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Your search term(s) "Renal Tubular Acidosis" returned 12 results.

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Renal Tubular Acidosis. Bethesda, MD: National Kidney and Urologic Diseases Information Clearinghouse. 2008. 6 p.

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, and progressive renal failure. This fact sheet reviews the diagnosis, the subtypes of RTA, therapy, and current research activities in RTA. To diagnose RTA, the doctor will check the acid-base balance in samples of the patient’s blood and urine. Physicians use a three-category classification system to describe the different types of RTA. Type 1, also called classic distal RTA, is an inherited disorder associated with diseases that affect many organ systems such as the autoimmune disorders Sjögren’s syndrome and lupus erythematosus. Type 2 is called proximal RTA and occurs most frequently in children as part of a disorder called Fanconi’s syndrome; it can also occur as a side effect of treatment with ifosfamide, a drug used in chemotherapy. Type 4 is caused by another defect in the kidney tubule but is different from classic or proximal RTA because it results in high levels of potassium in the blood instead of low levels. If treated early, most people with RTA will not develop permanent kidney failure. Therefore, the goal is early recognition and adequate therapy, which will need to be maintained and monitored throughout the patient’s lifetime. The fact sheet concludes with a summary of research programs in Renal tubular acidosis (RTA) area and a brief description of the activities of the National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC), a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) that provides information about diseases of the kidneys and urologic system to patients and their families, the general public, and health care professionals. Readers are referred to the National Kidney Foundation at www.kidney.org or 1–800–622–9010, the American Association of Kidney Patients at www.aakp.org or 1–800–749–2257, and the American Kidney Fund at www.kidneyfund.org or 1–800–638–8299 for more information.

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Urinary Stone Disease. IN: Tanagho, E.; McAninch, J., eds. Smith’s General Urology. 17th ed. Columbus, OH: McGraw Hill. 2008. pp 246-277.

This lengthy chapter about urinary stone disease is from an updated edition of a comprehensive textbook about urology that offers an overview of the diagnosis and treatment of diseases and disorders common to the genitourinary tract. The author notes that urinary stones are common, yet their cause remains uncertain. The author begins with a discussion of the etiology, role of urinary ions, stone varieties, and symptoms and signs at the presentation of urinary tract stones. Symptoms can include pain, hematuria, infection, associated fever, nausea, and vomiting. The author reviews diagnostic approaches to urinary stones and outlines the treatment options, including conservative observation, dissolution agents, relief of obstruction, extracorporeal shock wave lithotripsy, ureteroscopic stone extraction, percutaneous nephrolithotomy, open stone surgery, pyelolithotomy, anatrophic nephrolithotomy, radial nephrotomy, and ureterolithotomy. The chapter includes a section on special situations, including renal transplantation, pregnancy, dysmorphia, obesity, medullary sponge kidney, renal tubular acidosis, associated tumors, pediatric patients, caliceal diverticula, and kidney malformations. Prevention strategies are also outlined, including metabolic evaluation and the use of oral medications. A brief review of bladder, urethral, and prepucial stones is given. The chapter is illustrated with numerous black-and-white drawings and photographs. The chapter concludes with an extensive list of references, categorized by topic. 24 figures. 110 references.

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Renal Tubular Acidosis. IN: Nilsson, K.R.; Piccini, J.P., eds. Osler Medical Handbook. Philadelphia, PA: Saunders. 2006. pp. 784-788.

Renal tubular acidosis (RTA) is a common finding in many of the tubulointerstitial diseases and is characterized by a normal anion gap metabolic acidosis. This chapter on renal tubular acidosis is from a handbook that provides the essentials of diagnosis and treatment, as well as the latest in evidence-based medicine, for residents working bedside, in-patient care. The chapter begins with a presentation of essential Fast Facts and concludes with Pearls and Pitfalls useful to the practicing internist. The body of the chapter is divided into sections: Epidemiology, Clinical Presentation, Diagnosis, and Management. Specific topics covered in this chapter include the subtypes of RTA, including distal RTA (types I and IV) and proximal RTA (type II); the use of the urine anion gap to distinguish distal RTA from the other major cause of a normal anion gap metabolic acidosis (gastrointestinal bicarbonate loss); and treatment, which is necessary to prevent the complications of RTA, including osteoporosis, kidney stones, and hyperkalemia. The chapter concludes with a list of references, each labeled with a 'strength of evidence' grade to help readers determine the type of research available in that reference source. 3 figures. 1 table. 3 references.

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Renal Tubular Disorders. IN: Hogg, R., ed. Kidney Disorders in Children and Adolescents: A Global Perspective of Clinical Practice. New York, NY: Informa Healthcare USA. 2006. pp 165-180.

This chapter about renal tubular disorders is from a textbook that presents a global perspective of clinical practice regarding kidney disorders in children and adolescents. The author notes that hereditary renal tubular transport disorders can lead to profound problems in the homeostasis of electrolytes, minerals, or organic solutes in the body and thus can be associated with significant morbidity. However, not all tubular disorders are associated with significant clinical abnormalities. Most patients with renal tubular disorders present in the neonatal period or the 1st year of life. The author summarizes the general characteristics of hereditary tubular transport disorders, reviews some aspects of the pathophysiology and genetic aspects of a few of the diseases, describes the clinical features of the tubulopathies, and briefly summarizes the therapy of some of the disorders that are seen in children. Specific disorders considered include classic cystinuria, hereditary isolated glycosuria, Dent’s disease, proximal renal tubular acidosis, Bartter’s and Gitelman’s syndromes, Liddle syndrome, pseudohypoaldosteronism type 1, distal renal tubular acidosis, and nephrogenic diabetes insipidus. The author concludes that molecular genetics and molecular biology studies have led to the identification of numerous renal tubular disease-causing mutations, have provided important insight into the defective molecular mechanisms underlying various tubulopathies, and have greatly increased the understanding of the physiology of renal tubular transport. 9 figures. 2 tables. 55 references.

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Renal Tubulointestitial Diseases. IN: Nilsson, K.R.; Piccini, J.P., eds. Osler Medical Handbook. Philadelphia, PA: Saunders. 2006. pp. 731-740.

The renal tubulointerstitial diseases are a heterogeneous group of disorders with characteristic features that may include sterile pyuria and white blood cell casts, parenchymal concentrating defects resulting in polyuria and nephrogenic diabetes insipidus, and tubular defects such as renal tubular acidosis (RTA). This chapter on renal tubulointerstitial diseases is from a handbook that provides the essentials of diagnosis and treatment, as well as the latest in evidence-based medicine, for residents working bedside, in-patient care. The chapter begins with a presentation of essential Fast Facts and concludes with Pearls and Pitfalls useful to the practicing internist. The body of the chapter is divided into sections: Epidemiology, Clinical Presentation, Diagnosis, and Management. Specific topics covered in this chapter include acute interstitial nephritis (AIN), a condition that can be caused by drugs, infection, and immunologic disease; acute tubular necrosis (ATN), the most common cause of in-hospital acute renal failure (ARF), often caused by medications, iodinated contrast dye, and hypotension; patients at high risk for contrast nephropathy, including those with preexisting renal dysfunction, diabetes mellitus, multiple myeloma, and advanced age; and the problem of rhabdomyolysis leading to ARF via intratubular obstruction and ATN. The chapter concludes with a list of references, each labeled with a 'strength of evidence' grade to help readers determine the type of research available in that reference source. 2 figures. 1 table. 18 references.

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Kidney Diseases in Childhood [for parents]. KidsHealth, Nemours Center for Children's Health Media, The Nemours Foundation. 2003. 4 p.

This brochure provides information about kidney diseases in childhood. From a health series for families, the brochure first briefly reviews the role of the kidneys in overall health, the process of filtration, and the hormones produced by the kidneys (erythropoietin, renin, and the active form of vitamin D). The brochure then reviews the most common kidney diseases in children, including congenital anomalies such as posterior urethral valve obstruction and fetal hydronephrosis; multicystic kidney disease; and other diseases affecting the kidneys, including renal tubular acidosis, Wilms tumor, nephritis, nephrosis, and the nephrotic syndrome. The brochure then discusses when to contact a health care provider regarding signs or symptoms of urinary tract disease and outlines the diagnostic tests used to confirm various kidney diseases, including kidney function tests and imaging studies. The brochure is one of a series that explains just how each body system, part, and process is necessary for living.

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Nephrolithiasis: Reducing the Risk of Recurrence. Contemporary Urology. 15(2): 36, 39-40, 42, 47-48, 50-52. February, 2003.

Nephrolithiasis (kidney stones) is a common disorder, with a reported lifetime incidence of up to 13 percent in North America. This article addresses ways to reduce the risk of recurrent kidney stones. The authors contend that recurrent stones are preventable with dietary modifications and medical therapy, but appropriate evaluation of both recurrent and first-time stone formers is vital. The authors review the pathophysiology and treatment of kidney stones and describe a simple approach to evaluation aimed at identifying high risk patients. Topics include hypercalciuria, excessive amounts of calcium in the urine; hypercalcemia, excessive amounts of calcium in the blood; hyperoxaluria, excessive amounts of calcium oxalate in the urine; hyperuricosuria, excessive amounts of uric acid in the urine; hypocitraturia, low amounts of citrate in the urine; hypomagnesuria, low amounts of magnesium in the urine; renal tubular acidosis; and patient evaluation and risk assessment. 1 figure. 3 tables. 31 references.

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Alkali Therapy in Renal Tubular Acidosis: Who Needs it?. JASN. Journal of the American Society of Nephrology. 13 (8): 2186-2188. August 2002.

Renal tubular acidosis (RTA) is a renal (kidney) tubule disorder that causes acidosis by restricting the reduction of urinary pH and thereby the titration of urinary buffers and the excretion of acid. The acidosis of type 1 RTA (classic) results in osteoporosis and other disorders of bone demineralization. Alkali (base pH) therapy has been given to children with RTA to heal osteopenia and to encourage normal growth. This article considers the use and indications of alkali therapy in adults with RTA. The authors review recent studies in this area, including studies investigating the impact of high net acid dietary load. The authors also consider the therapeutic potential of alkali in the increasingly large number of elderly people who are likely to be impaired by RTA. The authors conclude that with the scope of its recognized expression so expanded, the frequency of its consequent occurrence so increasing, and the potential societal benefits of its treatment so enormous (and so inexpensively achieved), RTA may be coming of age as a disorder of public health importance. 41 references.

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Alterations of the Kidney in Liver Disease. In: Arias, I.M., et al. Liver: Biology and Pathobiology, Fourth Edition. Philadelphia, PA: Lippincott Williams and Wilkins. 2001. p.649-660.

This chapter on alterations of the kidney in liver disease is from a textbook on the pathobiology and biology of the liver. The authors discuss the physiologic relationship between liver and kidney, considering more specifically the presence and activity of intrahepatic receptors, which contribute to the regulation of renal salt and water excretion; organic renal impairment, principally due to precipitation of immunoglobulins and cryoglobulins in glomeruli, and development of cirrhotic glomerulonephritis, such as membranous glomerulonephritis (MGN) or membranoproliferative glomerulonephritis (MPGN); metabolic renal damage, as represented by renal tubular acidosis (RTA); renal functional impairment (RFI), due to renal impairment and hemodynamic alterations with hyperdynamic circulation resulting in ascites and edema; and pathogenesis of the hepatorenal syndrome (HRS). 1 figure. 1 table. 109 references.

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Hereditary Distal Renal Tubular Acidosis: New Understandings. In: Coggins, C.H.; Hancock, E.W., Eds. Annual Review of Medicine: Selected Topics in the Clinical Sciences, Volume 52. Palo Alto, CA: Annual Reviews Inc. 2001. p. 471-484.

The primary or hereditary form of distal renal tubular acidosis (dRTA), although rare, has received increased attention recently because of dramatic advances in the understanding of its genetic basis. This review article discusses several recent important studies that have begun to unravel the genetic defects causing different types of primary or hereditary dRTA (the authors do not discuss acquired dRTA). The final regulation of renal acid excretion is effected by various acid and base transporters localized in specialized cells in the cortical collecting and outer medullary collecting tubules. Inherited defects in two of the key acid or base transporters involved in distal acidification, as well as mutation in the cytosolic carbonic anhydrase gene, can cause dRTA. The syndrome is inherited in both autosomal dominant and recessive patterns; patients with recessive dRTA present with either acute illness or growth failure at a young age, sometimes accompanied by deafness, whereas dominant dRTA is usually a milder disease and involves no hearing loss. Hypokalemia (low levels of potassium in the blood), metabolic acidosis, nephrocalcinosis (calcium phosphate in the tubules of the kidney, resulting in kidney insufficiency), and renal calculi (kidney stones) are seen in both autosomal recessiave and dominant dRTA but tend to be more severe and more common in autosomal recessive dRTA. Growth retardation is also much more common and severe in recessive dRTA, probably because the recessive form occurs earlier in life and causes severe metabolic acidosis. The severity of the acidosis manifesting at an early age is the key determinant of delayed growth. 2 figures. 1 table. 64 references.

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