Acute Renal Failure.ppt
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1、Acute Renal Failure,Deb Goldstein Argy Resident September, 2005,Acute Renal Failure,Rapid decline in the GFR over days to weeks. Cr increases by 0.5 mg/dL GFR 10mL/min, or 25% of normalAcute Renal Insufficiency Deterioration over days-wks GFR 10-20 mL/min,Definitions,Anuria: No UOP Oliguria: UOP400-
2、500 mL/d Azotemia: Incr Cr, BUN May be prerenal, renal, postrenal Does not require any clinical findings Chronic Renal Insufficiency Deterioration over mos-yrs GFR 10-20 mL/min, or 20-50% of normal ESRD = GFR 5% of nl,ARF: Signs and Symptoms,Hyperkalemia Nausea/Vomiting HTN Pulmonary edema Ascites A
3、sterixis Encephalopathy,Causes of ARF in hospitalized pts,45% ATN Ischemia, Nephrotoxins 21% Prerenal CHF, volume depletion, sepsis 10% Urinary obstruction 4% Glomerulonephritis or vasculitis 2% AIN 1% Atheroemboli,ARF: Focused History,Nausea? Vomiting? Diarrhea? Hx of heart disease, liver disease,
4、previous renal disease, kidney stones, BPH? Any recent illnesses? Any edema, change in urination? Any new medications? Any recent radiology studies? Rashes?,Physical Exam,Volume Status Mucus membranes, orthostatics Cardiovascular JVD, rubs Pulmonary Decreased breath sounds Rales Rash (Allergic inter
5、stitial nephritis) Large prostate Extremities (Skin turgor, Edema),W/U for ARF,Chem 7 Urine Urine electrolytes and Urine Cr to calculate FeNa Urine eosinophils Urine sediment: casts, cells, protein Uosm Kidney U/S - r/o hydronephrosis,FeNa = (urine Na x plasma Cr) (plasma Na x urine Cr),FeNa 1% 1. P
6、RERENAL Urine Na 20. Functioning tubules reabsorb lots of filtered Na 2. ATN (unusual) Postischemic dz: most of UOP comes from few normal nephrons, which handle Na appropriately ATN + chronic prerenal dz (cirrhosis, CHF) 3. Glomerular or vascular injury Despite glomerular or vascular injury, pt may
7、still have well-preserved tubular function and be able to concentrate Na,More FeNa,FeNa 1%-2% 1. Prerenal-sometimes 2. ATN-sometimes 3. AIN-higher FeNa due to tubular damageFeNa 2% ATN Damaged tubules cant reabsorb Na,Calculating FeNa after pt has gotten Lasix.,Caution with calculating FeNa if pt ha
8、s gotten Loop Diuretics in past 24-48 h Loop diuretics cause natriuresis (incr urinary Na excretion) that raises U Na-even if pt is prerenal So if FeNa1%, you dont know if this is because pt is euvolemic or because Lasix increased the U Na So helpful if FeNa still 1% 1. Fractional Excretion of Lithi
9、um (endogenous) 2. Fractional Excretion of Uric Acid 3. Fractional Excretion of Urea,A 22yo male with sickle cell anemia and abdominal pain who has been vomiting nonstop for 2 days. BUN=45, Cr=2.2.,A. ATN B. Glomerulo-nephritis C. Dehydration D. AIN from NSAIDs,Prerenal ARF,Hyaline casts can be seen
10、 in normal pts NOT an abnormal finding UA in prerenal ARF is normal Prerenal: causes 21% of ARF in hosp. pts Reversible Prevent ATN with volume replacement Fluid boluses or continuous IVF Monitor Uop,Prerenal causes,Intravascular volume depletion Hemorrhage Vomiting, diarrhea “Third spacing” Diureti
11、cs Reduced Cardiac output Cardiogenic shock, CHF, tamponade, huge PE Systemic vasodilation Sepsis Anaphylaxis, Antihypertensive drugs Renal vasoconstriction Hepatorenal syndrome,Intrinsic ARF,Tubular (ATN) Interstitial (AIN) Glomerular (Glomerulonephritis) Vascular,You evaluate a 57yo man w/ oliguri
12、a and rapidly increasing BUN, Cr.,ATN Acute glomerulonephritis Acute interstitial nephritis Nephrotic Syndrome,ATN,Muddy brown granular casts (last slide) Renal tubular epithelial cell casts (below),More ATN,Broad casts (form in dilated, damaged tubules),ATN Causes,1. Hypotension Relative low BP May
13、 occur immediately after low BP episode or up to 7 days later! 2. Post-op Ischemia Post-aortic clamping, post-CABG 3. Crystal precipitation 4. Myoglobinuria (Rhabdo) 5. Contrast Dye ARF usually 1-2 days after test 6. Aminoglycosides (10-26%),ATNWhat to do,Remove any offending agent IVF Try Lasix if
14、euvolemic pt is not peeing Dialysis Most pts return to baseline Cr in 7-21 days,Which UA is most compatible w/contrast-induced ATN?,Spec grav 1.012, 20-30 RBC, 15-20 WBC, +Eos Spec grav 1.010, 1-3 WBC, 5-10 renal tubular cells, many granular casts, occasional renal tubular cell casts, no eos Spec gr
15、av 1.012, 5-10 RBC, 25-50 WBC, many bact, occasional fine granular casts, no eos Spec grav 1.020, 10-20 RBC, 2-4 WBC, 1-3 RBC casts, no eos,ATN,B. Spec grav 1.010, 1-3 WBC, 5-10 renal tubular cells, many granular casts, occasional renal tubular cell casts, no eos Dilute urine: failure to concentrate
16、 urine No RBC casts or WBC casts in ATN Eos classically in AIN or renal atheroemboli, but nonspecific,56yo woman with previously normal renal function now has BUN=24, Cr 1.8. Which drug is responsible?,Indinavir for her HIV Gentamicin for her SBE Motrin for her OA Cyclosporin for her SLE,WBC Casts,C
17、ells in the cast have nuclei (unlike RBC casts)Pathognomonic for Acute Interstitial Nephritis,Acute Interstitial Nephritis,70% Drug hypersensitivity 30% Antibiotics: PCNs (Methicillin), Cephalosporins, Cipro Sulfa drugs NSAIDs Allopurinol.15% Infection Strep, Legionella, CMV, other bact/viruses 8% I
18、diopathic 6% Autoimmune Dz (Sarcoid, Tubulointerstitial nephritis/Uveitis),AIN from Drugs,Renal damage is NOT dose-dependent May take wks after initial exposure to drug Up to 18 mos to get AIN from NSAIDS! But only 3-5 d to develop AIN after second exposure to drugFever (27%) Serum Eosinophilia (23%
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