【持续性肾脏替代治疗CRRT英文精品课件】Acute Kidney Injury.pptVIP

Atheroembolic AKI Clinical Manifestations AKI days to weeks after manipulation, anticoagulation Systemic signs, signals of inflammation Rash Livedo reticularis Decreased complement due to activation by exposed atheromata Eosinophilia/eosinophiliuria Occlusion of distal arteriolar beds AKI Visual field deficits Gangrenous digits, palpable pulses Pancreatitis GI bleeding Acute Kidney Injury Clinical features of Acute Interstitial Nephritis Onset usually 3-5 days with most drugs, but may be sooner with rifampin, or much later with NSAIDS Rising SCr which resolves upon d/c of offending drug Fever, hematuria, pyuria: Urine eosinophils Mild to moderate proteinuria; much higher to NS in NSAIDS Eosinophilia and morbilliform rash also s/sx in AIN Occasionally see hyperkalemia and distal RTA Bx not usually necessary for dx, assuming reversal of sx’s; may be needed for complicated cases Prednisone 40 mg PO x 2 wks sometimes utilized to shorten AKI interval Acute Kidney Injury: AIN causes DRUGS ACEI Allopurinol Cephalosporins Cimetidine Fluoroquinolones Loop diuetics NSAIDS PCN Phenytoin Rifampin Sulfonamides Tegretol Thiazides INFECTION Bacterial Agents causing pyelonephritis Legionella Brucella Yersinia Viral Hantavirus HIV CMV,EBV,HSV AKI: Glomerulonephritis (RPGN)/Systemic Vasculitis Immune-Complex Mediated SLE Cryoglobulinemic vasculitis Henoch-Sch?nlein purpura Post-strep GN Direct Ab attack Anti-GBM disease Goodpasture’s syndrome Pauci-immune vasculitis Microscopic polyangiitis Wegener’s granulomatosis Churg-Strauss syndrome Thrombotic Microangiopathy TTP HUS Scleroderma renal crisis Preeclampsia Malignant hypertension Acute Glomerulonephritis (RPGN) Accounts for a minority of AKI: ~5% May have severe morbidity, mortailty Extra-renal manifestations may be present Pulmonary Dermal GI Hematologic HTN may be present, especially in absence of prior Hx UA: differentiates from ATN, AIN Dysmorphic RBC, RBC casts, proteinuria 0.5gm/24h Serologies, complement activation