Info
🌱 來自: Huppert’s Notes
Renal Tubular Acidosis (RTA)🚧 施工中
Renal Tubular Acidosis (RTA)
RTA Type I (Distal)
• Pathophysiology: Defect in collecting tubule’s ability to excrete H+ due to congenital causes, multiple myeloma, autoimmunity, amphotericin B toxicity
• Labs: Urine pH >5.5; hypokalemia (secrete K+ instead of H+); non-anion gap metabolic acidosis
• Clinical features: ↑Risk kidney stones (increased calcium and phosphate excretion into alkaline urine)
• Treatment: Sodium bicarb to correct acidosis; phosphate salts promote excretion of titratable acid
RTA Type II (Proximal)
• Pathophysiology: Carbonic anhydrase mutation → HCO3– is not reabsorbed. Associated with multiple myeloma (rule out!), lead poisoning, amyloid, Fanconi syndrome
• Labs: Urine pH <5.5; hypokalemia; non-anion gap metabolic acidosis. Fanconi: +glycosuria.
• Clinical features: No risk of kidney stones like type I; risk of hypophosphatemic rickets
• Treatment: Sodium restriction increases Na+ resorption in proximal tubule with bicarb asbsorbed as well. Do not give bicarb because it will be excreted.
RTA Type IV (Hyperkalemic)
• Pathophysiology: Hypoaldosteronism or lack of collecting tubule response to aldosterone; common with interstitial renal diagnosis or diabetic nephropathy
• Labs: Acidic urine; hyperkalemia, non-anion gap metabolic acidosis. No stones.