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OBJECTIVES

Acute Renal Failure (ARF)

Puan Fatimatuzzahra Abd. Aziz USM 2 September 2010

Provide the definition, terms and types associated with ARF. Explain the pathogenesis and clinical course of ARF. Discuss assessment of renal function function. Identify the type of ARF based on laboratory parameters. List and explain the treatment of ARF.

Anatomy
2 Kidneys 2 Ureters Bladder Urethra

What do the KIDNEYs do?

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Definition
Abrupt decline (24-48 hours) in renal function: Inability of kidney to excrete metabolic waste products. Inability to maintain acid base balance acid-base balance. Abrupt increase [Scr] > 50% in patients with previously normal renal function or An increase of 1mg/ml in those with preexisting renal disease.

Daily urine output Classification

Pre-renal, Intrinsic, post-renal Anuric, oliguric, non-oliguric

Normal > 400ml/day Anuric < 50ml/day Oliguric :50 - 400 ml/day Nonoliguric > 400 ml/ day

A: Pre- Renal Azotemia B: Post renal Obstruction C: Intrinsic ARF

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Causes of ARF
Pre-renal: blood flow Caused by: vomiting, diarrhea, poor fluid intake, fever, use of diuretics, and heart failure cardiac failure, liver dysfunction or septic failure dysfunction, shock

Causes of ARF
Intrinsic Due to kidney damage Eg:
Interstitial nephritis, acute glomerulonephritis, tubular necrosis, ischemia, toxins

Causes of ARF
Post-renal : Obstruction in upper/lower urinary tract. Sign & symptoms: force of urine stream, dribbling, polyuria. Resolves rapidly after remove the obstruction. Eg: prostatic hypertrophy, cancer of the prostate or cervix, or retroperitoneal disorders neurogenic bladder bilateral renal calculi, papillary necrosis, coagulated blood, bladder carcinoma, and fungus .

Pathogenesis

RBF
Prostacyclin, PGE2 Tubular water & Na reabsortions , secretion ADH Insufficient O2 & nutrients for tubular metabolic needs

To maintain intravascular volume Necrosis result in renal tissues death

Clinical Course & Prognosis

Depend on:
Etiology identified quickly and is reversible then clinical course is short. Presence of co-mobidities liver disease, hypoalbuminemia, heart failure, geriatrics then prognosis higher mortality SCr increase < 1-2mg/dL then prognosis is good Amount of urine produced mortality: oliguric/anuric > non-oliguric The need renal replacement therapy (mortality higher)

Phases

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Oliguric Phase
Progressive decrease in UO Duration: days to several weeks. Nonologuric: better prognosis Monitor fluid & electrolyte

Diuretic Phase
UO May indicate begining of renal repair Duration: few days to several weeks or longer. Kid Kidney still unable t concentrate urine till bl to t t i result in substantial water and sodium loss.

Recovery Phase
Duration: depend on severity (several weeks to months). Normal kidney function, normalization of urine production, kidney able to diluting & concentrating urine urine.

Clinical Manifestation

Symptoms of ARF
Decrease urine output (70%) Edema, esp. lower extremity

Symptoms of ARF
Heart failure Nausea, vomiting

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Symptoms of ARF
Pruritus Mental changes Anemia Tachypenic Cool, pale, moist skin

Clinical Manifestation
Identify etiology; 90% reversible Delay diagnosis: severe injury Diagnostic approach;
History taking Medical drug previous renal disease Medical, drug, Physical examination such as Vital signs: hypotension = volume depletion Skin: hydration status Urinalysis To classify the cause/type High specific gravity:pre-renal & functional ARF Proteinurea, hematuria: glomerular injury Glucosuria, aminoaciduria; proximal tubular dysfunction

Clinical Manifestation...
i. Laboratory data. To detect presence of renal disease Increase : K+, urea, creatinine blood level Decresae: creatinine clearance To determine type of ARF Urine osmolality > 500mOsm/L: prerenal due to ADH stimulation (prerenal) Table below:
Lab. Tests Urine sediment Urinary RBC Urinary WBC Urine sodium FENa(%) Urine/serum Osmolality urine/serum craetinie BUN/Scr Prerenal Azotemia Normal None None <20 <1 >1.5 >40:1 >20 Acute Intrinsic RF Cast, cellular debris 2-4+ 2-4+ >40 1-2 >1.3 <20:1 15 Postrenal Obstruction Cellular debris Variable 1+ >40 Variable < 1.5 <20:1 15

ii.

Goals of Therapy
Identify & remove ARF cause Prevent progression to irreversible renal injury

Prevention of ARF
Prevention in high risk patients is important due to high mortality Once risk identified strategies can be implemented to reduce likelihood of ARF 1.Nephrotoxin Avoidance Utili d l Utilized least nephrotoxic d t h t i drug Minimum dose 2. Sodium Loading Sodium loading increase tubular sodium which will cause decrease in renal blood flow, GFR and tubular flow Minimize delivery of nephrotoxin to tubules thus reduce risk of tubular injury.

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Prevention of ARF...
3.
Hydration Ensure patient is not dehydrated before administration of nephrotoxic drug Volum expansion allows: optimal renal perfusion reduce tubular workload may reduce tubules susceptibility to damage tubule s Also increase urine output hence minimizing kidney exposure to toxin Usually use normal saline: Expand intravascular compartment and increase renal perfusion Rate 1-2 ml/kg/hr started 3 6 hrs prior to adm of nephrotoxic drug Urine output 2ml/kg/hr is best indicator for sufficient hydration status

Pharmacological Treatment
Nonoliguric: better prognosis Diuretics:
UO :
Easier management of fluid and electrolyte balance Able to administer adequate nutrition Reduced risk of pulmonary edema Reduced need for renal replacement

urine flow may prevent tubular obstruction prevent glomerulus vasoconstriction

Diuretics: Loop Diuretic

Before initiation of diuretic:
Patients hydation status is good Monitor fluid lost. Assessment of intravascular volume: y (vital sign, oral g , Physical examination ( mucosa & daily body weight)

Eg: Frusemide, Ethacrynic acid,Torsemide, Bumetamide. Frusemide:

low cost, available in oral and parenteral forms forms, good safety and efficacy profiles. Continuous infusion better the intermittent dosing. Dosing: Loading dose: 40-80 mg frusemide Continuous infusion at 10-20mg/hr

First line:
loop diuretic & mannitol

Diuretic: Mannitol
Osmotic diuretic Dosing:
Start :12.5 - 25gm infuse intravenously over 3-5 min (20% solution)

Dopamine
Controversial Those with no response to diuretics Low dose: p improve RBF 0.5 2 g/kg/min

Limitation:
only via parenterally can caused ARF thus need to monitor urine output, osmolality dan serum electrolytes

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Thank you