Acute Renal Failure

Stephanie Chieng Mei Ling

22/7/09
 Introduction
 Deterioration of renal function over a period of hours to days
which result in the failure of kidney :
(i) To excrete nitrogenous waste product (urea & creatinine)
(ii) To maintain fluid & electrolyte homeostasis
 Glomerular filtration rate (GFR): is the rate at which
ultrafiltrate is formed at the glomerulus.
 Normal value of GFR: 100-120mls/min
 Introduction (cont’)
 3 classes ARF: prerenal/hypoperfusion state,
intrarenal/intrinsic renal parenchymal injury & postrenal/
urinary obstructive disorder.
 Can be further described according to the amount of urine
produced per day as anuric (<50mL/d), oliguric (50-
400mL/d), non-oliguric (>400mL/d)
 Types & Causes of ARF
Prerenal ARF
> Intravascular volume depletion is the most common cause.
- Sudden & severe drop in BP (shock) or interruption of blood flow to the
kidneys due to injury/ illness.
- eg blood loss/fluid loss (vomiting, diarrhoea), cardiac failure, sepsis,
dehydration etc.
> Prerenal azotemia- due to diseases that leads to a decrease
in the effective arterial blood volume. These diseases include
HF, liver failure, and nephrotic syndrome.
- Drugs: NSAIDs & ACE I are known to cause prerenal azotemia.
Intrinsic ARF
Intrinsic renal parenchymal injury
- Direct damage to the kidneys by inflammation, toxins, drugs,
infection or reduced blood supply.
- Classified as tubular, glomerular, interstitial & vascular.
 Injury to tubules most often caused by ischemia or nephrotoxins.

If not treated, can lead to ‘acute tubular necrosis’-more severe

ischemic insult to kidneys.
 Glomerulonephritis- uncommon cause of ARF. Can be due to
diseases such as SLE.
 Acute interstitial nephritis- often results from an allergic rxn to a
drug. Can also be due to autoimmune disease, infection.
Cont’
 Vascular disease- microvascular & macrovasular. Depending
on location(s), vascular causes can be pre or intrarenal.
- Microvascuar commonly present as microangiopathic
hemolytic anemia & ARF secondary to small vessel
thrombosis or occlusion.
- Macrovascular causes of ARF in elderly should be
suspected renal artery stenosis or thrombosis, aortic disease
or acute dissection
 Post-renal ARF
Postrenal/ urinary obstructive disorder
- Obstruction of the outflow tracts of the kidneys such as at
renal pelvis, ureter or bladder neck.
- Causes: prostatci hypertrophy, catheters, tumors etc.
- Recovery of renal function is directly proportional to the
duration of the obstruction.
 Investigation Markers
 Urea (1.7- 8.3 mmol/L)
-Poor marker of renal fn: variable reabsorption in renal tubules, varies
with diet & hydration state, level increases w protein breakdown &
decreased in other disease (eg liver disease)
 Serum Creatinine (64-122 micromol/L)
- Fairy constant daily production w minimal tubular reabsorption.
-However, may vary with dietary intake (higher level2 hrs post high
red meat intake). Levels peak in the evening, low in morning.
-Generally, elevations implies impairments of RF & reduction of
GFR.
Investigation Marker (2)
 Creatinine Clearance (105-150ml/m)
- Based on Cockcroft & Gault formula
CrCL= (140-age) x IBW (kg)/ Serum Cr (micromol/l) x 0.814
For female= multiple the whole equation with 0.85
Mild RF : 25-50ml/min
Moderate: 10-25ml/min
Severe: <10ml/min

 Any abnormalities of electrolytes values

 Management
 The initial care –focus on reversing underlying cause, correcting
fluid & electrolyte imbalances, and preventing further renal injury
by providing supportive measures.
Fluid Management
- In oliguric RF, strategy is to have fluid restriction.
- Hypovolaemia must be corrected
- Hypotension must be quickly corrected with fluid challenge, or if
there is no volume deficit, use of an appropriate inotrope is
advocate
 Patients with volume deficit
(i) In hypotensive patients
-Fluid challenge with 250ml of NS over 15min. If BP does not
improve or CVP measurement does not increase by 2cm repeat
fluid challenge (up to 500-1000ml of NS may be required). Stop if
CVP increases to satisfactory level i.e 5-10cm H2O
-If volume is restored, with gd BP , but urine outflow is poor
(<40mL/hr), IV frusemide can be given either by slow bolus of 40-
120mg repeated as necessary or by infusion (dilute in NS) at a rate
of 10-30mg/hr with max daily dose of 1g.
Patients with volume deficit (2)
-If vol is restored, with gd BP , but urine output remains poor
despite frusemide & inotrope, restrict fluid to 500ml/24hr plus
measured losses. Avoid K+ & food rich in K+.
-If good BP is obtained & good urine flow is established
(>40ml/hr), continue with a slower fluid replacement regimen.
-If volume is restored, but BP is still low, use an appropriate
inotrope (eg dopamine)
Patients w/hout volume deficit
(ii) In normotensive patients
-Fluid challenge should also be given to correct fluid deficit.
-If gd urine flow is established (>40m/hr), continue with slower
fluid replacement regimen.
-If vol restored but urine outflow is poor (<40ml/hr), start
IV frusemide as mentioned above.
-Start IV frusemide & if necessary with an inotrope as mentioned
before.
-If urine flow does not improve, restrict fluid.
 Metabolic acidosis
 pH< 7.1 or with HCO3 <10mmol/L may need to be treated with
Sodium Bicarbonate. A rough estimation of the amount (mmol)
required can be calculated by:
0.5 X body weigh (kg) X Base deficit
base deficit= 24- actual HCO3
1ml of 8.4% NaHCO3 provides 1mmol of NaHCO3
 Treatment usually titrated slowly by infusing bicarbonate (eg 1ml
of 8.4% NaHCO3 per kg over 30min) & regularly checking the
plasma pH & bicarbonate.
 Nutrition
 In patients with ARF the main determinants of nutrient
requirements (and outcome) are the degree of hypercatabolism
caused by the disease associated with ARF, the nutritional state,
and the type and frequency of dialysis therapy.
 Protein- 0.8-1.2g/kg/d (high intake if in hypercatabolic state)
 NaCl- 2-4g/d
 Caloric intake- 35-50kcal/kg/d
 Potassium- 40mmol/d (if dialysed)
 Oral feeding should be initiated whenever possible.
 Dialysis
 Needed if medical Tx fails to control fluid/electrolyte derangement
eg fluid overload, metabolic acidosis
Indications for initiating dialysis are:
 BU> 30mmol/l
 Severe hyperK (>6mmol/l)
 Severe metabolic acidosis (pH<7.1)
 Volume overload +/- pulmonary oedema not responsive to diuretics
 Development of uremic Sx eg CNS (asterixis, neuromuscular
irritability,coma, seizure) and GI (nause & vomiting, haemorrhage)
symptoms.
 GFR< 10-15ml/min
 Types of dialysis
 Depending on clinical situations- haemodialysis, peritoneal
dialysis, CRRT (continuous renal replacement therapy)
 Patients with severe tissue breakdown (eg rhabdomyolysis,
trauma, burns, sepsis) gave enhanced urea production- require
haemodialysis or CRRT.
 In other cases of ARF in which the catabolic component is less
prominent, peritoneal dialysis may be adequate.
 Diuretic resistance
 Decreased response to loop diuretics- diuretic resistance
 Some common causes of resistance in ARF: excessive Na intake,
inadequate diuretics dose or inappropriate regimen, reduced
bioavailability (from GI oedema), reduced RBF (drugs,
intravascular depletion), nephrotic syndrome (diuretics bind to
proteins in renal tubule, reducing diuretic effects)
 Strategies to overcome: increasing the dose/ dosing frequency;
continuous IV infusion of the diuretic; concomitant
administration of loop diuretic with diuretics that act on distal
convoluted tubule (thiazides) or the collecting duct
(spironolactone, amiloride) for synergistic effect
 References
 Helms R.A., Quan D.J., Herfindal E.T et al. Textbook of Therapeutics: Drug and
Disease Management.
 Sarawak Handbook of Medical Emergencies
 Needham E. Management of Acute Renal Failure. American Family Physician.
2005 November; 72: 1739-46. Adapted from
http://www.aafp.org/afp/20051101/1739.pdf
 Druml W. Nutrition and Metabolism in Acute Renal Failure. Adapted from
http://www.kidneyatlas.org/book1/adk1_18.pdf
 Mitch E.W., Klahr S.Handbook of Nutrition and Kidney:Nutritional Support in
Acute Renal Failure. 3rd edition.