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Renal Tubular Acidosis Type 1

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

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 >>

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: The Clinical Entity

Renal Tubular Acidosis: The Clinical Entity

Renal Tubular Acidosis: The Clinical Entity Department of Pediatrics, Hospital de Cruces, Vizcaya, Spain. Correspondence to Professor J. Rodrguez-Soriano, Department of Pediatrics, Hospital de Cruces, Plaza de Cruces s/n, Baracaldo, 48903 Vizcaya, Spain. Phone: 34-94-6006357; Fax: 34-94-6006044; E-mail: jsoriano{at}hcru.osakidetza.net The term renal tubular acidosis (RTA) is applied to a group of transport defects in the reabsorption of bicarbonate (HCO3), the excretion of hydrogen ion (H+), or both. This condition was first described in 1935 ( 1 ), confirmed as a renal tubular disorder in 1946 ( 2 ), and designated renal tubular acidosis in 1951 ( 3 ). The RTA syndromes are characterized by a relatively normal GFR and a metabolic acidosis accompanied by hyperchloremia and a normal plasma anion gap. In contrast, the term uremic acidosis is applied to patients with low GFR in whom metabolic acidosis is accompanied by normo- or hypochloremia and an increased plasma anion gap. The renal acid-base homeostasis may be broadly divided into two processes: (1) reabsorption of filtered HCO3, which occurs fundamentally in the proximal convoluted tubule; and (2) excretion of fixed acids through the titration of urinary buffers and the excretion of ammonium, which takes place primarily in the distal nephron. The mechanisms for proximal reabsorption of approximately 80 to 90% of filtered HCO3 are displayed in Figure 1 . The foremost processes occurring in this segment are H+ secretion at the luminal membrane via a specific Na+- H+ exchanger (NHE-3) and HCO3 transport at the basolateral membrane via a Na+- HCO3 cotransporter (NBC-1). In the proximal tubules, carbonic acid (H2CO3) is formed within the cell by the hydration of CO2, a reaction catalyzed by a soluble cytoplasmic carbonic 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 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 >>

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 >>

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 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 >>

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 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 >>

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 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 >>

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 >>

Case Of Distal Renal Tubular Acidosis (type 1) Presenting With Musculoskeletal Pain | Rheumatology | Oxford Academic

Case Of Distal Renal Tubular Acidosis (type 1) Presenting With Musculoskeletal Pain | Rheumatology | Oxford Academic

Sir, Musculoskeletal symptoms are often the presenting complaint in patients with renal tubular acidosis (RTA) [ 1 ]. The biochemical picture can, however, be incomplete during the early stage of RTA, thus making it difficult to diagnose. We present a 46-yr-old lady, referred with a 9-month history of widespread myalgia and arthralgia. Past history included hyperthyroidism requiring subsequent thyroidectomy followed by thyroxine replacement. At presentation she was receiving regular lithotripsy, having had recurrent renal stones for 4 yr. Her family history included her grandmother, father and one sister suffering from renal problems, and her brother had recently been diagnosed with nephrolithiasis. Examination of the cardiovascular, respiratory and abdominal systems was unremarkable. She had generalized muscle weakness but her tendon reflexes, plantar responses and sensory examination were normal. There were no joint abnormalities. She had a wide-based gait and was using one elbow crutch. Investigations showed a normal full blood count, erythrocyte sedimentation rate (ESR), sodium, potassium, urea and creatinine; she was negative for antinuclear antibody (ANA) and rheumatoid factor (RF); alkaline phosphatase was 337 IU/l (normal range 40140 IU/l), aspartate aminotransferase 13 IU/l (normal range 1060 IU/l), bilirubin 7 mol/l (normal range 517 mol/l), parathyroid hormone 3.3 pmol/l (normal range 0.95.4 pmol/l) and 25-hydroxyvitamin D3 25.5 IU (normal range 850); urinary calcium and creatine kinase were normal. The raised alkaline phosphatase was shown to be bone-derived. The bone scan, requested because of the high alkaline phosphatase, showed symmetrical abnormal uptake in both sacroiliac regions and in both femoral heads, suggestive of avascular necrosis. It also sho Continue reading >>

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