Pathophys |
- ↓ renal perfusion, with maximized renal compensation to retain Na
- No damage to kidney structures
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- Kidney parenchyma is damaged leading to ↓ GFR
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- Obstruction from renal pelvis to urethra (typically b/l or solitary kidney to cause AKI)
- Increased pressure damages nephrons, causes hydronephrosis
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Etiology |
- Hypovolemia
- Poor forward pressure - hypotension, CHF, MI
- Hemodynamic - afferent vasoconstriction (NSAIDs, cyclosporine/tacrolimus, amphotericin B), efferent vasodilation (ACEi, ARB), IV dye
- Hypercalcemia
- Hepatorenal syndrome
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- Glomerular
- Vascular -
- Interstitial - "allergic reaction" in the kidney. Meds (penicillins, cephalosporins, sulfonamides, phenytoin, PPIs, NSAIDS), systemic disease (sarcoid, Sjogren's)
- Tubular (ATN) - ischemic (prolonged prerenal, sepsis, hypotension), nephrotoxic (aminoglycosides, methotrexate, amphotericin, cisplatin, myoglobin, IV contrast)
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- Prostate (BPH, cancer), neurogenic bladder, intraureteral (stone/clot/tumors), extraureteral (compression from tumor, retroperitoneal fibrosis)
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Management |
- Look at volume status: prerenal does not = dry/give IVF; may need inotropes or diuresis to improve cardiac output/renal perfusion
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- ATN - treat low perfusion state, identify risk factors, withdraw offending agents
- maintain fluid, electrolyte, acid-base balance
- renal replacement therapy as needed (AEIOU), but mostly just wait for kidney to recover...(7-21 d), usually return to baseline
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- Straight cath/Foley
- Renal u/s to rule out hydronephrosis
- Post-obstructive diuresis over next 24 hrs
- Make sure to maintain fluid balance/PO intake; q12 electrolytes
- Cr should downtrend soon (e.g. next morning)
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