Acute Renal Failure

 
Presented by Peter Fumo, MD, FACP
 Pre-renal Azotemia
 
Intra-renal Azotemia
 
Post-renal Azotemia
Counterregulatory Responses to Decrease in Effective
Circulating Blood Volume
 
Increased Sympathetic Tone
 
Increase in renin-angiotensin system characterized by a
increase in angiotensin II and aldosterone
 
Increase in ADH
Net Effects:
 
Increased efferent arteriolar tone due to AII to maintain SNGFR
 
Decreased afferent arteriolar tone due to increased nitric oxide
and prostaglandin synthesis stimulated by AII to maintain
SNGFR
 
Increased tubular sodium reabsorption proximally due to AII
and distally due to aldosterone
 
Increase in water reabsorption and urinary concentration due to
ADH
 
Increase in urea reabsorption due to increased sodium and water
reabsorption
Urinary indices will therefore display
low urinary sodium (<20 Meq/l)
 
Low fractional excretion of sodium (< 1%)
 
Low fractional excretion of urea (< 35%)
 
High urine osmolarity (> 600 mOsm)
 
Urinalysis will show high urine SG and low urine pH
 
BUN/Cr ratio will be > 20:1
Renal autoregulation will help maintain GFR and creatinine clearance

Pre-renal azotemia simply means diminished renal blood flow and is

reversible
 
Low cardiac output due to low preload due to volume depletion,
third-spacing or pulmonary hypertension (e.g. acute PE)
 
Low cardiac output due to pump failure, valvular heart disease or
tamponade
 
Systemic vasodilation with shunting of blood away from renal
vasculature such as in septic shock or liver failure
 
Defects in autoregulation or medications that interfere with
autoregulation
Treatments include:
 
Restoring intravascular volume
 
Stopping certain medications such as NSAIDs, ARBs or ACE
Is
 
Allowing BP to drift up with defective autoregulation
 
 
Inotropic support with pump failure
 
Norepinephrine, volume and perhaps vasopressin with
vasodilatory shock
Post-renal Azotemia
 
Due to obstruction to urinary outflow
 
Diagnosed usually by ultrasound
 
Urinalysis is bland
 
Hyperkalemic metabolic acidosis common
 
Treatment is to relieve the obstruction
Intrarenal Etiologies include:
 
Vascular
 
Acute Tubular Necrosis
 
Acute Glomerulonephritis
 
Acute Interstitial Nephritis
 
Tubular Obstruction
Acute Tubular Necrosis
 
Most common inpatient etiology
 
Can be ischemic or due to nephrotoxins
 
Urinalysis shows isosthenuric urine with granular casts,
usually seen with ischemic oliguric ATN
 
Urinary sodium >40 mEq/l, fractional excretion of sodium >
3% and fractional excretion of urea >35% with oliguria
 
Urine osmolarity < 400 mOsm
 
BUN/Cr ratio < 10:1
Nephrotoxic ATN can be due to endogenous toxins such as
hemoglobin and myoglobin, or exogenous toxins such as
aminoglycosides or dye
 
Hemoglobin or myoglobin gives a positive dipstick for blood
in the absence of RBCs
 
Rhabdomyalysis can give rise in serum creatinine > 2
mg/dl/day
 
Treatment of ischemic ATN is to restore renal perfusion
 
Treatment of nephrotoxic ATN is usually fluids and to stop
offending nephrotoxins
Vascular etiologies:
 
Acute injury to renal vessels
 
Characterized by elevations in BP, nonspecific urinalysis but
often proteinuria and hematuria
 
Urinary indices can look like pre-renal azotemia
 
Examples include malignant hypertension, TTP and HUS which
are all characterized by schistocytes
 
Atheroemboli for which eosinophilia and eosinophiluria
common
 
Renal infarction-elevated LDH, ALT
Acute Glomerulonephritis
 
Usually develops in outpatient setting
 
Urinalysis is key to diagnosis and show proteinuria, hematuria
and RBC casts
 
Can see low urine sodium and isosthenuric urine
 
Relatively rare cause compared to others
 
Biopsy required for definitive diagnosis
 
Treatment usually entails immunosuppression
Acute Interstitial Nephritis
 
Usually allergic in origin from medications such as antibiotics
 
Can see rash, fever, eosinophilia
 
Urinalysis shows hematuria, pyuria, WBC casts and
eosinophils
 
NSAIDs do not give eosinophilia, eosinophiluria or rash but
does give proteinuria due to MCD
 
Treatment is to remove offending drug and perhaps steroids
Tubular obstruction
 
Can be due to endogenous proteins such as Bence-Jones
proteins (SSA positive)
 
Can be due to endogenous crystals such as uric acid (acid
urine, pleomorphic crystals and urine uric acid to creatinine
ratio > 1)
 
Exogenous crystals due to medications such as acyclovir, sulfa
drugs and indinivir
 
Treatment is intravenous fluids, forced diuresis and urinary
alkalinization with uric acid
General Diagnostic Approach
Careful assessment of volume status
Careful look at medications
Careful look at recent radiologic studies
Urinalysis
Urinary Indices especially if oliguric
Differential for eosinophilia and smear for schistocytes
CPK, LDH and uric acid levels
Renal ultrasound
If renal ultrasound does not show obstruction, azotemic
medication avoidance and trial of intravenous fluids does not
improve BUN and creatinine, then most likely etiology is
intrarenal
 
Renal biopsy usually indicated for suspicion of acute GN,
unclear diagnosis, if immunosuppression being considered or
if certain medication that cannot be withdrawn potentially
implicated
Overview of Treatment
 
Avoid nephrotoxins and renal dose medications that are
renally excreted
 
Low protein, low sodium and low potassium diet
 
Phosphate binders
 
Daily assessment of volume status and symptoms
 
Daily weight, I/Os and screen 8
Indications for Dialysis
 
Uremic symptoms
 
Uremic Signs
 
Congestive heart failure unresponsive to diuretics
 
Severe hyperkalemia especially if associated with EKG
changes
 
Intractable acidosis