Renal tubular acidosis (RTA)

• In RTA, there is a normal anion gap metabolic acidosis in patients with normal or almost normal renal function.
• Basically all present with low pH and hypokalemia (except type 4)
  • Think H⁺ and K⁺ antagonize each other during excretion (due to Na⁺/K⁺ vs Na⁺/H⁺), increased excretion of one leads to decreased excretion of the other.
• Renal tubular acidosis is caused by defects in the tubular transport of HCO₃^- and/or H⁺.
• Most forms of RTA are asymptomatic; rarely, life-threatening electrolyte imbalances may occur.

Proximal renal tubular acidosis (type 2)

• Isolated proximal RTA: The proximal convoluted tubule cells are unable to reabsorb HCO₃^-.
• Fanconi syndrome: Impaired reabsorption of HCO₃^- and other compounds (e.g., potassium, glucose, phosphate, and amino acid reabsorption) in the PCT

Distal renal tubular acidosis (type 1)

• The α-intercalated cells of the distal tubule are unable to secrete H⁺.

Mixed RTA (type 3)

• Type 1 RTA with HCO₃^- wasting

Hyperkalemic renal tubular acidosis (type 4)

• Aldosterone deficiency and/or resistance in the collecting duct and distal convoluted tubule cause hyperkalemia, which inhibits ammonia synthesis in the proximal convoluted tubule and decreases urinary ammonium excretion.

Liddle syndrome