Renal tubular acidosis overview: Difference between revisions
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==Historical Perspective== | ==Historical Perspective== | ||
Renal tubular acidosis was first described as separate entity by Dr. Lightwood in 1935. Later Dr.Butler in 1936 described the pathophysiology and genetic inheritance of renal tubular acidosis in the children. | |||
==Classification== | ==Classification== | ||
Based on underlying defect in concentration of urine process in renal tubule, renal tubular acidosis can be classified into type 1 (distal), type 2 (proximal), type 4 (hypoaldosteronism) and voltage-dependent RTA. | |||
==Pathophysiology== | ==Pathophysiology== | ||
==Causes== | ==Causes== | ||
Primary causes of renal tubular acidosis include genetic [[mutations]] causing defects in the kidney anion exchanger [kAE1] in distal tubule intercalated cells and congenital adrenal hyperplasia. Secondary causes include medications and autoimmune diseases. | |||
==Differentiating Renal tubular acidosis from Other Diseases== | ==Differentiating Renal tubular acidosis from Other Diseases== | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
The estimated annual incidence of distal renal tubular acidosis is 10 in 100,000 population. Renal tubular acidosis is more common in infants than other group of population. There is racial predilection for renal tubular acidosis. | |||
==Risk Factors== | ==Risk Factors== | ||
Common risk factors in the development of renal tubular acidosis include childhood[[urinary tract obstruction]], [[diabetes mellitus]], [[primary biliary cirrhosis]], [[nephrocalcinosis]], [[nephrolithiasis]], [[Amphotericin B Nephrotoxicity|Amphotericin-B therapy]], [[cisplatinum]], [[Adrenal insufficiency|Untreated adrenal insufficiency]]. | |||
==Screening== | ==Screening== | ||
Screening for renal tubular acidosis is usually not recommended for asymptomatic patients. Screening is only recommended for patients with increased risk of having proximal RTA or metabolic disorders associated with the development of Fanconi syndrome. | |||
==Natural History, Complications, and Prognosis== | ==Natural History, Complications, and Prognosis== | ||
If left untreated renal tubular acidosis leads to growth failure and chronic kidney failure. Common complications associated with renal tubular acidosis include volume depletion, electrolyte disturbances, nephrocalcinosis, osteoporosis, growth retardation, renal rickets. Prognosis of renal tubular acidosis is generally good with appropriate therapy. | |||
==Diagnosis== | ==Diagnosis== | ||
===Diagnostic Study of Choice=== | ===Diagnostic Study of Choice=== | ||
Revision as of 12:54, 1 June 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
Historical Perspective
Renal tubular acidosis was first described as separate entity by Dr. Lightwood in 1935. Later Dr.Butler in 1936 described the pathophysiology and genetic inheritance of renal tubular acidosis in the children.
Classification
Based on underlying defect in concentration of urine process in renal tubule, renal tubular acidosis can be classified into type 1 (distal), type 2 (proximal), type 4 (hypoaldosteronism) and voltage-dependent RTA.
Pathophysiology
Causes
Primary causes of renal tubular acidosis include genetic mutations causing defects in the kidney anion exchanger [kAE1] in distal tubule intercalated cells and congenital adrenal hyperplasia. Secondary causes include medications and autoimmune diseases.
Differentiating Renal tubular acidosis from Other Diseases
Epidemiology and Demographics
The estimated annual incidence of distal renal tubular acidosis is 10 in 100,000 population. Renal tubular acidosis is more common in infants than other group of population. There is racial predilection for renal tubular acidosis.
Risk Factors
Common risk factors in the development of renal tubular acidosis include childhoodurinary tract obstruction, diabetes mellitus, primary biliary cirrhosis, nephrocalcinosis, nephrolithiasis, Amphotericin-B therapy, cisplatinum, Untreated adrenal insufficiency.
Screening
Screening for renal tubular acidosis is usually not recommended for asymptomatic patients. Screening is only recommended for patients with increased risk of having proximal RTA or metabolic disorders associated with the development of Fanconi syndrome.
Natural History, Complications, and Prognosis
If left untreated renal tubular acidosis leads to growth failure and chronic kidney failure. Common complications associated with renal tubular acidosis include volume depletion, electrolyte disturbances, nephrocalcinosis, osteoporosis, growth retardation, renal rickets. Prognosis of renal tubular acidosis is generally good with appropriate therapy.