ACUTE RENAL FAILURE

DR. S.RAGHAV MD
 DEFINITION
ABRUPT DECREASE IN RENAL
FUNCTION RESULTING IN THE
ACCUMULATION OF
NITROGENOUS COMPOUNDS
SUCH AS UREA AND
CREATININE
 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 normal

Acute Renal Insufficiency

 Deterioration over days-wks
 GFR 10-20 mL/min
 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
 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
 Asterixis
 Encephalopathy
Causes of ARF in hospitalized
patients
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, 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 vs Chronic Renal
Failure

 History
» Known Chronic
» Recent Toxic Exposure
» Recent Hypoxic Insult
» Recent Trauma
» Known Diseases Associated with ARF
» Prev. Abnormal Lab Results Suggesting
Chronic
 Acute vs Chronic Renal
Failure

 Rapidly Rising Creatinine = Acute

 Kidney Size
» Small = Chronic
 Renal Ultrasound
» Increased Echogenicity = Chronic
 Urine Flow Rate
» Oliguric or Anuric usually = Acute
 ACUTE RENAL FAILURE
CLASSIFICATION BY URINE
VOLUME

OLIGURIC: <400 CC/ 24 Hrs

NON-OLIGURIC: >500 CC/24 Hrs

ANURIC <50 CC/24 Hrs

 ETIOLOGY OF ACUTE RENAL
FAILURE

 PRE-RENAL 55-60%

 POST RENAL <5%

 RENAL 35-40%
 PRE-RENAL ACUTE RENAL
FAILURE

 MOST COMMON CAUSE OF ARF

 RESULTS FROM DECREASED RENAL
PERFUSION
 TREATMENT OF THE CAUSE RESTORES
RENAL FUNCTION TUBULAR FUNCTION
INTACT *
 PROLONGED PRE-RENAL FAILURE MAY
LEAD TO ATN
 CAUSES OF PRE-RENAL
AZOTEMIA

 Intravascular volume depletion

 Decreased cardiac output
 Systemic vasodilation
» Antihypertensives
» Sepsis
 Renal vasoconstriction
 Drugs impairing autoregulation
» Ace inhibitors NSAID
MECHANISMIS OF PRE
RENAL ARF
 POST-RENAL ACUTE RENAL
FAILURE

 ACCOUNTS FOR 2-15% OF ALL ARF

 OBSTRUCTION TO URINE FLOW
» INCREASED TUBULAR PRESSURE
» VASOCONSTRICTION
– DECREASED RENAL BLOOD FLOW
 MUST BE BILATERAL TO RESULT IN ARF
» UNLESS : SINGLE KIDNEY OR PRIOR
CHRONIC RENAL FAILURE
 POST RENAL ACUTE RENAL
FAILURE

 SUSPECT OBSTRUCTION IN ANURIA

 ETIOLOGY MAY BE AGE DEPENDENT
» YOUNG = CONGENITAL ABNORMALITY
» OLDER MALE = PROSTATIC
ENLARGEMENT
 ARF MOST OFTEN ASSOCIATED WITH
LESIONS IN:
» BLADDER, PROSTATE OR URETHRA
 Intrinsic ARF
1. Tubular (ATN)
2. Interstitial (AIN)
3. Glomerular
(Glomerulonephritis)
4. Vascular
RENAL-ACUTE RENAL FAILURE

 VASCULAR DISEASE
» VASCULITIS (SLE, POLYARTERITIS
ETC.)
» SCLERODERMA
» THROMBOEMBOLIC DISEASE
» MALIGNANT HYPERTENSION
 RENAL--ACUTE RENAL
FAILURE

 GLOMERULAR DISEASE
» ACUTE GLOMERULONEPHRITIS
– POST INFECTIOUS GN
– CRESCENTIC GN
 ANCA POSITIVE DISEASES
– GOODPASTURE’S DIS.
 ANTI- GLOMERULAR BASEMENT
ANTIBODY
 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
RBC CAST
ACUTE INTERSTITIAL NEPHRITIS
DRUG INDUCED

 PENICILLINS  NSAID
 SULFONAMIDES (FENOPROFEN)
 CEPHALOSPORIN  ALLOPURINOL
 RIFAMPIN ( 2ND  PHENYTOIN
TIME)  THIAZIDES
 QUINOLONES  FUROSEMIDE
 CIMETIDINE
Acute Interstitial Nephritis

 Fever
 Rash
 Eosinophilia
 Pyuria
 WBC Casts
 AIN Management

 Remove offending agent

 Most patients recover full kidney
function in 1 year
 Poor prognostic factors
» ARF > 3 weeks
» Advanced age at onset
WBC Cast
RENAL --ACUTE RENAL FAILURE

 ACUTE TUBULAR NECROSIS

» ISCHEMIC INJURY
» TOXIC INJURY
– ENDOGENOUS TOXINS
 HEMOGLOBINURIA

 MYOBLOBINURIA (RHABDOMYOLYSIS)

 ENDOTOXEMIA
RENAL-- ACUTE RENAL FAILURE

 ACUTE TUBULAR NECROSIS

» EXOGENOUS TOXINS
– AMINOGLYCOSIDES
– RADIOGRAPHIC CONTRAST
– HEAVY METAL COMPOUNDS
– ETHYLENE GLYCOL
– METHANOL
– CARBON TETRACHLORIDE
– CIS PLATIN
 HIGH RISK SETTINGS FOR ATN

CLINICAL SETTING FREQUENCY

 GEN.MED. --SURG. 3-5%
 INTENSIVE CARE 5-25%
 OPEN HEART SURG 5-20%
 AMINOGLYCOSIDE 10-30%
 BURNS 20-60%
 RHABDOMYOLYSIS 20-30%
 CIS-PLATIN 15-25%
 ATN
 Muddy brown granular casts (last slide)
 Renal tubular epithelial cell casts (below)
DIAGNOSTIC APPROACH TO ARF

 HISTORY
 PHYSICAL EXAMINATION
 ASSMENT OF URINE VOLUME
 URINE ANALYSIS
 BLOOD CHEMISTRY
 BLOOD AND URINE INDICES
 RADIOLOGIC STUDIES
Treatment of ARF
 Hyperkalemia

 Increase in serum potassium levels

more than 5.5mEq/L.
 May result in cardiac arrest and death.

 Clinical setting in which it occurs

» Acute renal failure
» Chronic renal failure
Table 5-3. Treatment of hyperkalemia

Medication Mechanism of action Dosage Peak effect

Calcium Antagonism of 10-30 ml of 10% solution IV -5 min

gluconate membrane over 2 min

Insulin and Increased K+entry Insulin, 10 U IV bolus 30-60 min

Glucose into the cells followed by 0.5 mU/kg of
body weight per minute in
50 ml of 20% glucose

Sodium Increased K+entry 44-50 mEq IV over 5 min; 30-60 min

bicarbonate into the cells can be repeated within 30
min
Albuterol Increased K+entry
into the cells 20 mg in the nebulized form 30-60 min

Kayexalate Removal of the 20 g of resin with 100 ml of 2-4 hr

excess K+ 20% sorbitol; can be
repeated every 4-6 hr

Hemodialysis Removal of the Dialysis bath K+ concentration 30-60 min

excess K+ variable
INDICATIONS FOR DIALYSIS IN
ACUTE RENAL FAILURE
 UREMIC SYMPTOMS
~ nausea
~ neurologic
 SEVERE FLUID OVERLOAD
 REFRACTORY ELECTROLYTE

DISORDERS
~hyperkalemia
 SEVERE REFRACTORY ACIDOSIS
INDICATIONS FOR DIALYSIS IN
ACUTE RENAL FAILURE

 PERICARDITIS
 NEUROPATHY
 MENTAL STATUS CHANGE
 SEIZURES
 BLEEDING
 TOXINS----ETHYLENE GLYCOL,
METHANOL
 PROPHYLACTIC
~recent studies fail to document benefit
 Indications for acute dialysis

AEIOU
 Acidosis (metabolic)
 Electrolytes (hyperkalemia)
 Ingestion of drugs/Ischemia
 Overload (fluid)
 Uremia
MORTALITY ASSOCIATED WITH
SETTING OF ATN

 OVERALL MORTALITY 40-60%

 POST TRAUMATIC 70-90%
 MEDICAL CAUSE 15-40%
 SURGICAL CAUSE 40-80%
 NON-OLIGURIC 26% *
 OLIGURIC 50% *
THANK YOU