Acute Renal Failure

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Acute Renal Failure

• Dr Ajith Cherian MD,DM.

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Defenition.

• Acute renal failure (ARF) is a syndrome
  characterized by rapid decline in GFR (hours to
  days), retention of nitrogenous waste products,
  and perturbation of extracellular fluid volume
  and electrolyte and acid-base homeostasis.
• ARF complicates approximately 5 of hospital
  admissions and up to 30 of admissions to
  intensive care units.

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Definitions

• Anuria No UOP
• Oliguria UOPlt400-500 mL/d
• Azotemia Incr Cr, BUN
• May be prerenal, renal, postrenal
• Does not require any clinical findings
• Chronic Renal Insufficiency
• Deterioration over months-yrs
• GFR 10-20 mL/min, or 20-50 of normal
• ESRD GFR lt5 of normal

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Acute Renal Failure

• (1) diseases that cause renal hypoperfusion
  without compromising the integrity of renal
  parenchyma (prerenal ARF, prerenal azotemia)
  (55)
• (2) diseases that directly involve renal
  parenchyma (intrinsic renal ARF, renal azotemia)
  (40)
• (3) diseases associated with urinary tract
  obstruction (postrenal ARF, postrenal azotemia)
  (5)

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• Most ARF is reversible, the kidney being
  relatively unique among major organs in its
  ability to recover from almost complete loss of
  function.
• ARF is associated with major in-hospital
  morbidity and mortality.

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• Autoregulatory dilatation of afferent arterioles
  is maximal at mean systemic arterial blood
  pressures of 80 mmHg, and hypotension below this
  level is associated with a precipitous decline in
  GFR.
• Lesser degrees of hypotension may provoke
  prerenal ARF in the elderly and in pts with
  diseases affecting the integrity of afferent
  arterioles (e.g., hypertensive nephrosclerosis,
  diabetic vasculopathy).
• Drugs that interfere with adaptive responses in
  the renal microcirculation may trigger
  progression of prerenal ARF to ischemic intrinsic
  renal ARF .

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• Cyclooxygenase inhibitors NSAIDs or
  angiotensin-converting enzyme (ACE) activity (ACE
  inhibitors) and angiotensin II receptor blockers
  are the major culprits and should be used
  judiciously in the setting of suspected renal
  hypoperfusion.

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• Hepatorenal Syndrome This is a particularly
  aggressive form of ARF,with many of the features
  of prerenal ARF, that frequently complicates
  hepatic failure due to advanced cirrhosis or
  other liver diseases, including malignancy,
  hepatic resection, and biliary obstruction.
• Carries a mortality rate of 90.

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• Frequent offenders are the antimicrobial agents,
  such as acyclovir,foscarnet, aminoglycosides,
  amphotericin B, and pentamidine.
• ARF complicates 10 to 30 of courses of
  aminoglycoside antibiotics, even in the presence
  of therapeutic levels

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contrast nephropathy

• Intrarenal vasoconstriction is a pivotal event in
  ARF that is triggered by radiocontrast agents
  cyclosporine, and tacrolimus (FK506).
• .

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Contrast-Induced ARFPrevalence

• Less than 1 in patients with normal renal
  function
• Increases significantly with renal insufficiency

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Contrast-Induced ARFRisk Factors

• Renal insufficiency
• Diabetes mellitus
• Multiple myeloma
• High osmolar (ionic) contrast media
• Contrast medium volume

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Contrast-induced ARFClinical 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

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Contrast-induced ARFProphylactic Strategies

• Use I.V. contrast only when necessary
• Hydration
• Minimize contrast volume
• Low-osmolar (nonionic) contrast media
• N-acetylcysteine, fenoldopam

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• The syndrome appears to be dose-related, and its
  incidence is only slightly reduced in high-risk
  individuals by use of more expensive low
  osmolality nonionic contrast agents.

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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?

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ARF Signs and Symptoms

• Hyperkalemia
• Nausea/Vomiting
• HTN
• Pulmonary edema
• Ascites
• Asterixis
• Encephalopathy

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Physical Exam

• Volume Status
• Mucus membranes, orthostatics
• Cardiovascular
• JVP, pericardial rubs
• Pulmonary
• Decreased breath sounds
• Rales
• Rash (Allergic interstitial nephritis)
• Large prostate
• Extremities (Skin turgor, Edema)

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• Findings of CRF include anemia, neuropathy, and
  radiologic evidence of renal osteodystrophy or
  small scarred kidneys.
• Anemia may also complicate ARF and renal size may
  be normal or increased in several chronic renal
  diseases (e.g.,diabetic nephropathy, amyloidosis,
  polycystic kidney disease).

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W/U for ARF

• RFT-urea,creatinine .
• Potassium,Sodium,Uric acid.
• Urine
• Urine electrolytes and Urine Cr to calculate FeNa
• Urine eosinophils
• Urine sediment casts, cells, protein
• Uosm
• Kidney U/S - r/o hydronephrosis

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FeNa (urine Na x plasma Cr)
(plasma Na x urine Cr)

• (UNa, urine sodium concentration PCr, plasma
  creatinine concentration PNa, plasma sodium
  concentration UCr, urine creatinine
  concentration)
• FeNa lt1
• 1. PRERENAL
• Urine Na lt 20. Functioning tubules reabsorb lots
  of filtered Na
• 2. Glomerular or vascular injury
• Despite glomerular or vascular injury, pt may
  still have well-preserved tubular function and be
  able to concentrate Na

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• FeNa gt2
• ATN
• Damaged tubules can't reabsorb Na

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Calculating FeNa after pt has received Loop
Diuretics

• 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 FeNagt1, you dont know if this is because
  pt is euvolemic or because Lasix increased the U
  Na
• So helpful if FeNa still lt1, but not if FeNa gt1

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Urinary Sediment
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A 22yr male with sickle cell anemia and abdominal
pain who has been vomiting nonstop for 2 days.
BUN45, Cr2.2.

• A. ATN
• B. Glomerulo-nephritis
• C. Dehydration
• D. AIN from NSAIDs

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A 22yr male with sickle cell anemia and abdominal
pain who has been vomiting nonstop for 2 days.
BUN45, Cr2.2.

• A. ATN
• B. Glomerulo-nephritis
• C. Dehydration
• D. AIN from NSAIDs

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Prerenal ARF

• Hyaline casts can be seen in normal pts
• NOT an abnormal finding
• UA in prerenal ARF is normal

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Intrinsic ARF

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

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Urinary Sediment

• WBC Cells and WBC Casts
• Acute interstitial nephritis
• Acute pyelonephritis

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White Blood Cells
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White Blood Cell Cast
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WBC Casts

• Cells in the cast have nuclei
• (unlike RBC casts)
• Pathognomonic for Acute Interstitial Nephritis

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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)

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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...

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AIN Management

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

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Intrinsic ARF

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

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Urinary Sediment

• RTE cells, Renal Tubular Epithelial Cell casts,
  pigmented granular (muddy brown) casts
• Acute tubular necrosis

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Renal Tubular Epithelial Cell Cast
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Pigmented Granular Casts
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You evaluate a 57yr man w/ oliguria and rapidly
increasing BUN, Cr.

1. ATN
2. Acute glomerulonephritis
3. Acute interstitial nephritis
4. Nephrotic Syndrome

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

1. ATN
2. Acute glomerulonephritis
3. Acute interstitial nephritis
4. Nephrotic Syndrome

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ATN

• Muddy brown granular casts

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ATN

• Renal tubular epithelial cell casts

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ATN

• Broad casts (form in dilated, damaged tubules)

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ATNWhat to do

• Remove any offending agent
• IVF
• Try Lasix if euvolemic pt is not urinating
• Dialysis
• Most pts return to baseline Cr in 7-21 days

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ATN Prerenal
Cr increases at 0.3-0.5 /day increases slower than 0.3 /day
U Na, FeNa UNagt40 FeNa gt2 UNalt20 FeNalt1
UA epi cells, granular casts Normal
Response to volume Cr wont improve much Cr improves with IVF
BUN/Cr 10-151 gt201
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Intrinsic ARF

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

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Urinary Sediment

• RBC casts or dysmorphic RBCs
• Acute glomerulonephritis
• Small vessel vasculitis

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Red Blood Cell Cast
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Red Blood Cells
Monomorphic
Dysmorphic
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Dysmorphic Red Blood Cells
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Dysmorphic Red Blood Cells
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You evaluate a 32yo woman with HTN, oliguria, and
rapidly increasing Cr, BUN. You spin her urine

1. ATN
2. Acute glomerulonephritis
3. Acute interstitial nephritis
4. Nephrotic Syndrome

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

1. ATN
2. Acute glomerulonephritis
3. Acute interstitial nephritis
4. Nephrotic Syndrome

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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

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What are these?
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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

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• Imaging in ARF

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Hydronephrosis
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Normal Renal Ultrasound
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Hydronephrosis
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Hydronephrosis
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• Management in ARF

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Prevention

• What works?
• Maintenance of euvolemia
• Avoidance of nephrotoxins when possible
• NSAIDs, aminoglycoside, Amphotericin, IV contrast
• BP control--avoidance of excessive hypo- or
  hypertension

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Contrast-Induced Nephrotoxicity

• If Crgt1.4, use pre-procedure prophylaxis

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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

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Prevention

• What doesnt work?
• Empiric use of
• Diuretics (i.e., Furosemide, Mannitol)
• Dopamine (or Dopamine agonists such as
  Fenoldopam)
• Calcium-channel blockers

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Acute Renal Failure Treatment

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

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Hyperkalemia

• Highly Arrhythmogenic
• Usually with progressive EKG changes
• Peaked T waves ---gt Widened QRS--gt Sinus wave
• Kgt 5.5 meq/L needs evaluation/intervention
• Usually in setting of Decrease GFR but
• medication also a common cause
• ACEI
• NSAIDS
• Septran, Heparin

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Dialysis Indications

• Refractory hyperkalemia
• Metabolic acidosis
• Volume overload
• Mental status changes

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• THANK YOU.