紊乱文档.pptVIP

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紊乱文档

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 AT

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