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Renal Tubular Acidosis Diagnosis Criteria

Singhvi

Singhvi

Primary Sjgren's Syndrome presenting as quadriplegia and respiratory involvement due to renal tubular acidosis causing hypokalemia is rare and the significance of managing such case with potassium citrate instead of potassium chloride is highlighted. KEY WORDS : Primary Sjgren's syndrome, Quadriplegia, Renal tubular acidosis, Hypokalemia Acute flaccid quadriplegia is a common neurological problem. Though most of them are Guillian Barre syndrome but one has to keep in mind hypokalemia which can mimic the syndrome. Routinely hypokalemia is corrected by potassium in the chloride form, whereas in renal tubular acidosis giving potassium as chloride may not be enough and potassium citrate has to be given which is converted to bicarbonate correcting acidosis and the potassium level. Primary Sjgren's Syndrome presenting as acute flaccid quadriplegia is rare. We present a patient who also developed renal tubular acidosis and further discuss here the management in relation to hypokalemia in the setting of acidosis. A 30 year female presented with a 24 hour history of pain in both the thighs followed by rapid and progressive weakness of all four limbs. When reviewed at the emergency, the patient was gasping and sustained a respiratory arrest for which she was promptly intubated and shifted to the intensive care unit where she was put on mechanical ventilation. On further inquiry she did not have any preceding history of fever, rash, diarrohea, flulike symptoms, recent vaccination or joint or muscle pain ,photosensitivity or polyuria. There were no prior such episodes and family history was also noncontributory. Significantly, she was a case of primary hypothyroidism for the last 4 years and taking thyroxine supplementation. She had normal menstrual cycles. Preliminary examination Continue reading >>

Renal Tubular Acidosis

Renal Tubular Acidosis

Patients with renal tubular acidosis (RTA) are often asymptomatic but may present with complaints of muscular weakness related to associated hypokalemia. Patients with severe acidemia can show hyperventilation or Kussmaul breathing due to respiratory compensation. Patients with RTA have a low arterial pH and serum bicarbonate with hyperchloremia and a normal serum anion gap. The urine pH exceeds 5.5 in classic distal RTA, but is lower than 5.0 in patients with untreated proximal RTA and is low also in hyperkalemic distal RTA. Alkali therapy is the mainstay of treatment. Potassium supplementation may be required for hypokalemia, and low-potassium diets are used if hyperkalemia is present. If hyperkalemic distal RTA is due to mineralocorticoid deficiency, fludrocortisone can be given unless it is contraindicated due to the presence of fluid overload or uncontrolled hypertension. Proximal RTA occurs most often as a component of Fanconi syndrome, which is characterized by generalized dysfunction of the proximal tubule, with the resultant urinary loss of bicarbonate, calcium, phosphate, urate, amino acids, glucose, and other organic acids and bases. In children, Fanconi syndrome causes growth retardation, renal rickets, and severe metabolic acidosis. Adult cases exhibit similar urinary losses, but the clinical impact is largely restricted to metabolic acidosis. Fanconi syndrome is marked by the appearance in the urine of all amino acids. Specific amino aciduria as seen in isolated cystinuria, glucose loss in isolated glycosuria, and isolated phosphaturia do not constitute Fanconi syndrome. The term renal tubular acidosis (RTA) describes any one of a number of disorders, in which the excretion of fixed acid (distal RTA) or the reabsorption of filtered bicarbonate (proximal R 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 >>

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 | 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 >>

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 >>

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

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 Is Highly Prevalent In Critically Ill Patients

Renal Tubular Acidosis Is Highly Prevalent In Critically Ill Patients

Renal tubular acidosis is highly prevalent in critically ill patients Brunner et al.; licensee BioMed Central.2015 Hyperchloremic acidosis is frequent in critically ill patients. Renal tubular acidosis (RTA) may contribute to acidemia in the state of hyperchloremic acidosis, but the prevalence of RTA has never been studied in critically ill patients. Therefore, we aimed to investigate the prevalence, type, and possible risk factors of RTA in critically ill patients using a physical-chemical approach. This prospective, observational trial was conducted in a medical ICU of a university hospital. One hundred consecutive critically ill patients at the age 18, expected to stay in the ICU for 24h, with the clinical necessity for a urinary catheter and the absence of anuria were included. Base excess (BE) subset calculation based on a physical-chemical approach on the first 7days after ICU admission was used to compare the effects of free water, chloride, albumin, and unmeasured anions on the standard base excess. Calculation of the urine osmolal gap (UOG) - as an approximate measure of the unmeasured urine cation NH4 + - served as determinate between renal and extrarenal bicarbonate loss in the state of hyperchloremic acidosis. During the first week of ICU stay 43 of the patients presented with hyperchloremic acidosis on one or more days represented as pronounced negative BEChloride. In 31 patients hyperchloremic acidosis was associated with RTA characterized by a UOG 150mosmol/kg in combination with preserved renal function. However, in 26 of the 31 patients with RTA metabolic acidosis was neutralized by other acid-base disturbances leading to a normal arterial pH. RTA is highly prevalent in critically ill patients with hyperchloremic acidosis, whereas it is often neutraliz 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 >>

Renal Tubular Acidosis In Children - Symptoms & Treatment

Renal Tubular Acidosis In Children - Symptoms & Treatment

Does your child complain of intense pain when he is urinating? Does he exhibit any obvious growth impairments? If you nodded along anxiously, you might want to consult the doctor, as he may be suffering from renal tubular acidosis or RTA. In the meanwhile, read our post below to learn more about Renal Tubular Acidosis symptoms, causes, types and treatments in children. What Is Renal Tubular Acidosis? Renal tubular acidosis or RTA is a disorder in which kidneys are unable to extract excess acid from the blood. The acids are flushed from the body through the urine. Any problem with the task makes the blood acidic and causes health problems (1). It is important for children with RTA to receive prompt treatment for the same. Any delay in treatment may cause poor growth in the child along with other kidney disorders (2). [ Read: Kidney Stones In Children ] All body functions utilize chemical reactions for various tasks. These chemical reactions produce acid. With RTA, acidosis (excessive acid) becomes the norm. Kidneys remove acids in the urine. They also bring bicarbonate (a base) back into the blood. This is the way kidneys maintain a perfect balance of acid and base in the body (3). This filtration process in the kidneys is carried by nephrons. These nephrons are small filtering units (4). Each nephron has a tiny tube (renal tubule) attached to it, which carries out the filtration process. Due to genetic defects, health problems and use of drugs, renal tubule function can have functional problems. This can cause RTA (5). Types Of RTA In Children: RTA can be of different types. Type 1 Renal Tubular Acidosis or Distal RTA – It is the most commonly-occurring RTA. ‘Distal’ means distance. In this type of distal renal tubular acidosis, the defect in the tube is at a dist 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 >>

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 >>

Distal Renal Tubular Acidosis

Distal Renal Tubular Acidosis

Distal renal tubular acidosis (dRTA) or Type 1 renal tubular acidosis (RTA) is the classical form of RTA, being the first described. Distal RTA is characterized by a failure of acid secretion by the alpha intercalated cells of the cortical collecting duct of the distal nephron . This failure of acid secretion may be due to a number of causes, and it leads to an inability to acidify the urine to a pH of less than 5.3. Radiograph of a rickets sufferer, a complication of both distal and proximal RTA. Because renal excretion is the primary means of eliminating acid from the body, there is consequently a tendency towards acidemia . This leads to the clinical features of dRTA: [1] Urinary stone formation (related to alkaline urine, hypercalciuria , and low urinary citrate). [2] Nephrocalcinosis (deposition of calcium in the substance of the kidney) Bone demineralisation (causing rickets in children and osteomalacia in adults) The symptoms and sequelae of dRTA are variable and range from being completely asymptomatic , to loin pain and hematuria from kidney stones , to failure to thrive and severe rickets in childhood forms as well as possible renal failure and even death. dRTA commonly leads to sodium loss and volume contraction, which causes a compensatory increase in blood levels of aldosterone . [3] Aldosterone causes increased resorption of sodium and loss of potassium in the collecting duct of the kidney, so these increased aldosterone levels cause the hypokalemia which is a common symptom of dRTA. [3] The pH of patient's blood is highly variable, and acidemia is not necessarily characteristic of sufferers of dRTA at any given time. One may have dRTA caused by alpha intercalated cell failure without necessarily being acidemic; termed incomplete dRTA, which is characteri Continue reading >>

Renal Tubular Acidosis With Hypokalemia Symptoms

Renal Tubular Acidosis With Hypokalemia Symptoms

Renal Tubular Acidosis with Hypokalemia Symptoms As understood today, renal tubular acidosis is a derangement characterized by an impairment of acidifying the urine despite systemic acidosis, even though glomerular function is intact.1 Well-established diagnostic criteria define the disorder as a clinical entity,1-5,19 but recognition, as a rule, is delayed until symptoms of the associated nephrolithiasis stimulate further investigation. Since nephrocalcinosis and nephrolithiasis are secondary manifestations of the disorder, the diagnosis, in most instances, is not made early in the course of the disease. In the case to be presented here the disorder has been encountered in an exceptionally early stage. Symptoms of hypokalemia alone dominated the clinical picture without any suggestive evidence of kidney stones or intrinsic renal disease. Following basic workup the diagnosis has been substantiated by a positive ammonium chloride loading test and has been amplified by x-ray studies and a percutaneous biopsy of the kidney. Continue reading >>

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