4. 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
5. 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
6. 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
7. 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
8. 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
9. 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
11. 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
12. 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
13. 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
14. 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
15. 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
16. 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
17. 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
18. 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
19. 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
20. Indications for Dialysis
Uremic symptoms
Uremic Signs
Congestive heart failure unresponsive to diuretics
Severe hyperkalemia especially if associated with EKG
changes
Intractable acidosis
