Refractory Type 1 Renal Tubular Acidosis With Amiloride

Successful Management Of Refractory Type 1 Renal Tubular Acidosis With Amiloride

Successful Management of Refractory Type 1 Renal Tubular Acidosis with Amiloride 1Department of Internal Medicine, University of Maryland School of Medicine, Baltimore, MD, USA 2Division of Nephrology, University of Maryland Medical Center Midtown Campus, Baltimore, MD, USA 3Department of Medicine, Division of Nephrology, Johns Hopkins School of Medicine, Baltimore, MD, USA 4Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA 5Nephrology Center of Maryland, Baltimore, MD, USA Correspondence should be addressed to Patrick Oguejiofor ; [email protected] Received 14 July 2016; Revised 2 December 2016; Accepted 14 December 2016; Published 3 January 2017 Copyright 2017 Patrick Oguejiofor 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. A 28-year-old female with history of hypothyroidism, Sjgrens Syndrome, and Systemic Lupus Erythematosus (SLE) presented with complaints of severe generalized weakness, muscle pain, nausea, vomiting, and anorexia. Physical examination was unremarkable. Laboratory test showed hypokalemia at 1.6 mmol/l, nonanion metabolic acidosis with HCO3 of 11 mmol/l, random urine pH of 7.0, and urine anion gap of 8 mmol/l. CT scan of the abdomen revealed bilateral nephrocalcinosis. A diagnosis of type 1 RTA likely secondary to Sjgrens Syndrome was made. She was started on citric acid potassium citrate with escalating dosages to a maximum dose of 60 mEq daily and potassium chloride over 5 years without significant improvement in serum K+ and HCO3 levels. She had multiple emergency room visits for persistent muscle pain, generalized weakness, Continue reading >>

Renal Tubular Acidosis

Renal Tubular Acidosis

Renal tubular acidosis (RTA) is a disease that occurs when the kidneys fail to excrete acids into the urine, which causes a person's blood to remain too acidic. Without proper treatment, chronic acidity of the blood leads to growth retardation, kidney stones, bone disease, chronic kidney disease, and possibly total kidney failure. The body's cells use chemical reactions to carry out tasks such as turning food into energy and repairing tissue. These chemical reactions generate acids. Some acid in the blood is normal, but too much acidacidosiscan disturb many bodily functions. Healthy kidneys help maintain acid-base balance by excreting acids into the urine and returning bicarbonatean alkaline, or base, substanceto the blood. This "reclaimed" bicarbonate neutralizes much of the acid that is created when food is broken down in the body. The movement of substances like bicarbonate between the blood and structures in the kidneys is called transport. One researcher has theorized that Charles Dickens may have been describing a child with RTA in the character of Tiny Tim from A Christmas Carol. Tiny Tim's small stature, malformed limbs, and periods of weakness are all possible consequences of the chemical imbalance caused by RTA.1 In the story, Tiny Tim recovers when he receives medical treatment, which would likely have included sodium bicarbonate and sodium citrate, alkaline agents to neutralize acidic blood. The good news is that medical treatment can indeed reverse the effects of RTA. To diagnose RTA, doctors check the acid-base balance in blood and urine samples. If the blood is more acidic than it should be and the urine less acidic than it should be, RTA may be the reason, but additional information is needed to rule out other causes. If RTA is the reason, additional in Continue reading >>

Renal Tubular Acidosis Type 1

Renal Tubular Acidosis Type 1

SDN members see fewer ads and full resolution images. Join our non-profit community! Can someone explain to me why in Renal tubular acidosis 1 you get hypokalemia??? I understand that the H+ uniporter in the intercalated cell in the collecting tubule is not working so H+ is retained, and you get metabolic acidosis. I always equate hyperkalemia with acidosis. So if you are retaining the H+ shouldnt you also be retaining the K+? Dont the H+ and K+ go in the same direction? Also based on the pic in FA in renal section it looks like the H+ is a uniporter and K+ is a uniporter and they go in the same direction which is secreted out of the tubule. However in wiki (i know i shouldnt be using this, it says that the H+ and K+ are antiporters). Can someone please clarify this for me? Thanks!!!! Can someone explain to me why in Renal tubular acidosis 1 you get hypokalemia??? I understand that the H+ uniporter in the intercalated cell in the collecting tubule is not working so H+ is retained, and you get metabolic acidosis. I always equate hyperkalemia with acidosis. So if you are retaining the H+ shouldnt you also be retaining the K+? Dont the H+ and K+ go in the same direction? Also based on the pic in FA in renal section it looks like the H+ is a uniporter and K+ is a uniporter and they go in the same direction which is secreted out of the tubule. However in wiki (i know i shouldnt be using this, it says that the H+ and K+ are antiporters). Can someone please clarify this for me? Thanks!!!! With respect to Na reabsorption, you lose K first to pick up Na and maintain neutrality. Once you are low on K you start dumping H+ into the lumen. There are Na, K, and H channels for this purpose. There are also several other channels/transporters in the collecting duct which I learned a lo Continue reading >>

Kidney Tubular Acidosis

Kidney Tubular Acidosis

Kidney tubular acidosisalso called renal tubular acidosis (RTA)is a condition that occurs when the kidneys do not properly filter acids from the blood into the urine causing the blood to become too acidic. Without treatment and over time, acidity of the blood can lead to one or more of the following: There are four types of renal tubular acidosis: Type 1. Type 1 renal tubular acidosisalso called distal RTAoccurs relatively far from the beginning of the renal tubule (the part of the kidney where acid and waste products are removed from the blood). A main effect of distal RTA is low blood potassium levels, which can cause extreme weakness, irregular heartbeat, paralysis and, more rarely, death. Type 1 RTA can be inherited or a symptom of: Type 2. Type 2 renal tubular acidosisalso called proximal RTAoccurs closer to the beginning of the renal tubule. This type of RTA occurs more often in infants as part of a disorder called Fanconi syndrome (a disorder in which certain needed minerals are passed into the urine instead of being reabsorbed into the bloodstream). Proximal RTA can also occur as a symptom of some inherited disorders that keep the body from effectively breaking down and using nutrients. Examples of inherited disorders that can lead to proximal RTA include cystinosis (a condition in which the amino acid cystine builds up in the body and damages cells) and Wilson's disease. Type 3. Type 3 renal tubular acidosis is considered to be a combination of Type 1 RTA and Type 2 RTA. Type 4. Type 4 renal tubular acidosisalso called hyperkalemic RTAoccurs when a part of the kidney called the distal tubule fails to move electrolytes from the blood to the urine, causing a buildup of electrolytes in the blood. Hyperkalemic RTA can happen if there is a deficiency of the hormone Continue reading >>

Type 1 (distal) Renal Tubular Acidosis - Deranged Physiology

Type 1 (distal) Renal Tubular Acidosis - Deranged Physiology

This form of renal tubular acidosis is a failure of the cortical collecting duct to decrease chloride resorption in response to acidosis. The defect seems to be in the activity of alpha-intercalated cells of the collecting duct. The mechanism of distal renal tubular acidosis There are a few mechanisms discussed in the literature, each of which can result in a diminished urinary acidification, and in a normal anion gap metabolic acidosis. The key feature of the renal tubular mechanisms involved here is the import of systemic ammonia, as well as the de novo synthesis of ammonia from glutamine within the renal tubule. (This ammonia also leaks out of the kidney into the systemic circulation, but in itself it is not a significant contributor to systemic ammonia levels , in case you are wondering.) Firstly, one can completely destroy the water-impermeable membranes which separate the peritubular capillary and the tubular lumen. This would lead to an equilibration of bicarbonate and chloride, with the resulting failure to excrete one and retain the other. This is exactly what happens when amphotericin attacks the tubule. Any interference with NH3 and H+ excretion in the alpha-intercalated cells is another such mechanism. The ionized NH4+, the combination of excreted NH3 and H+ remains in the lumen of the tubule (where it is trapped by its charge). This positive charge is balanced by the chloride anions, which are already present in the tubule. Any defect of ammonia excretion would therefore decrease the concentration of chloride anions in the tubular fluid. This chloride would have to be retained. The main defect in this case seems to be a problem with ATP-powered H+ secretion, which is normally an acidity-regulated process. As pH drops, so the activity of this protein should Continue reading >>

Renal Tubular Acidosis

Renal Tubular Acidosis

Renal tubular acidosis (RTA) refers to the non-anion gap metabolic acidosis which develops due to derangement of usual metabolic processes in the kidneys. The kidneys have a critical role in maintaining stable physiologic pH and they do so through several mechanisms throughout the nephron. Proximally, filtered bicarbonate is resorbed and distally acid is excreted then buffered in the urine. If the kidneys lose the ability to carry out these functions, renal tubular acidosis results. The three major forms of renal tubular acidosis are differentiated by the specific type and location of the mechanistic defect. An understanding of the basic physiology of the handling of acid by the kidney allows one to use clinical and laboratory clues to diagnose the type of RTA. The three key renal mechanisms to handle acid are listed below with the form of RTA associated with defects at that site. Reclaiming filtered bicarbonate in the proximal tubule - proximal (type 2) renal tubular acidosis The reclamation of bicarbonate is accompanied by excretion of a proton (H+) and occurs primarily in the proximal tubule (90% of filtered bicarbonate). A decrease in proximal tubular bicarbonate resorptive capacity results in proximal (type 2) RTA. During the development of proximal RTA, bicarbonate is excreted into the urine because the filtered concentration exceeds the resorptive threshold of the proximal tubule, raising the urine pH. However, due to urinary loss, the subsequent serum and filtered bicarbonate concentrations decrease below the resorptive threshold such that filtered bicarbonate is then resorbed normally. Therefore the bicarbonaturia is self-limited and the serum bicarbonate concentration usually stabilizes between 14 and 20 meq/L. The urine pH is only transiently elevated during Continue reading >>

Distal Renal Tubular Acidosis Type 1

Distal Renal Tubular Acidosis Type 1

0 evaluations from distal renal tubular acidosis type 1 patients report major effectiveness of Venlafaxine for depressed mood (0%) 1 evaluation from a distal renal tubular acidosis type 1 patient reports moderate effectiveness of Venlafaxine for depressed mood (50%) 1 evaluation from a distal renal tubular acidosis type 1 patient reports slight effectiveness of Venlafaxine for depressed mood (50%) 0 evaluations from distal renal tubular acidosis type 1 patients report none effectiveness of Venlafaxine for depressed mood (0%) 0 evaluations from distal renal tubular acidosis type 1 patients report that they could not tell effectiveness of Venlafaxine for depressed mood (0%) 0 evaluations from distal renal tubular acidosis type 1 patients report severe overall side effects for Venlafaxine (0%) 0 evaluations from distal renal tubular acidosis type 1 patients report moderate overall side effects for Venlafaxine (0%) 2 evaluations from distal renal tubular acidosis type 1 patients report mild overall side effects for Venlafaxine (100%) 0 evaluations from distal renal tubular acidosis type 1 patients report no overall side effects for Venlafaxine (0%) 0 evaluations from distal renal tubular acidosis type 1 patients report major effectiveness of Gabapentin for pain (0%) 0 evaluations from distal renal tubular acidosis type 1 patients report moderate effectiveness of Gabapentin for pain (0%) 0 evaluations from distal renal tubular acidosis type 1 patients report slight effectiveness of Gabapentin for pain (0%) 1 evaluation from a distal renal tubular acidosis type 1 patient reports none effectiveness of Gabapentin for pain (100%) 0 evaluations from distal renal tubular acidosis type 1 patients report that they could not tell effectiveness of Gabapentin for pain (0%) 0 evaluatio Continue reading >>

Orphanet: Distal Renal Tubular Acidosis

Orphanet: Distal Renal Tubular Acidosis

Only comments seeking to improve the quality and accuracy of information on the Orphanet website are accepted. For all other comments, please send your remarks via contact us . Only comments written in English can be processed. Check this box if you wish to receive a copy of your message Distal renal tubular acidosis (dRTA) is a disorder of impaired net acid secretion by the distal tubule characterized by hyperchloremic metabolic acidosis. The classic form is often associated with hypokalemia whereas other forms of acquired dRTA may be associated with hypokalemia, hyperkalemia or normokalemia. Inheritance: Autosomal dominantorAutosomal recessiveorNot applicable Prevalence of dRTA is unknown but is often underreported. The hereditary forms of dRTA are more prevalent in areas of high consanguinity (Arabic peninsula and North Africa) whereas acquired dRTA has been reported more frequently in Western countries. Disease onset can occur at any age, depending on cause. Hereditary dRTA subtypes include autosomal dominant (AD) and autosomal recessive (AR) dRTA (see these terms). A recessive subtype of dRTA associated with anemia has also been described in Southeast Asia. AR forms are frequently diagnosed in infants and young children. AD dRTA is mostly diagnosed in adolescents and young adults. Patients with dRTA can be asymptomatic or can present with polyuria, polydipsia, weakness and fatigue (symptoms associated with hypokalemia). Failure to thrive, rickets, stunting of growth (seen in children) and osteomalacia or osteopenia (seen in adults) are a result of urinary calcium wastage and a loss of calcium salts from the bones. Hypercalciuria, nephrolithiasis and nephrocalcinosis usually occur. Low plasma potassium levels in those with the classic form of dRTA can also cause ca 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 >>

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