Renal Tubular Acidosis (RTA)

The 2 most important metabolic acidosis with normal anion gap (6-12) are:

1. RTA
2. Diarrhoea

RTA has positive urine anion gap (UAG) whereas diarrhea has negative UAG.

Type1 dRTA (fairly common)

• the intercalated cells' apical H+/K+ antiporter is non-functional, resulting in potassium-wasting and proton (H+) retention

Causes:

• Hereditary: Marfan’s, Ehler’s Danlos $, Sickle Cell Disease
• Autoimmune: Sjogren’s, SLE, Thyroiditis
• Drugs: Lithium, amphotericin, analgesics, vit D

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DISTAL-O

D - Vit D excess

I -Inflammatory/ auto-Immune- such as chronic active hepatitis, Sjogren’s syndrome, interstitial nephritis

S -Sickle Cell Disease

T -Transplanted kidney, Toluene

A -Amphotericin, analgesics (drugs)

L -Lithium

O -Obstructive uropathy; Others- medullary sponge kidney

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Since calcium stones demonstrate a proclivity for deposition at higher pHs (alkaline), the substance of the kidney develops stones bilaterally; this does not occur in the other RTA types. (RTA does not mean the tubule is always acidic)

• Normal anion gap metabolic acidosis/acidemia (NAGMA) - Hypokalaemic, hyperchloraemic metabolic acidosis
• HYPOkalemia
• Urinary stone formation [related to alkaline urine (pH always >5.5), hypercalciuria, and low urinary citrate]
• Nephrocalcinosis (deposition of calcium in the substance of the kidney)