An abrupt (within 48hr) reduction in kidney function currently defined as an absolute increase in serum creatinine of either >0.3 mg/dL or a percentage increase of >50% or a reduction in UOP (documented as oliguria of <0.5 ml/kg/hr for >6hr)

1. Overview of Acute Renal Failure
Mednotez

2. AKI (Acute Kidney Injury)
• Definition and diagnostic Criteria
– An abrupt (within 48hr) reduction in kidney function
currently defined as an absolute increase in serum
creatinine of either >0.3 mg/dL or a percentage increase of
>50% or a reduction in UOP (documented as oliguria of
<0.5 ml/kg/hr for >6hr)

3. Definition and classification/staging system for acute kidney injury (AKI)
• AKI stage Creatinine criteria Urine output criteria
• AKI stage I Increase of serum creatinine by
≥ 0.3 mg/dl (≥ 26.4 μmol/L)
or
increase to ≥ 150% – 200% from baseline < 0.5 ml/kg/hour for > 6 hours
•
-------------------------------------------------------------------------------------------------------------------
• AKI stage II Increase of serum creatinine to
> 200% – 300% from baseline < 0.5 ml/kg/hour for > 12 hours
•
-------------------------------------------------------------------------------------------------------------------
• AKI stage III increase of serum creatinine to
> 300% from baseline < 0.3 ml/kg/hour for > 24 hours
or or
serum creatinine ≥ 4.0 mg/dl anuria for 12 hours
≥ 354 μmol/L) after a rise of at least 44 μmol/L
or
treatment with renal replacement therapy

4. Epidemiology
• Prevalence
– 1% all patients admitted to hospital
– 10-30% patients admitted to ICU
• Etiology
– Hemodynamic 30%
– Parenchymal 65%
• Acute tubular necrosis 55%
• Acute glomerulonephritis 5%
• Vasculopathy 3%
• Acute interstitial nephritis 2%
– Obstruction 5%

5. Mortality
• Dialysis requiring 40-90%
• Increased mortality even in patients not requiring
dialysis
• 25% increase in creatinine associated with a mortality
rate of 31% compared with 8% for matched patients
without renal failure

6. Non-Oliguric vs. Oliguric vs. Anuric
• Oliguric renal failure.
– Functionally, urine output less than that required to
maintain solute balance (can’t excrete all solute taken in).
– Defined as urine output < 400ml/24hr.
• Anuric renal failure.
– Defined as urine output < 100ml/24hr.
– Less common – suggests complete obstruction, major
vascular catastrophy, or more commonly severe ATN.

7. Non-Oliguric vs. Oliguric vs. Anuric
• Classifying by urine output may help establish a
cause.
– Oliguria – more common with obstruction, prerenal
azotemia
– Nonoliguric – intrarenal causes – nephrotoxic ATN, acute
GN, AIN.
• More importantly, assists in prognosis.
– Significantly higher mortality with oliguric renal failure.
– 80% vs. 25% mortality in Oliguric vs. non-oliguric ARF
– Nonoliguric renal failure may also suggest greater liklihood
of recovery of function.

8. Evaluation of Renal Failure
• Is the renal failure acute or chronic?
– laboratory values do not discriminate between acute
vs. chronic
– oliguria supports a diagnosis of acute renal failure
• Clues to chronic disease
– Pre-existing illness – DM, HTN, age, vascular disease.
– Uremic symptoms – fatigue, nausea, anorexia, pruritis,
altered taste sensation, hiccups.
– Small, echogenic kidneys by ultrasound.

9. Acute Renal Failure
Clinical Assessment (Volume Status,
Urinalysis and Ultrasound)
Pre-Renal Intra-Renal Post-Renal
Absolute Decrease
In ECF Volume
GI losses
Hemorrhage
Decreased
Renal
Blood Flow
Heart failure
Renal artery
stenosis
Altered Intra-Renal
Hemodynsmics
Drug-induced
NSAIDS/COX-2
Inhibitors
Calcineurin inhibitors
ACE inhibitors
AII Receptor Blockers
Sepsis
Hypercalcemia
Cirrhosis/Hepatorenal
syndrome
Abdominal compartment
syndrome
Tubulointerstitial
Disorders
Tubular Injury
Ischemic
Nephrotoxic
Interstitial Nephritis
Allergic-type
NSAID-type
Glomerular Disorders
Glomerulonephritis
Thrombotic
microangiopathies
Atheroembolic
disease
Anatomic Obstruction
Bladder Outlet
Prostate
Pelvic Tumor
Ureteral
Tumor
Stones
Stricture
Tubular Obstruction
Crystals
Calcium oxalate
(Ethylene glycol
poisoning)
Drugs
Indinovir
Methotrexate
Proteins
Myeloma cast
nephropathy
Clinical Approach to Acute Renal Failure

10. 5 Key Steps in Evaluating Acute Renal
Failure
1) Obtain a thorough history and physical;
review the chart in detail
2) Do everything you can to accurately
assess volume status
3) Always order a renal ultrasound
4) Look at the urine
5) Review urinary indices

11. Acute Renal Failure
–Identify an insult
• Volume depletion (diarrhea, blood loss, emesis, over-
diuresis), Hypotension, CHF.
• Drug exposure – toxin or reduction of renal perfusion.
• Contrast exposure.
• Infections – inflammatory mediators v. direct infection
• Endogenous toxins/insults – myoglobin,hemoglobin,
uric acid.

12. Acute Renal FAilure
• Symptoms:
– Fever, rash, joint pains, myalgias
• Concern for SLE, vasculitis, acute interstitial nephritis.
– Dyspnea – heart failure.
– Hemoptysis – Goodpasture’s, Wegener’s.
– Preceding bloody diarrhea – HUS.
– Preceding pharyngitis – post-Strep GN, post-
infectious GN.

13. Acute Renal Failure
• Urine output.
– Abrupt anuria.
• Acute obstruction, severe acute GN, sudden vascular
catastrophe.
– Slowly diminishing.
• Ureteral stricture.
• Prostatic enlargement.
– Presence of hematuria
• Painless – suggests GN.
• Painful – suggest ureteral obstruction.

14. Acute Renal Failure
• Physical Exam.
– Skin – new rashes.
• Livedo reticularis – atheroemboli, SLE, cryoglobulins.
• Petechiae – HSP.
• Malar rash – SLE.
– Eye
• Papilledema – malignant HTN.
• Roth’s spots – endocarditis.
– CV
• Rub – suggestive of uremic pericarditis, lupus.
• Gallop – suggesting CHF.

15. Acute Renal Failure
• Physical Exam.
– Assessing volume status.
• Is the patient intravascularly volume depleted?
– Neck veins – JVP
– Peripheral edema or lack of.
– Orthostatic vitals.
– Not always straightforward.
– Pt. may be edematous (low albumin) or have
significant right sided heart disease.

16. • BUN/Creatinine ratio.
– > 20:1 – suggest prerenal or obstruction.
– Can be elevated by anything leading to increased urea
production/absorption.
• GI bleed
• TPN
• Steroids
• Drugs – Tigecycline.
• Creatinine in anephric state typically only rises
1mg/dl/day.
– If greater – should be concerned for rhabdomyolysis

17. ATN vs. Prerenal Azotemia
Indices Prerenal ATN
UNa < 20 > 40
FeNa < 1% > 4%
U/PCreat > 40 < 20
FeUN < 35% >70%

18. Confounding Variables in the Diagnosis of Pre-
renal Azotemia versus ATN
• A low urine Na can also be seen in:
– Contrast induced ATN
– Early ATN or obstruction
– Acute Glomerulonephritis and Nephrotic Syndrome
• Diuretics can elevate the urine Na
• Jaundice may induce “muddy brown” cast formation

19. Urinary Sediment
• Can be helpful in identifying underlying disease
states (proteinuric disease, underlying chronic GN) as
well as examining acute insult.

20. Urinary Sediment Findings inUrinary Sediment Findings in
Intra-Renal Acute Renal FailureIntra-Renal Acute Renal Failure
Intra-renal Acute
Renal Failure
Dysmorphic Hematuria
Red cell casts
Oval fat bodies
Fatty Casts
Muddy brown casts
Renal tubular epithelial
cells and casts
White cells
White cell casts
Eosinophiluria
Glomerulonephritis
Atheroembolic disease
Thrombotic
microangiopathy
Minimal change
disease
Focal segmental
glomerulosclerosis
Albuminuria
Tubular proteinuria
Tubular epithelial
injury
-Ischemic
-Nephrotoxic
Interstitial nephritis
Urinary tract
infection
Crystalluria
Drug toxicity
Urate crystals
-Urate nephropathy
Calcium oxalate crystals
-ethylene glycol

21. Acute Renal failure
• Introduction to casts…
Hyaline Casts:
Better seen with low
light.
Non-specific.
Composed of Tamm-
Horsfall mucoprotein.

22. Acute Renal Failure
UpToDate Images.
Waxy Casts:
Smooth appearance.
Blunt ends.
May have a “crack”.
Felt to be last stage of
degenerating cast –
representative of chronic
disease.
Granular Casts:
Represent degenerating
cellular casts or aggregated
protein.
Nonspecific.

23. Acute Renal Failure
Fatty Casts:
Seen in patients with
significant proteinuria.
Refractile in appearance.
May be associated with free
lipid in the urine.
Can see also “oval fat
bodies” – RTE’s that have
ingested lipid.
Polarize – demonstrate
“Maltese cross”.
UpToDate Images.

24. Acute Renal Failure
Muddy Brown
Casts:
Highly suggestive of
ATN.
Pigmented granular
casts as seen in
hyperbilirubinemia can
be confused for these.
UpToDate Images.

25. Acute Renal Failure
UpToDate Images.
White Blood Cell
Casts:
Raises concern for
interstitial nephritis.
Can be seen in other
inflammatory disorders.
Also seen in
pyelonephritis.

26. Acute Renal Failure
• Hematuria
Nonglomerular hematuria:
Urologic causes.
Bladder/Foley trauma.
Nephrolithiasis.
Urologic malignancy.
May be “crenated” based upon age
of urine, osmolality – NOT
dysmorphic.

27. Acute Renal Failure
Red Blood Cell
Casts:
Essentially diagnostic of
vasculitis or
glomerulonephritis.
Dysmorphic Red Cells:
Suggestive of glomerular
bleeding as seen with
glomerulonephritis.
Blebs, buds, membrane
loss.
Rarely reported in other
conditions – DM, ATN.

28. Acute Renal Failure
Crystals – Pretty and important.
Uric acid crystals:
Seen in any setting of
elevated uric acid and an
acidic urine.
Seen with tumor lysis
syndrome.
Calcium oxalate crystals:
Monohydrate – dumbell
shaped, may be needle-like.
Dihydrate – envelope shaped.
Form independent of urine pH.
Seen acutely in ethylene glycol
ingestion.
UpToDate Images.

29. Diagnostic Evaluation ofDiagnostic Evaluation of
Renal FailureRenal Failure
Cumulative
% Correct
Diagnosis
Hx, PE, Labs Therapeutic
Trials
Renal
Biopsy
100-
80-
60-
40-
20-
0-
60%
25%
15%

30. Diagnosis-Observation andDiagnosis-Observation and
Therapeutic TrialsTherapeutic Trials
 Fluid replacementFluid replacement
 Relief of obstructionRelief of obstruction
 Discontinuation of medicationsDiscontinuation of medications

31. Renal Biopsy-When?Renal Biopsy-When?
 Exclude pre- and post-renal failure, andExclude pre- and post-renal failure, and
clinical findings are not typical for ATNclinical findings are not typical for ATN
 Extra-renal manifestations that suggest aExtra-renal manifestations that suggest a
systemic disordersystemic disorder
 Heavy proteinuriaHeavy proteinuria
 RBC castsRBC casts

32. Case 1
A 42 year male is admitted to the SICU after sustaining
multiple trauma. His course is complicated by
Enterobacter sepsis with profound hypotension
requiring support with intravenous dopamine. The
urine output has gradually decreased to only 300 ml
per day. The urine sodium is 78.

34. Ischemic Acute Renal Failure
• A form of ATN often following a prerenal insult
• Late proximal tubule and medullary thick ascending limb
most susceptible
• Severity of renal failure correlates with duration of insult
• Treatment is to optimize renal perfusion, avoid
additional nephrotoxic insults and other supportive
measures

35. Conditions that Lead to Pre-renal Acute Renal Failure
Generalized
or Localized Reduction in
Renal Blood Flow
Ischemic
Acute Renal Failure
Intravascular Volume Depletion
Decreased Effective Circulating Volume
CHF Cirrhosis Nephrosis
Medications
CYA, Tacrolimus
ACE inhibitors NSAIDS
Radiocontrast Amphotericin B
Aminoglycosides
Hepatorenal
Syndrome
Sepsis
Large-vessel Renal Vascular Disease
Renal Artery Thrombosis
Renal Artery Embolism
Renal Artery Stenosis or Crossclamping
Small-vessel Renal Vascular Disease
Vasculitis Atheroemboli
Thrombotic Microangiopathies
Transplant Rejection

36. Phases of Ischemic Epithelial Tubular
Injury
Time
GFR
Pre-renal
Initiation
Extension
Maintenance
Recovery

38. Risk Factors for Ischemic Tubular
Injury
• Volume depletion
• Aminoglycosides
• Radiocontrast
• NSAIDs, Cox-2 inhibitors
• Sepsis
• Rhabdomyolysis
• Preexisting renal disease
• HTN
• Diabetes mellitus
• Age > 50
• Cirrhosis

39. Case 2
A 56 y.o. male presents with complaints of persistent
fever, chills, sore throat, and myalgias for the past 14
days. Ten days ago he started taking amoxicillin he
had on hand for dental prophylaxis. His physical
exam is remarkable for fever to 38.6o
C, an exudative
pharyngitis and a diffuse maculopapular rash.

40. Case 2
Laboratory Data Result Normal Range
Serum
Na 134 mEq/L 135-145
K 5.7 mEq/L 3.5-5
Cl 106 mEq/L 100-111
Total CO2 14 mEq/L 24
BUN 46 mg/dL 4-15
Creatinine 3.8 mg/dL 0.6-1.0
Glucose 96 mg/dL 60-100
Whole blood
WBC 12 x109/L 4.5-11.0
Hgb 11 gm/dL 13.5-17.5
Hct 33 % 41.0-53.0
Platelets 216 x109/L150-440
Urine
Specific gravity 1.010 1.002-1.036
Protein 2+ Negative
Blood Trace Negative
Glucose Negative Negative
The urine sediment shows 3-5 RBC’s/h.p.f., 20-25 WBC’s/h.p.f., coarse granular and white
cell casts, and rare red cell casts.

41. Case 2

42. Acute Interstitial Nephritis-Etiology
• Allergic/Drug induced
• Autoimmune
– Sarcoid -SLE
– Sjogren’s
• Toxins
– Chinese herb nephropathy -Heavy metals
– Light chain cast nephropathy
• Infiltrative
– Leukemia
– Lymphoma
• Infections (Legionella, CMV, HIV, Toxoplasma)

43. Acute Interstitial Nephritis
Clinical Presentation
• Non-oliguric ARF
• Fever in allergic and infectious types (except NSAID type)
• Rash in allergic type (except NSAID induced)
• Eosinophilia
• UA: WBC casts
Eosinophiluria (allergic)
Hematuria (NSAID related)

44. Common Causes of Drug Induced AIN
• NSAIDS
• Antibiotics
– Penicillins
• methacillin
• Ampicillin, amoxacillin, carbenacillin, oxacillin
• Cephalosporins
– Quinolones (ciprofloxacin)
– Anti-tuberculous medications (rifampin, INH, ethambutol)
– Sulfonamides (TMP-SMX, furosemide, thiazides)
• Miscellaneous
– Allopurinol, cimetidine, dilantin

45. NSAID versus Beta-lactam AIN
Beta-lactam NSAID
Duration of exposure 2 weeks 5 months
Fever/rash/eosinophilia 80% 20%
Eosinophiluria 80% 15%
> 3 gm proteinuria < 1% 83%
Rate of recovery Fast Slow
Chronic renal failure Rare Common
Benefit of steroids Probably Probably not

46. Acute Interstitial Nephritis
Diagnosis
• Eosinophiluria
– > 1-5% considered positive
– Sensitivity 50-90%, specificity 50-80%
Pretest Prob Post-test Prob
+Eos -Eos
30% 65% 5%
50% 81% 11%
80% 95% 33%
• False positives in UTIs, RPGN, and atheroembolic disease
• Renal biopsy if considering steroid therapy and for prognosis

47. Acute Interstitial Nephritis
Treatment
• Withdrawal of offending agent
• Treatment of underlying process if infectious/autoimmune
etiology
• Trial of corticosteroids, especially in allergic presentations
1 mg/kg/day or 2 mg/kg every other day
– No randomized trials proving efficacy
– Reversal of renal failure usually seen in < 6 weeks

48. Rhabdomyolysis
• Often develops in the setting of crush injury, especially if
superimposed circulatory shock
• Hallmarks of diagnosis
– CK > 10,000
– (+) dipstick for blood but no RBCs
• Treatment
– Volume expansion (judiciously if severe oliguria or
azotemia)
– Fasciotomy when indicated for compartment syndrome
(“second wave phenomenon”)
• Avoid calcium repletion unless neuromuscular manifestations
present
• Rebound hypercalcemia in recovery phase

49. Common Nephrotoxic Agents
• Antimicrobial agents
– Aminoglycosides
– Amphotericin B
– Acyclovir
– Foscarnet
– Pentamidine
• Chemotherapeutic agents
– cisplatin
– mitomycin C
– streptozocin
• Vasoactive drugs
– NSAIDS
– ACE inhibitors
– CSA and tacrolimus
• Radiocontrast agents

50. Factors that ReduceFactors that Reduce
Glomerular Capillary PressureGlomerular Capillary Pressure
Afferent
Arteriole
Efferent
Arteriole
Vasoconstriction
NSAIDs
Cox-2 Inhibitors
Cyclosporine A
Tacrolimus
Iodinated contrast
Hypercalcemia
Hepatorenal syndrome
Vasodilation
ACE inhibitors
Angiotensin Receptor
Blockers

51. Aminoglycoside Nephrotoxicity
• Generally presents 1 week after exposure
• Non-oliguric
• Low trough levels do not guard against nephrotoxicity
• Incidence of ATN
– 10% after 1 week
– 40% after 2 weeks
• Risk factors for ATN
– Advanced age - Superimposed sepsis
– Liver disease - Hypotension

52. Radiocontrast-Induced
Acute Renal Failure
• Induces renal vasoconstriction and direct cytotoxicity via
oxygen free radical formation
• Risk factors:
– Renal insufficiency - Diabetes
– Advanced age - > 125 ml contrast
– Hypotension
• Usually non-oliguric ARF; irreversible ARF rare

53. Prevention of Radiocontrast Nephropathy
Intervention Strength of
Evidence
Clarity of
Risk-Benefit
Grade of Recommendation
Volume expansion
with normal saline
Good Clear A: Intervention is always indicated
and acceptable
Volume expansion
with sodium
bicarbonate
Fair Clear B: Intervention may be effective and is acceptable
Iso-osmolar contrast Fair Clear B: Intervention may be effective and is acceptable
Theophylline Fair Unclear C: May be considered; minimal or
no relative impact
N-acetylcysteine Good Unclear C: May be considered; minimal or
no relative impact
Hemofiltration Fair Unclear I: Insufficient evidence to recommend for or against
Fenoldopam Good Unclear D: Not useful
Hemodialysis Good Unclear D: Not useful

54. Contrast Induced Nephropathy
• Assess CIN risk
– eGFR <30 – Hospital admission, Nephrology consult, Dialysis planning, renal protection
– eGFR 30-59 – Discontinue NSAIDs, IV volume expansion, Intra-arterial: isoosmolar, Intra-
venous: iso-osmolar or low osmolar contrast; limit contrast volume
– eGFR >60, Discontinue metformin
• Optimal Volume Status
• Low-osmolality contrast media
• F/U Creatinine 24 – 72hr after contrast exposure
• Adequate IV volume expansion with isotonic crystalloid for 3 – 12hr
before the procedure and continue for 6 – 24hr afterward. Oral fluid data
is insufficient
• No adjunctive medical or mechanical treatment has been proved to be
efficacious
• Prophylactic hemodialysis and hemofiltration not validated

55. Acute Renal Failure due to
Intratubular Obstruction
• Crystalluria
– Ethylene glycol: Calcium oxalate
– Tumor lysis: Urate and Calcium phosphate
– Medications
• Acyclovir
• Methotrexate
• Sulfonamides
• Anti-retroviral agents
• Myeloma cast nephropathy

56. Acute Urate Nephropathy
• Acute oliguric renal failure associated with urate levels >
18 mg/dl
• Associated with overproduction and excretion of urate in
patients undergoing chemotherapy or with a heavy tumor
burden
• Urine urate/creatinine > 1
• Prevention: allopurinol 600-900 mg/d + NS (uo > 2.5 l/d)
• Urinary alkalinization may worsen calcium phosphate
precipitation and NS is as effective as urinary
alkalinization alone
• Early dialysis indicated for oliguric ARF to decrease urate
burden

57. Renal Disease Associated
with Multiple Myeloma
• Myeloma cast nephropathy
– direct precipitation of casts in tubules
– Factors favoring cast precipitation:
-affinity of light chains for Tamm-Horsfall protein
-high luminal Cl-
-volume depletion
– Plasmapheresis may be beneficial
• Hypercalcemic nephropathy
• Glomerular lesions (MPGN, Amyloid, Light chain deposition
disease)

58. Case 3
A 35-year-old Hispanic female presents with a one
month history of periorbital and lower extremity
edema. Over two days prior to presentation she has
experienced arthralgias in her wrists and elbows. On
physical examination she is in no acute distress.
Blood pressure is 162/94, temperature 37.4 . Her
skin exam is significant for a malar erythematous
rash. The heart and lungs are normal. There is 3+
edema to the thighs bilaterally.

59. Case 3
Laboratory Data Result Normal Range
Serum
Na 138 mEq/L 135-145
K 4.2 mEq/L 3.5-5
Cl 108 mEq/L 100-111
Total CO2 17 mEq/L 24
BUN 75 mg/dL 4-15
Creatinine 3.5 mg/dL 0.6-1.0
Glucose 83 mg/dL 60-100
Anti-neutrophil antibody 1:160 Negative
Whole blood
WBC 5.9 x109/L 4.5-11.0
Hgb 11.9 gm/dL 13.5-17.5
Hct 34 % 41.0-53.0
Platelets 153 x109/L 150-440
Urine
Specific gravity 1.015 1.002-1.036
Protein 3+ Negative
Blood 3+ Negative
RBC >50/h.p.f. 0-4
Sodium 10 mEq/L Variable
Creatinine 35 mg/dL Variable

60. Case 3

61. Acute Glomerulopathies
• RPGN most commonly seen with:
– Lupus nephritis (DPGN, class IV)
– Pauci-immune GN (ANCA associated)
– Anti-GBM disease
– less commonly: IgA, post-infectious
• Nephrotic presentations of ARF
– Collapsing FSGS (HIV nephropathy)
– Minimal change disease with ATN
• Thrombotic microangiopathies (HUS, TTP, malignant
hypertension, scleroderma kidney, pre-eclampsia)

62. Atheroembolic Renal Disease
• ARF in patient with erosive atherosclerosis
• Often follows aortic manipulation (angiography, surgery,
trauma) or anticoagulation
• Pattern is often an acute worsening of renal function due to
showering of emboli, followed by more insidious progression
over several weeks to months due to ongoing embolization of
atheromatous plaques
• Livedo reticularis
• Nephritic sediment, eosinophilia, eosinophiluria, low C3
• Poor prognosis

63. Livedo Reticularis

64. Hepatorenal Syndrome
Major Criteria
• Chronic or acute liver disease with advanced hepatic failure and portal
hypertension
• Low GFR, as indicated by a serum creatinine >1.5 mg/dL or a creatinine
clearance < 40 mL/min
• Absence of shock, ongoing bacterial infection, fluid loss, and current or
recurrent treatment with nephrotoxic drugs. Absence of gastrointestinal fluid
losses (repeated vomiting or intense diarrhea) or renal fluid losses (as indicated
by weight loss > 500 gm/d for several days in patients with ascites without
peripheral edema or > 100 gm/d in patients with peripheral edema)
• No sustained improvement in renal function (decrease in serum creatinine to
1.5 mg/dL or less or increase in creatinine clearance to 40 ml/min or more)
after withdrawal of diuretics and expansion of plasma volume with 1.5 L of
isotonic saline
• Proteinuria < 500 mg/d and ultrasonographic evidence of obstructive uropathy
or parenchymal renal disease.

65. Hepatorenal syndrome
Minor Criteria
• Urine volume < 500 mL/day
• Urine sodium < 10 mEq/L
• Urine osmolality > plasma osmolality
• Urine red blood cells < 50 per high-power
field
• Serum sodium concentration < 130 mEq/L

66. Obstructive Uropathy
• Urine output in partial obstruction
Normal Obstruction
GFR 150 L/day 10 L/day
Tubular resorption 148 L/day 8 L/day
Urine output 2 L 2L
• Urine Na low over first 24-48 hours, then > 40
• Ultrasound 90% sensitive
• Prognosis depends on duration (< 1 week favorable, poor
if > 12 weeks)

67. Other AKI….
• Abdominal Compartment Syndrome
– Presence of IAP >20 that is associated with a single or multiple organ
system failure. Causes severe oliguric or anuric renal failure. Tx:
surgical decompression.
• Acute Phosphate Nephropathy
– AKI from Nephrocalcinosis after use of oral sodium phosphate
(phospho soda) for colonoscopy.
• Orlistat associated AKI
– AKI from Oxalate nephropathy due to enhancing oxalate absorption
with increased urinary excretion.
• IVIG associated AKI
– AKI from osmotic nephrosis from sucrose-containing formulation.
• Herbal, Home remedies
– Arsenal X, Chromium picolinate, Chineses Herb Xi Xin with aristolochic
acid; tea from Mouring Cypress, Snake gallbladder, Star fruit (oxalate),
Ma Huang (ephedra), Noni Juice

68. Hyaline Casts

69. Red Cell Cast

70. Muddy Brown Casts

71. Fatty Cast