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For further information, see CMDT Part 21-17: Metabolic Acidosis
For further information, see CMDT Part 21-19: Normal Anion Gap Acidosis
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Essentials of Diagnosis
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General Considerations
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Renal tubular acidosis (RTA)
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Hyperchloremic acidosis with a normal anion gap and normal or near normal glomerular filtration rate, in the absence of diarrhea
Three major types of RTA can be differentiated by the clinical setting: urinary pH, urinary anion gap, serum K+ level
Type I (distal H+ secretion defect)
Characterized by selective deficiency in H+ secretion by alpha intercalated cells in the collecting tubule
Enhanced K+ excretion occurs probably due to less competition from H+ in the distal nephron transport system
Develops as a consequence of paraproteinemias, autoimmune disease, and drugs and toxins such as amphotericin
Type II (proximal HCO3– reabsorption defect)
Due to a defect in the ability of the proximal tubule to reabsorb filtered HCO3–
Hypokalemia results when a patient is treated with HCO3– without adequate K+ supplementation
Can exist with other proximal reabsorption defects resulting in glucosuria, aminoaciduria, phosphaturia, and uricosuria (Fanconi syndrome)
Causes include plasma cell myeloma and nephrotoxic drugs and carbonic anhydrase inhibitors (acetazolamide)
Type IV (hyporeninemic hypoaldosteronism)
Most common RTA in clinical practice
Due to a defect in aldosterone action that impairs distal nephron Na+ reabsorption and therefore K+ and H+ excretion
Common causes include diabetic nephropathy and tubulointerstitial renal ...