机体对酸碱平衡的调节机制及代谢性酸中毒精品.ppt

Proximal RTA Laboratory finding hyperchloremic acidosis hypophosphatemia alkaline phosphatase elevation hypokalemia, hypouricemia urine glucose, amino acid, phosphorous Proximal RTA Treatment restore systemic acidosis:10-25 mEq/kg/day treatment of osteomalacia: VitD correct hypokalemia: potassium salt Classic Distal RTA Major Causes: Autoimmune disorder Hypercalciuria and Nephrocalcinosis Drug or Toxin Tubulointerstitial Diseases Associated with genetic disorder Classic Distal RTA Clinical Feature Hyperchloremic metabollc acidosis Hypokalemia Urine concentration defect Nephrocalcinosis nephrolithiasis Absence of Fanconi syndrome Classic Distal RTA Laboratory feature: severe acidosis severe hypokalemia urine pH6.0 hyper calciuria bicarbonaturia:FE:5-15% U:B pCO2? Classic Distal RTA Treatment: Correction of systemic acidosis (1-1.5mEq/kg/day) Correction of hypokalemia Distal RTA with Hyperkalemia Type: Generalized defect of collecting tubule Type 4 RTA Hyperkalemia dRTA Selective Hypoaldosteronism Drug indued Pseudohypoaldosteronism Distal RTA with Hyperkalemia Pathophysiologic disorders mineral corticoid deficiency mineral corticoid resistance renal tubule dysfunction combination impairment of renal potassium and net acid excretion Mineralocorticoid Deficiency Primary : Generalized:Addison’s disease Isolated: Selective Ald deficiency defect Seconday: Hyporeninemic hypoaldosteronism Pharmacologic hypoaldosteronism: heparin, NSAID, ACEI ketoconazole, amino glutathimide Mineralocorticoid Resistance With salt wasting pseudohypoaldosteronism type I without salt wasting pseudohypoaldosteronism type II drug indued interstitial nephritis sickle cell disease chronic renal allograft rejection Drug induced Hyperkalamia Impairment of RAS cyclooxygenase inhibitors ACEI AT1 recepor antagonist