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Acute Renal Failure

SIS_IX_271109

Acute Renal Failure


Rapid decline in the GFR over days to weeks.
An increase in Plasma creatinine concentration to >200micromol/L = Biochemical defination

Review
Serum Creatinine (mg/dl)

9.0

8.0
7.0 6.0

5.0
4.0 3.0 2.0

1.0
0

20

40

60

80 100 120 140 160 180

Inulin Clearance (ml/min per 1.73m2)

Definitions
Anuria: No UOP Oliguria: UOP<400-500 mL/d Azotemia: Incr Cr, BUN May be prerenal, renal, postrenal Does not require any clinical findings Chronic Renal Insufficiency Deterioration over mos-yrs ( usually >3 months) ESRD = GFR <5%

Definition
Acute Kidney Injury:
an abrupt decrease in kidney function characterized by a rise in serum creatinine of more than or equal to 0.3 mg/dl or an increase to more than or equal to 1.5 fold from the baseline or normal creatinine level or a urine output of less than 0.5 ml/kg/hr for more than 6 hours with exclusion of chronic kidney insufficiency.

Definition of Acute Kidney Injury (AKI) based on Acute Kidney Injury Network
Stage 1 Increase in Serum Creatinine 1.5-2 times baseline OR 0.3 mg/dl increase from baseline 2-3 times baseline 3 times baseline OR 0.5 mg/dl increase if baseline>4mg/dl OR Any RRT given Urine Output <0.5 ml/kg/h for >6 h

2 3

<0.5 ml/kg/h for >12 h <0.3 ml/kg/h for >24 h OR Anuria for >12 h

Classification/staging system for acute kidney injurya

Serum creatinine criteria

Urine output criteria

stage Increase in serum creatinine of more than or equal to 0.3 mg/dl ( 26.4 mol/l) or increase to more than or equal to 150% to 200% (1.5- to 2-fold) from baseline Increase in serum creatinine to more than 200% to 300% (> 2- to 3-fold) from baseline Increase in serum creatinine to more than 300% (> 3-fold) from baseline (or serum creatinine of more than or equal to 4.0 mg/dl [ 354 mol/l] with an acute increase of at least 0.5 mg/dl [44 mol/l]) Less than 0.5 ml/kg per hour for more than 6 hours Less than 0.5 ml/kg per hour for more than 12 hours Less than 0.3 ml/kg per hour for 24 hours or anuria for 12 hours

2b

3c

aModified

from RIFLE (Risk, Injury, Failure, Loss, and End-stage kidney disease) criteria. The staging system proposed is a highly sensitive interim staging system and is based on recent data indicating that a small change in serum creatinine influences outcome. Only one criterion (creatinine or urine output) has to be fulfilled to qualify for a stage. b200% to 300% increase = 2- to 3-fold increase. cGiven wide variation in indications and timing of initiation of renal replacement therapy (RRT), individuals who receive RRT are considered to have met the criteria for stage 3 irrespective of the stage they are in at the time of RRT. Mehta et al. Critical Care 2007 11:R31 doi:10.1186/cc5713

Chronic Kidney Disease: a long-standing, progressive deterioration of renal function, kidney damage for more than 3 months, defined by structural or functional abnormalities of the kidney, with or without decreased GFR.

In the presence of increased serum creatinine, the following features will diagnose CKD and hence will exclude subjects from enrollment:
Past documents: increased serum creatinine History: uraemic symptoms > 2 months (any 2 or more of the below mentioned):
Nausea/vomiting Pruritus Nocturia Leg and/or facial swelling

Physical examination: ( 1 of the following):


Pigmentation Left ventricular hypertrophy Fundoscopic changes

Ultrasound Abdomen:
Decreased size Decreased cortical thickness Increased echogenicity Scarring Multiple cyst

Normochromic anemia in absence of systemic inflammatory conditions Renal osteodystrophy Serum creatinine > 10mg/dl with normal urine output

Acute Renal Failure


Intravascular volume depletion
Hemorrhage AGE Sodium depletion (diuresis)

Pre-renal Causes

Redistribution of ECF
Third space accumulation (pancreatitis, Cirrhosis) Edematous disorders (Reduction of effective circulating volume e.g. CCF, NS, Cirrhosis)

Drugs : NSAID, ACE etc Sepsis

Prerenal ARF
Volume depletion: vomiting, diarrhea, decreased intake, diuretics, third-spacing
Hypotension: sepsis, drugs, blood loss Decreased cardiac output Renal artery stenosis, embolism, or thrombosis

Renal
Vascular: Hypertension, Wegeners, PAN
Glomerular: Post-strep GN, Lupus, RPGN, Hepatitis related, IgA nephropathy, Tubular: Acute Tubular Necrosis (ATN) Medication toxicity, toxins Interstitial: Acute Interstitial Nephritis (AIN)

Intra-renal renal (e.g ) Acute Tubular Necrosis


Ischemia Toxins (antibiotics, contrast), hemolysis, rhabdomyolysis, heat stroke Clinical course: initiation, maintenance, and recovery diuretic phases Clinical clues: Muddy brown, granular casts on urinalysis

Acute Renal Failure


Nephrotoxic ATN
Endogenous Toxins
Heme pigments (myoglobin, hemoglobin) Myeloma light chains

Exogenous Toxins
Antibiotics (e.g., aminoglycosides, amphotericin B) Radiocontrast agents Heavy metals (e.g., cis-platinum, mercury) Poisons (e.g., ethylene glycol)

Acute Tubular Necrosis

Acute Tubular Necrosis

Postrenal
BPH Stones (usually unilateral with single kidney) Tumor (lymphoma, ovarian, prostate)

Urethral stricture
Neurologic (i.e. overflow incontinence)

Review

Renal Blood Flow


F = P/R RAP RVP RBF = Raff + Reff

RBF ~

RAP Raff + Reff

Review

Raff
RAP

Reff
PGC

Pre-Renal Azotemia Pathophysiology


Renal hypoperfusion
Decreased RBF and GFR Increased filtration fraction (GFR/RBF)

Increased Na and H2O reabsorption


Oliguria, high Uosm, low UNa Elevated BUN/Cr ratio

Clinical Presentation of Acute Renal Failure

Acute Renal Failure

Prerenal decreased renal perfusion 80% of cases

Renal intrinsic renal disease 10% of cases

Postrenal obstruction 10%

ARF: Signs and Symptoms


Sign of underline cause - BP, Volume Hyperkalemia Nausea/Vomiting HTN Pulmonary edema Ascites Asterixis Encephalopathy

ARF: Focused History


Nausea? Vomiting? Diarrhea? Hx of heart disease, liver disease, 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 interstitial nephritis) Large prostate Extremities (Skin turgor, Edema)

Acute Interstitial Nephritis


Causes
Allergic interstitial nephritis
Drugs

Infections
Bacterial Viral

Sarcoidosis

Allergic Interstitial Nephritis


Clinical Characteristics
Fever Rash Arthralgias Eosinophilia Urinalysis
Microscopic hematuria Sterile pyuria Eosinophiluria

Acute Interstitial Nephritis


Usually drug induced
methicillin, rifampin, NSAIDS

Develops 3-7 days after exposure Fever, Rash , and eosinophilia common U/A reveals WBC, WBC casts, + Hansel stain Often resolves spontaneously Steroids may be beneficial ( if Scr>2.5 mg/dl)

Acute Interstitial Nephritis

Atheroembolic ARF
Associated with emboli of fragments of atherosclerotic plaque from aorta and other large arteries Diagnose by history, physical findings (evidence of other embolic phenomena--CVA, ischemic digits, blue toe syndrome, etc), low serum C3 and C4, peripheral eosinophilia, eosinophiluria, rarely WBC casts Commonly occur after intravascular procedures or cannulation (cardiac cath, CABG, AAA repair, etc.)

Cholesterol Embolization

Chlosterol embolization is an often unrecognized cause of acute renal failure which may be indistinguishable from the bland variety of allergic interstitial nephritis except by biopsy. In addition to ARF, other manifestations of the occlusion of small arteries by atheroembolic material include skin mottling (livedo reticularis), blue toes and distal digital infarcts with intact peripheral pulses. Transient eosinophilia, hypocomplementemia, and an elevated sedimentation rate are sometimes also seen.

Your 68yo male inpatient with baseline Cr=1.2 had negative cardiac cath 4 days ago, now Cr=1.8 and blanching rash.
A. Renal Artery Stenosis B. ContrastInduced Nephropathy C. Abdominal Aortic Aneurysm D. Cholesterol Atheroemboli

Why do his toes look like this?

Contrast-Induced ARF
Prevalence
Less than 1% in patients with normal renal function Increases significantly with renal insufficiency

Contrast-Induced ARF
Risk Factors
Renal insufficiency Diabetes mellitus Multiple myeloma High osmolar (ionic) contrast media Contrast medium volume

Contrast-induced ARF
Clinical Characteristics
Onset - 24 to 48 hrs after exposure Duration - 5 to 7 days Non-oliguric (majority) Dialysis - rarely needed Urinary sediment - variable Low fractional excretion of Na

Contrast-induced ARF
Prophylactic Strategies
Use I.V. contrast only when necessary Hydration Minimize contrast volume Low-osmolar (nonionic) contrast media N-acetylcysteine, fenoldopam

Rhabdomyolytic ARF
Diagnose with serum CPK (usu. > 10,000), urine dipstick (+) for blood, without RBCs on microscopy, pigmented granular casts Common after trauma (crush injuries), seizures, burns, limb ischemia occasionally after IABP or cardiopulmonary bypass Treatment is largely supportive care. Alkalinization of urine .

Acute Glomerulonephritis
Rare in the hospitalized patient Most common types: acute post-infectious GN, crescentic RPGN Diagnose by history, hematuria, RBC casts, proteinuria (usually non-nephrotic range), low serum complement in post-infectious GN), RPGN often associated with antiGBM or ANCA Usually will need to perform renal biopsy

Acute Glomerulonephritis (2)


If diagnosis is post-infectious, disease is usually self-limited, and supportive care is usually all that is necessary. For RPGN, may need immunosuppressive therapy with steroids Cytoxan, plasmapheresis (if assoc. with anti-GBM)

Acute Renal Failure


Post-renal Causes
Intra-renal Obstruction
Acute uric acid nephropathy Drugs (e.g., acyclovir)

Extra-renal Obstruction
Renal pelvis or ureter (e.g., stones, clots, tumors, papillary necrosis, retroperitoneal fibrosis) Bladder (e.g., BPH, neuropathic bladder) Urethra (e.g., stricture)

Acute Renal Failure


Diagnostic Tools
Urinary sediment Urinary indices
Urine volume Urine electrolytes

Radiologic studies

Urinary Sediment (1)


Bland
Pre-renal azotemia Urinary outlet obstruction

Urinary Sediment (2)


RBC casts or dysmorphic RBCs
Acute glomerulonephritis Small vessel vasculitis

Red Blood Cell Cast

Red Blood Cells

Monomorphic

Dysmorphic

Dysmorphic Red Blood Cells

Dysmorphic Red Blood Cells

Urinary Sediment (3)


WBC Cells and WBC Casts
Acute interstitial nephritis Acute pyelonephritis

White Blood Cell Cast

Urinary Sediment (4)


RTE cells, RTE cell casts, pigmented granular (muddy brown) casts
Acute tubular necrosis

Renal Tubular Epithelial Cell Cast

Pigmented Granular Casts

Acute Renal Failure


Urine Volume (1)
Anuria (< No urine/ 50/100 ml/24h)
Acute bilateral arterial or venous occlusion Bilateral cortical necrosis Acute necrotizing glomerulonephritis Obstruction (complete) ATN (very rare)

Acute Renal Failure


Urine Volume (2)
Oliguria (100-500 ml/24h)
Pre-renal azotemia ATN

Non-Oliguria (> 500 ml/24h)


ATN Obstruction (partial)

Acute Tubular Necrosis


Clinical Characteristics
Characteristic Incidence Toxin-induced UV (ml/24h) UNa (mEq/L) FENa (%) Dialysis required Mortality Oliguric ATN 41% 8% < 400 68 + 6 6.8 + 1.4 84% 50% Non-Oliguric ATN 59% 30% 1,280 + 75 50 + 5 3.1 + 0.5 26% 25%

Acute Renal Failure


Urinary Indices
ATN PR 40 PR 40 1.0 20 ATN ATN 20 PR PR PR 1.0 ATN ATN

UOsm (mOsm/L)

(U/P)Cr

UNa (mEq/L)

RFI

FENa

Hydronephrosis

Normal Renal Ultrasound

Hydronephrosis

Hydronephrosis

Management Principles
Establish urine output (fluids diuretics) Remove nephrotoxins, dose-adjust medications Careful volume and electrolyte management (using free daily weights, VS, I&Os, and labs) Ca, Mg, P also useful Provide nutrition (low K, low P)

Water and sodium restriction Protein restriction Potassium and phosphate restriction Adjust medication dosages Avoidance of further insults
BP support Nephrotoxins

Indications for Dialysis


Volume overload with CHF
Pericarditis Electrolyte abnormalities Toxins which can be removed by dialysis Life-threatening acidosis Uncontrolled bleeding

Hyperkalemia
Highly Arrhythmogenic
Usually with progressive EKG changes
Peaked T waves ---> Widened QRS--> Sinus wave

K> 5.5 meq/L needs evaluation/intervention Usually in setting of Decrease GFR but:
medication also a common cause
ACEI NSAIDS Septra, Heparin

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. PRERENAL 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 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 damage
FeNa >2% 1. ATN Damaged tubules can't reabsorb Na

Calculating FeNa after pt has gotten Lasix...


Caution with calculating FeNa if pt has 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 FeNa>1%, you dont know if this is because pt is euvolemic or because Lasix increased the U Na So helpful if FeNa still <1%, but not if FeNa >1% 1. Fractional Excretion of Lithium (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. Glomerulonephritis C. Dehydration D. AIN from NSAIDs

Prerenal ARF
Hyaline casts can be seen 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 Diuretics Reduced Cardiac output Cardiogenic shock, CHF, tamponade, huge PE.... Systemic vasodilation Sepsis Anaphylaxis, Antihypertensive drugs Renal vasoconstriction Hepatorenal syndrome

Intrinsic ARF
1. 2. 3. 4. Tubular (ATN) Interstitial (AIN) Glomerular (Glomerulonephritis) Vascular

You evaluate a 57yo man w/ oliguria and rapidly increasing BUN, Cr.

A. B. C. D.

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 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 euvolemic pt is not peeing Dialysis

Most pts return to baseline Cr in 7-21 days

ATN Cr increases at 0.3-0.5 /day

Prerenal increases slower than 0.3 /day UNa<20 FeNa<1% Normal

U Na, FeNa
UA Response to volume BUN/Cr

UNa>40 FeNa >2% epi cells, granular casts Cr wont Cr improves improve with IVF much 10-15:1 >20:1

Which UA is most compatible w/contrast-induced ATN?


A. Spec grav 1.012, 20-30 RBC, 15-20 WBC, +Eos B. Spec grav 1.010, 1-3 WBC, 5-10 renal tubular cells, many granular casts, occasional renal tubular cell casts, no eos C. Spec grav 1.012, 5-10 RBC, 25-50 WBC, many bact, occasional fine granular casts, no eos D. 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 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?
A. Indinavir for her HIV Gentamicin for her SBE Motrin for her OA Cyclosporin for her SLE

B.
C. D.

WBC Casts
Cells 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% Idiopathic 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 drug Fever (27%) Serum Eosinophilia (23%) Maculopapular rash (15%)
Bland sediment or WBCs, RBCs, non-nephrotic proteinuria WBC Casts are pathognomonic! Urine eosinophils on Wrights or Hansels Stain
Also see urine eos in RPGN, renal atheroemboli...

AIN Management
Remove offending agent Most patients recover full kidney function in 1 year Poor prognostic factors
ARF > 3 weeks Advanced age at onset

You evaluate a 32yo woman with HTN, oliguria, and rapidly increasing Cr, BUN. You spin her urine:

A. ATN B. Acute glomerulonephritis C. Acute interstitial nephritis D. Nephrotic Syndrome

Acute Glomerulonephritis

RBC casts: cells have no nuclei Casts in urine: think INTRINSIC renal dz If she has Lupus w/recent viral prodrome, think Rapidly Progressive Glomerulonephritis If she had a sore throat 10 days ago, think Postinfectious Proliferative Glomerulonephritis

What are these?

Glomerular Dz

Hematuria (dysmorphic RBCs) RBC casts Lipiduria (increased glomerular permeability) Proteinuria (may be in nephrotic range) Fever, rash, arthralgias, pulmonary sx Elevated ESR, low complement levels

Rapidly Progressive Glomerulonephritis


Type 1: Anti-GBM dz Type 2: Immune complex IgA nephropathy Postinfectious glomerulonephritis Lupus nephritis Mixed cryoglobulinemia Type 3: Pauci-immune Necrotizing glomerulonephritis (often ANCA-positive, assoc. w/vasculitis) Can present with viral-like prodrome Myalgias, arthralgias, back pain, fever, malaise Kidney bx : Extensive cellular crescents with or w/o immune complexes Can develop ESRD in days to weeks. Treat w/glucocorticoids & cyclophosphamide.

Postinfectious Proliferative Glomerulonephritis


Usually after strep infxn of upper respiratory tract or skin 8-14 day latent period
Can also occur in subacute bacterial endocarditis, visceral abscesses, osteomyelitis, bacterial sepsis

Hematuria, HTN, edema, proteinuria Positive antistreptolysin O titer (90% upper respiratory and 50% skin) Treatment is supportive
Screen family members with throat culture and treat with antibiotics if necessary

A 19yo woman with Breast Cancer s/p chemo in the ER has weakness, fever, rash. WBC=15.4, Hct 24, Cr 2.9, LDH 600, CK=600. UA=3+ prot, 3+blood, 20 RBC. What next test do you order? Whats her likely dx?
A. Nephrotic Syn B. Systemic Vasculitis C. Acute Glomerulonephritis D. Hemolytic-Uremic Syn E. Rhabdomyolysis

TTP
Order blood smear to r/o TTP TTP associated with malignancy, chemo TTP may mimic Glomerulonephritis on UA (RBCs, WBCs) Thrombocytopenia, anemia not consistent with nephrotic or nephritic syndrome Need CK in the thousands to cause ARF

Microvascular ARF
TTP/HUS HELLP syndrome Platelets form thrombi and deposit in kidneysGlomerular capillary occlusion or thrombosis Plasma exchange, steroids, Vincristine, IVIG, splenectomy....

Macrovascular ARF
Aortic Aneurysm Renal artery dissection or thrombosis Renal vein thrombus Atheroembolic disease
New onset or accelerated HTN? Abdominal bruits, reduced femoral pulses? Vascular disease? Embolic source?

Your 68yo male inpatient with baseline Cr=1.2 had negative cardiac cath 4 days ago, now Cr=1.8 and blanching rash.
A. Renal Artery Stenosis B. ContrastInduced Nephropathy C. Abdominal Aortic Aneurysm D. Cholesterol Atheroemboli

Why do his toes look like this?

Renal Atheroembolic Dz
1% of Cardiac caths: atheromatous debris scraped from the aortic wall will embolize Retinal Cerebral Skin (Livedo Reticularis, Purple toes) Renal (ARF) Gut (Mesenteric ischemia) Unlike in Contrast-Induced Nephropathy, Cr will NOT improve with IVF Diagnosis of exclusion: will NOT show up on MRI or Renal U/S; WILL show up on renal bx Tx: supportive

Post-Renal ARF
Urethral obstruction: prostate, urethral stricture. Bladder calculi or neoplasms. Pelvic or retroperitoneal neoplams. Bilateral ureteral obstruction (neoplasm, calculi). Retroperitoneal fibrosis.

Doc, your pt hasnt peed in 5 hrs....what do you want to do?


Examine pt: Dry? Septic (vasodilated)? Flush foley (sediment can obstruct outflow) Check I/Os (has she been drinking?) Give IV BOLUS (250-500cc IVF), see if pt pees in next 30-60 min
If she pees, then she was dry If she doesnt pee, then shes either REALLY dry or in renal failure

Check UA, UCx, urine lytes Consider Renal U/S if reasonable

Youre called to the ER to see...


A 35yo woman with previously normal renal function now with BUN=60, Cr=3.5. Do you call the Renal fellow to dialyze this pt? What if her K=5.9? What if her K=7.8?

Indications for acute dialysis


AEIOU
Acidosis (metabolic) Electrolytes (hyperkalemia) Ingestion of drugs/Ischemia Overload (fluid) Uremia

You admit this pt to telemetry and aggressively hydrate her. You recheck labs 6h later and BUN=85, Cr=4.2. Suddenly the pt starts to seize. Now what?

UremiaSo what?

General
Fatigue, weakness Pruritis Uremic encephalopathy Seizures Asterixis Anorexia, early satiety, N/V,

Mental status change

GI disturbance

Uremic Pericarditis Plt dysfunction/bleeding

A pt with chronic lung disease has acute pleuritic pain and desats to 92%RA. You want to r/o PE but her Cr=1.4. Can you get a CT with IV contrast?
A. B. C. D. E. F. Send her for Stat CT with IV contrast Send her for Stat CT without IV contrast Just give her heparin Begin IV hydration Begin pre-procedure Mannitol Get a VQ scan instead

Contrast-Induced Nephrotoxicity
Cr increases by 25% or >0.05 postprocedure Contrast causes renal vasoconstriction renal hypoxia Iodine itself may be renally toxic If Cr>1.4, use pre-procedure prophylaxis

Pre-Procedure Prophylaxis
1. IVF ( 0.9NS) 1-1.5 mg/kg/hour x12 hours prior to procedure and 6-12 hours after 2. Mucomyst (N-acetylcysteine) Free radical scavenger; prevents oxidative tissue damage 600mg po BID x 4 doses (2 before procedure, 2 after) 3. Bicarbonate (JAMA 2004) Alkalinizing urine should reduce renal medullary damage D5W with 3 amps HCO3; bolus 3.5 mL/kg 1 hour preprocedure, then 1mL/kg/hour for 6 hours postprocedure 4. Possibly helpful? Fenoldopam, Dopamine 5. Not helpful! Diuretics, Mannitol

Increase in Creatinine without AKI


Inhibition of tubular creatinine secretion Trimethoprim, Cimetidine, Probenecid Interference with creatinine assays in the lab (false elevation) glucose, acetoacetate, ascorbic acid, cefoxitin flucytosine

Increase in BUN without AKI


Increased production GI Bleeding Catabolic states (Prolonged ICU stay) Corticosteroids Protein loads (TPN-Albumin infusion)