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Renal Tubular Acidosis Diagnosis Criteria

Proximal Renal Tubular Acidosis

Proximal Renal Tubular Acidosis

URL of this page: //medlineplus.gov/ency/article/000497.htm Proximal renal tubular acidosis is a disease that occurs when the kidneys don't properly remove acids from the blood into the urine. As a result, too much acid remains in the blood (called acidosis ). When the body performs its normal functions, it produces acid. If this acid is not removed or neutralized, the blood will become too acidic. This can lead to electrolyte imbalances in the blood. It can also cause problems with normal function of some cells. The kidneys help control the body's acid level by removing acid from the blood and excreting it into the urine. Acidic substances in the body are neutralized by alkaline substances, mainly bicarbonate. Proximal renal tubular acidosis (Type II RTA) occurs when bicarbonate is not properly reabsorbed by the kidney's filtering system. Type II RTA is less common than Type I RTA. Type I is also called distal renal tubular acidosis . Type II most often occurs during infancy and may go away by itself. Cystinosis (body is unable to break down the substance cysteine) Drugs such as ifosfamide (a chemotherapy drug), certain antibiotics that are no longer used much (tetracycline), or acetazolamide Fanconi syndrome , a disorder of the kidney tubes in which certain substances normally absorbed into the bloodstream by the kidneys are released into the urine instead Inherited fructose intolerance , a disorder in which there is a lack of the protein needed to break down the fruit sugar fructose Multiple myeloma , a type of blood cancer Primary hyperparathyroidism , a disorder in which the parathyroid glands in the neck produce too much parathyroid hormone Sjgren syndrome , an autoimmune disorder in which the glands that produce tears and saliva are destroyed Wilson disease , an Continue reading >>

Prevalence And Characterization Of Renal Tubular Acidosis In Patients With Osteopenia And Osteoporosis And In Nonporotic Controls

Prevalence And Characterization Of Renal Tubular Acidosis In Patients With Osteopenia And Osteoporosis And In Nonporotic Controls

Prevalence and characterization of renal tubular acidosis in patients with osteopenia and osteoporosis and in nonporotic controls Department of Internal Medicine, Krankenhaus der Barmherzigen Brder, Graz, Austria Search for other works by this author on: Department of Internal Medicine, Krankenhaus der Barmherzigen Brder, Graz, Austria Search for other works by this author on: Department of Internal Medicine, Krankenhaus der Barmherzigen Brder, Graz, Austria Search for other works by this author on: Department of Internal Medicine, Krankenhaus der Barmherzigen Brder, Graz, Austria Search for other works by this author on: Department of Internal Medicine, Krankenhaus der Barmherzigen Brder, Graz, Austria Search for other works by this author on: Nephrology Dialysis Transplantation, Volume 15, Issue 7, July 2000, Pages 975980, Wolfgang Weger, Peter Kotanko, Martin Weger, Hannes Deutschmann, Falko Skrabal, Prevalence and characterization of renal tubular acidosis in patients with osteopenia and osteoporosis and in nonporotic controls, Nephrology Dialysis Transplantation, Volume 15, Issue 7, July 2000, Pages 975980, Background. Chronic metabolic acidosis may increase alkali mobilization from the bone and thus promote the development of osteoporosis. The objective of the current study was to compare urinary acidification in patients with reduced bone mineral content with that in control subjects with normal bone density. Methods. Fortysix subjects (41 females, 5 males) with osteopenia or osteoporosis were studied. In none of the subjects were overt metabolic acidosis, derangement of potassium homeostasis, or renal insufficiency present. Distal tubular acidification was studied by means of oral ammonium chloride loading test (0.1 g/kg body weight) and the oral frusemide test Continue reading >>

Approach To The Patient With Renal Tubular Acidosis - Oxford Medicine

Approach To The Patient With Renal Tubular Acidosis - Oxford Medicine

PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com).Oxford University Press, 2016. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy and Legal Notice ). The renal tubular acidoses are a collection of syndromes characterized by defective urinary acidification. These syndromes have classically caused some confusion, and many opine that the widely used numerical system (type 1, 2) should be abandoned. We consider distal renal tubular acidosis and proximal renal tubular acidosis separately, and briefly cover hypoaldosteronism.Distal (Type 1) renal tubular acidosis is a syndrome of hypokalaemia, metabolic acidosis, kidney stones, nephrocalcinosis, and osteomalacia or rickets. It is caused by failure of the acid secreting -intercalated cells in the distal nephron.Proximal (Type 2) renal tubular acidosis is a syndrome of metabolic acidosis that is almost always accompanied by the Fanconi syndrome of glycosuria, phosphaturia, uricosuria, aminoaciduria, and low-molecular-weight proteinuria. It is caused by a failure of bicarbonate reabsorption by the proximal tubular cells.Type 3 or mixed renal tubular acidosis, as originally described, has vanished (or was originally incompletely described). It is sometimes used to describe a mutation of carbonic anhydrase II, which causes both proximal and distal renal tubular acidosis, as well as cerebral calcification and osteopetrosis.Type 4 or hypoaldosteronism is a syndrome of hyperkalaemia and mild metabolic acidosis. It is due to a lack of aldosterone or resistance to its action. Access to the complete content on Oxford Medicine Online requires a subscription or purchase. Continue reading >>

Primary Distal Renal Tubular Acidosis - Nord (national Organization For Rare Disorders)

Primary Distal Renal Tubular Acidosis - Nord (national Organization For Rare Disorders)

NORD gratefully acknowledges Daniel Batlle, MD, Earle, del Greco Levin Professor of Nephrology/ Hypertension, Professor of Medicine, Northwestern University Feinberg School of Medicine, Division of Nephrology/ Hypertension, for assistance in the preparation of this report. Synonyms of Primary Distal Renal Tubular Acidosis Subdivisions of Primary Distal Renal Tubular Acidosis ATP6V1B1-associated distal renal tubular acidosis ATP6V0A4-associated distal renal tubular acidosis SLC4A1-associated distal renal tubular acidosis Primary distal renal tubular acidosis (dRTA) is a rare genetic disorder that affects the ability of the kidneys to remove acid from the blood. This leads to metabolic acidosis. Metabolic acidosis is a condition in which the circulating chemical acids and bases are out of balance. The blood of affected individuals contains too much acid and the urine contains too little acid. Chronic metabolic acidosis can lead to a variety of symptoms. The specific signs, symptoms, and severity of this disorder can vary from one person to another. There are different forms of primary distal renal tubular acidosis. They are caused by a variation (mutation) in one of at least three different genes; the SLC4A1 gene, the ATP6V0A4 gene, and the ATP6V1B1 gene. A variation in the SLC4A1 gene is usually inherited in an autosomal dominant pattern, and less often in an autosomal recessive pattern. Variations in the ATP6V0A4 and ATP6V1B1 genes are usually inherited in an autosomal recessive pattern. A mixture of sodium and potassium salts in the form of sodium citrate or potassium citrate liquid solutions is usually recommended. Liquid preparations, however, have poor palatability and acceptance among patients. In this case, sodium bicarbonate tablets are used instead or in additi Continue reading >>

Incidence Of Renal Tubular Acidosis In Nephrology Unit In Assiut University Childern Hospital

Incidence Of Renal Tubular Acidosis In Nephrology Unit In Assiut University Childern Hospital

You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. Incidence of Renal Tubular Acidosis in Nephrology Unit in Assiut University Childern Hospital The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. Verified August 2017 by Sally Ezzat Shafik mikhail, Assiut University. Recruitment status was: Not yet recruiting Information provided by (Responsible Party): Sally Ezzat Shafik mikhail, Assiut University Top of Page Study Description Study Design Groups and Cohorts Outcome Measures Eligibility Criteria Contacts and Locations More Information Providing summarized information on the clinical and biochemical characteristics and types of renal tubular acidosis in children in Assiut University Childern Hospital. Diagnostic Test: Arterial blood gases Diagnostic Test: Blood anion gap Diagnostic Test: serum electrolytes Diagnostic Test: renal function test Diagnostic Test: urine analysis 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, confirmed as a renal tubular disorder in 1946, and designated "renal tubular acidosis" in 1951. The RTA syndromes are characterized by a relatively normal GFR and a metabolic acidosis accompanied by hyperchloremia and a normal plasma anion gap. RTA is classified into 4 major forms: distal, proximal, hyperkalemic and combined RTA. Distal RTA is associated with reduced urinary acid secretion, proximal RTA ( pRTA ) is characterized by impaired bicarbonate (H 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 >>

Metabolic Acidosis Treatment & Management

Metabolic Acidosis Treatment & Management

Approach Considerations 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 while the serum HCO3- level remained at 15 mEq/L. In lactic acidosis and diabetic ketoacidosis, the organic anion can r Continue reading >>

Distal Renal Tubular Acidosis

Distal Renal Tubular Acidosis

I do not know why anyone would diagnose distal RTA (dRTA) very often. As I will show you it has colorful and unusual characteristics as unmistakable as rare, so diagnosis is not difficult. But many more people think they have than have it. In my 50 years of kidney stone prevention I have perhaps a few dozen examples or so, out of many thousands of stone formers. This is another of those long, elaborate articles only the most devoted read. Even so, elaborate as it is, this article tells only part of the story. It simplifies or simply ignores the mechanism for low potassium in dRTA, and left for another time its genetic causes, and also the bone and mineral disorders and treatment outcomes. I forgive myself, as just this part has been most taxing to write and is equally so to read. In a subsequent article I hope to expand on diagnosis and treatment, the bone and mineral disorders, genetic transporter disorders, and take up the novel modern issue of acid retention and its effects on kidneys. So consider the present article a part of my planned contribution. The featured illustration of kidney tissue from a patient with dRTA shows many crystal deposits on a radiograph (panel a), that at surgery mostly are calcified deposits (panel b) that nearly replace papillary tissue (panels c and d). Kidneys make urine more acid than blood because most of us eat a diet that imposes an acid load on the body and kidneys need to remove that acid.But apart from balancing acid excretion to diet acid load, unless kidneys acidify urine calcium phosphate crystals may form in such profusion as to block kidney tubules and produce kidney stones. This happens because as they conserve water kidneys concentrate urine calcium phosphate salts far above their levels in blood. If they simultaneously mak Continue reading >>

Payperview: Renal Tubular Acidosis In Sjgren's Syndrome: A Case Series - Karger Publishers

Payperview: Renal Tubular Acidosis In Sjgren's Syndrome: A Case Series - Karger Publishers

I have read the Karger Terms and Conditions and agree. Background: The exact frequency of distal and proximal renal tubular acidosis (RTA) in Sjgren's syndrome is unknown. Other features of Sjgren's syndrome like polyuria, glomerular manifestations, familial occurrence and pregnancy are not widely reported. The aim was to prospectively study the clinical features and outcome of distal and proximal RTA in Sjgren's syndrome and also report on other renal manifestations of Sjgren's syndrome. Methods: The present study is a prospective consecutive case series of patients who presented with a history suggestive of RTA and Sjgren's syndrome. All patients were followed for 1 year. The diagnosis of RTA was by fractional excretion of bicarbonate. The diagnosis of Sjgren's syndrome was according to the American-European classification system [modified by Tzioufas and Voulgarelis: Best Pract Res Clin Rheumatol 2007;21:989-1010]. Results: The total number of RTA patients diagnosed during this period was 149. Sjgren's syndrome accounted for 34.8% (52 of 149) of RTA patients. The important symptoms and laboratory parameters were oral and ocular symptoms in 23 (44.2%), dental caries in 12 (23%), body pains in 47 (90.3%), mean serum pH 7.202 0.03, mean serum bicarbonate, 14.03 1.66 mmol/l, and mean urine pH, 7.125 0.54. There were 30 (57.6%) patients with distal RTA and 22 (42.3%) patients with proximal RTA. Conclusions: The clinical implication of the present study is that RTA is a common feature of Sjgren's syndrome. It may be missed if the presentation is not due to oral and ocular symptoms. The present study is also the only one with a 1-year follow-up. Sjgren H: Zur Kenntnis der Keratoconjunctivitis sicca (Keratitis filiformis bei Hypofunktion der Trnendrsen). Acta Ophthalmol 193 Continue reading >>

Renal Tubular Acidosis (rta)

Renal Tubular Acidosis (rta)

Renal tubular acidosis (RTA)refers to anormal anion gap metabolic acidosis (also known as a hyperchloremic acidosis) caused by: decreased excretion of hydrogen ions and/or decreased reabsorption of sodium bicarbonate in the renal tubules The abnormal acid-base transport within the tubules cannot be solely explained by decreased a glomerular filtration rate (GFR) secondary to chronic kidney disease, obstructive uropathy, or some other non-specific nephropathic mechanism The precise pathophysiological mechanism underlying the disorder varies across RTA sub-types (I-IV), which are described in detail below. Normal Acid-Base Homeostasis within the Renal Tubules Acid-base handling in the renal tubule can be broken down into two stages: Proximal reabsorption of filtered bicarbonate Proximal Reabsorption of BicarbonateSoriano JR. Renal Tubular Acidosis: The Clinical Entity. JASN. 2002 The reabsorption of filtered bicarbonate in the proximal tubule depends on the activity of carbonic anhydrase and several transporters: Intracellular carbonic anhydrase (CA-II) creates carbonic acid from water and carbon dioxide, which in turn ionizes to form a hydrogen ion plus bicarbonate The newly created bicarbonate is passively transported into the blood along with sodium by the co-transporter NBC-1 The newly created hydrogen ion is excreted into the tubule by NHE-3, which is driven by the anti-transport of sodium (down its concentration gradient) Intraluminal carbonic anhydrase (CA-IV) combines the intraluminal bicarbonate and hydrogen ion into water and CO2, the latter of which diffuses back into the cell (and is used as substrate for CA-II), thus driving a net absorption of bicarbonate Distal Acidification of UrineSoriano JR. Renal Tubular Acidosis: The Clinical Entity. JASN. 2002 The ac 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 b Continue reading >>

Renal Tubular Acidosis | The Online Metabolic And Molecular Bases Of Inherited Disease | Ommbid | Mcgraw-hill Medical

Renal Tubular Acidosis | The Online Metabolic And Molecular Bases Of Inherited Disease | Ommbid | Mcgraw-hill Medical

Renal tubular acidosis (RTA) is a clinical syndrome characterized by hyperchloremic metabolic acidosis secondary to an abnormality in renal acidification. The acidification defect may be manifested by an inappropriately high urine pH, bicarbonaturia, and, by definition, reduced net acid excretion. Classical distal renal tubular acidosis and proximal renal tubular acidosis are frequently associated with hypokalemia. Distal renal tubular acidosis can also result from a generalized dysfunction of the distal nephron, in which case it is usually accompanied by hyperkalemia and may be associated with either hypoaldosteronism or aldosterone resistance. Proximal renal tubular acidosis may result from an isolated defect of acidification in the proximal nephron. The isolated defect in acidification could be the result of selective dysfunction of the Na+/H+ antiporter, the proximal tubule H+-ATPase or the Na+/HCO3 /CO3 = symporter. More commonly, proximal renal tubular acidosis occurs as one manifestation of a generalized defect in proximal tubule function. Patients with this generalized abnormality, the Fanconi syndrome, usually have glycosuria, aminoaciduria, citraturia, and phosphaturia. The acidification defect associated with this generalized tubular dysfunction may be the result of (a) impairment of cellular ATP generation, (b) cellular phosphate depletion, or (c) a selective abnormality of the basolateral Na+, K+-ATPase. Vitamin D deficiency is associated with the Fanconi lesion. The transport defect may be due to a combination of factors including reduction in 1,25-dihydroxy vitamin D3 levels, elevated parathyroid hormone levels, hypocalcemia, and intracellular phosphate depletion. The diagnosis of proximal renal tubular acidosis is based on the demonstration of a chronic 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 >>

Symptomatic Renal Tubular Acidosis (rta) In Patients With Systemic Lupus Erythematosus: An Analysis Of Six Cases With New Association Of Type 4 Rta

Symptomatic Renal Tubular Acidosis (rta) In Patients With Systemic Lupus Erythematosus: An Analysis Of Six Cases With New Association Of Type 4 Rta

Symptomatic renal tubular acidosis (RTA) in patients with systemic lupus erythematosus: an analysis of six cases with new association of type 4 RTA Correspondence to: L. B. Liou, Division of Rheumatology, Allergy and Immunology, Chang Gung Memorial Hospital, Kwei-San Hsiang, Tao-Yuan County, Taiwan 333. E-mail: [email protected] Search for other works by this author on: Rheumatology, Volume 44, Issue 9, 1 September 2005, Pages 11761180, S. L. Li, L. B. Liou, J. T. Fang, W. P. Tsai; Symptomatic renal tubular acidosis (RTA) in patients with systemic lupus erythematosus: an analysis of six cases with new association of type 4 RTA, Rheumatology, Volume 44, Issue 9, 1 September 2005, Pages 11761180, Objectives. We have analysed the association between different parameters of renal tubular acidosis (RTA) with clinical and laboratory parameters in patients with systemic lupus erythematosus (SLE). Methods. Review of hospital database records between 1978 and 2003 revealed six SLE patients with RTA. Correlations and comparisons were done by Spearman rank correlation coefficient and the 2 test. Results. Four patients had hypokalaemia (type 1 RTA) and two patients had hyperkalaemia (type 4 RTA). Three patients with type 1, but no patients with type 4 RTA, had medullary nephrocalcinosis. The majority of SLE patients with distal RTA (type 1 and type 4) had nephritis with proteinuria. No seronegative SLE was noted, and all patients were negative for anticardiolipin antibodies. There was a noticeable trend of higher serum potassium levels with increased SLE Disease Activity Index (SLEDAI; P<0.1) and nephritic manifestation (haematuria, P<0.1). The mean SLEDAI scores were 11.75 and 27.5 for type 1 and type 4 RTA patients, respectively. Conclusions. When present in patients with Continue reading >>

(pdf) Furosemide/fludrocortisone Test And Clinical Parameters To Diagnose Incomplete Distal Renal Tubular Acidosis In Kidney Stone Formers

(pdf) Furosemide/fludrocortisone Test And Clinical Parameters To Diagnose Incomplete Distal Renal Tubular Acidosis In Kidney Stone Formers

Background and objectives Incomplete distal renal tubular acidosis is a well known cause of calcareous nephrolithiasis but the prevalence is unknown, mostly due to lack of accepted diagnostic tests and criteria. The ammonium chloride test is considered as gold standard for the diagnosis of incomplete distal renal tubular acidosis, but the furosemide/udrocortisone test was recently proposed as an alternative. Because of the lack of rigorous comparative studies, the validity of the furosemide/udrocortisone test in stone formers remains unknown. In addition, the performance of conventional, nonprovocative parameters in predicting incomplete distal renal tubular acidosis has not been studied. Design, setting, participants, & measurements We conducted a prospective study in an unselected cohort of 170 stone formers that underwent sequential ammonium chloride and furosemide/udrocortisone testing. Results Using the ammonium chloride test as gold standard, the prevalence of incomplete distal renal tubular acidosis was 8%. Sensitivity and specicity of the furosemide/udrocortisone test were 77% and 85%, respectively, yielding a positive predictive value of 30% and a negative predictive value of 98%. Testing of several nonprovocative clinical parameters in the prediction of incomplete distal renal tubular acidosis revealed fasting morning urinary pH and plasma potassium as the most discriminative parameters. The combination of a fasting morning u rinary threshold pH ,5.3 with a pla sma potassium threshold .3. 8 mEq/L yielded a negative predictive value of 98% with a sensitivity of 85% and a specicity of 77% for the diagnosis of incomplete distal Conclusions The furosemide/udrocortisone test can be used for incomplete distal renal tubular acidosis screening in stone formers, but a Continue reading >>

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