Transcript Acute Renal Failure - Welcome to the QStation Web Site

Acute and Chronic
Renal Failure
Courtney Bunevich, DO
December 19, 2007
Acute Renal Failure
Rapid decline in the GFR over days to
weeks
 Serum Cr increases by >0.5 mg/dL
 GFR <10mL/min, or <25% of normal

Definitions
Anuria: No urine output
Oliguria: Urine output <400-500 mL/d
Azotemia: Increase in Serum Cr and BUN
 May
be prerenal, renal, or postrenal
 Does not require any clinical findings
Chronic Renal Insufficiency
 Deterioration
over months to years
 GFR 10-20 mL/min, or 20-50% of normal
ESRD: GFR <5% of normal
ARF: Signs and Symptoms
Hyperkalemia
 Nausea/Vomiting
 HTN
 Pulmonary edema
 Ascites
 Asterixis
 Encephalopathy

Causes of ARF in Hospitalized
Patients

45% ATN
 Ischemia,

21% Prerenal
 CHF,
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

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Nephrotoxins
volume depletion, sepsis
10% Urinary obstruction
4% Glomerulonephritis or vasculitis
2% AIN
1% Atheroemboli
ARF: Focused History
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Nausea? Vomiting? Diarrhea?
Hx of heart disease, liver disease, previous renal
disease, kidney stones, BPH?
Any recent illnesses?
Any edema, change in
urination?
Any new medications?
Any recent radiology studies?
Rashes?
Physical Exam
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Volume Status
 Mucus membranes, orthostatics
Cardiovascular
 JVD, rubs
Pulmonary
 Decreased breath sounds
 Rales
Rash (Allergic interstitial nephritis)
Large prostate
Extremities (Skin turgor, Edema)
Workup for ARF
BMP or RFP
 Urine

 Urine
electrolytes and Urine Cr to calculate
FeNa
 Urine eosinophils
 Urine sediment: casts, cells, protein
 Uosm

Kidney U/S to rule out hydronephrosis
FeNa = (urine Na x plasma Cr)
(plasma Na x urine Cr)
FeNa <1%

PRERENAL

ATN (unusual)
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Urine Na < 20 because functioning tubules reabsorb lots of
filtered sodium
Postischemic disease: most of UOP comes from few normal
nephrons, which handle sodium appropriately
ATN + chronic prerenal disease (cirrhosis, CHF)
Glomerular or vascular injury

Despite glomerular or vascular injury, pt may still have wellpreserved tubular function and be able to concentrate Na
FeNa
FeNa 1%-2%

Prerenal-sometimes

ATN-sometimes

AIN will have a higher FeNa due to tubular damage
FeNa >2%

ATN

Damaged tubules cannot reabsorb sodium
Calculating FeNa after Patient
Has Recieved Lasix

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Caution with calculating FeNa if pt has gotten
loop diuretics in past 24-48 h
Loop diuretics cause natriuresis that raises U
Na-even if the patient is prerenal
So if FeNa>1%, you do not know if this is
because patient is euvolemic or because lasix
increased the U Na
So, helpful if FeNa still <1%, but not if FeNa
>1%
Prerenal ARF
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Hyaline casts can be seen in normal pts
 NOT
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an abnormal finding
UA in prerenal ARF is normal
Prerenal: causes 21% of ARF in hospitalized
patients
Reversible
Prevent ATN with volume replacement
 Fluid
boluses or continuous IVF
 Monitor Uop
Prerenal causes

Intravascular volume depletion
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Hemorrhage
 Vomiting, diarrhea
 “Third spacing”
 Diuretics
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Reduced Cardiac output
 Cardiogenic shock, CHF, Tamponade
 Systemic vasodilation
 Sepsis
 Anaphylaxis, Antihypertensive drugs
Renal vasoconstriction
 Hepatorenal syndrome
Intrinsic ARF
1.
2.
3.
4.
Tubular (ATN)
Interstitial (AIN)
Glomerular
(Glomerulonephritis)
Vascular
You evaluate a 57yo man with
oliguria and rapidly increasing BUN
and Serum Cr
A.
B.
C.
D.
ATN
Acute glomerulonephritis
Acute interstitial nephritis
Nephrotic Syndrome
ATN
Muddy brown granular casts (last slide)
 Renal tubular epithelial cell casts (below)

More ATN
•Broad casts (form in dilated, damaged tubules)
ATN Causes

Hypotension
 Relative low BP
 May occur immediately
after low BP episode or up to
7 days later
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Post-op Ischemia
Post-aortic clamping, post-CABG
Crystal precipitation
Myoglobinuria
Contrast Dye
 ARF usually 1-2 days after IV contrast load
Aminoglycosides
ATN Treatment

Remove any offending agent
 IVF
 Try
Lasix if a euvolemic patient is not having
adequate urine output
 Dialysis

Most patients return to baseline Serum Cr
in 7 to 21 days
ATN
Cr
Prerenal
increases at increases
0.3-0.5 /day slower than
0.3 /day
U Na,
UNa>40
UNa<20
FeNa
FeNa >2%
FeNa<1%
UA
epithelial
Normal
cells,
granular
casts
Response Cr will not
Cr
to volume improve
improves
much
with IVF
Which UA is most compatible
with contrast-induced ATN?
A.
B.
C.
D.
Spec gravity 1.012, 20-30 RBC, 15-20 WBC,
positive for eosinophils
Spec gravity 1.010, 1-3 WBC, 5-10 renal
tubular cells, many granular casts, occasional
renal tubular cell casts, no eosinophils
Spec gravity 1.012, 5-10 RBC, 25-50 WBC,
many bacteria, occasional fine granular casts,
no eosinophils
Spec gravity 1.020, 10-20 RBC, 2-4 WBC, 1-3
RBC casts, no eosinophils
ATN
B. Spec gravity 1.010, 1-3 WBC, 5-10
renal tubular cells, many granular
casts, occasional renal tubular cell
casts, no eosinophils
 Dilute urine: failure to concentrate urine
 No RBC casts or WBC casts in ATN
 Eosinophils classically in AIN or renal
atheroemboli, but nonspecific
WBC Casts
Cells in the cast have
nuclei
(unlike RBC casts)
Pathognomonic for
Acute Interstitial
Nephritis
Acute Interstitial Nephritis
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70% Drug hypersensitivity
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15% Infection
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30% Antibiotics: PCN, Cephalosporins, Cipro
Sulfa drugs
NSAIDs
Allopurinol
Strep, Legionella, CMV
8% Idiopathic
6% Autoimmune Diseases

Sarcoid, Tubulointerstitial nephritis
AIN from Drugs
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Renal damage is NOT dose-dependent
May take weeks after initial exposure to drug
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Signs and Symtpoms
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Up to 18 months to get AIN from NSAIDS
But only 3-5 days to develop AIN after second exposure to drug
Fever (27%)
Serum Eosinophilia (23%)
Maculopapular rash (15%)
Labs
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Bland sediment or WBCs, RBCs, non-nephrotic proteinuria
WBC Casts are pathognomonic
Urine eosinophils on Wright’s or Hansel’s Stain
Also see urine eosinophils in RPGN and renal atheroemboli
AIN Management
Remove offending agent
 Most patients recover full kidney function
in 1 year
 Poor prognostic factors

 ARF
> 3 weeks
 Advanced age at onset
You evaluate a 32yo woman with HTN, oliguria,
and rapidly increasing Cr, BUN. You spin her
urine:
A.
B.
C.
D.
ATN
Acute
glomerulonephritis
Acute interstitial
nephritis
Nephrotic
Syndrome
Acute Glomerulonephritis
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RBC casts: cells have no nuclei
Casts in urine: think INTRINSIC renal disease
If she has Lupus with recent viral prodrome,
think Rapidly Progressive Glomerulonephritis
(RPGN)
If she had a sore throat 10 days ago, think
Postinfectious Proliferative Glomerulonephritis
Glomerular Disease
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Hematuria: dysmorphic RBCs
RBC casts
Lipiduria: increased glomerular
permeability
Proteinuria: may be in nephrotic range
Fever, rash, arthralgias, pulmonary
symptoms
Elevated ESR, low complement levels
Rapidly Progressive Glomerulonephritis
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Type 1: Anti-GBM disease
Type 2: Immune complex
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Type 3: Pauci-immune
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Necrotizing glomerulonephritis
Often ANCA-positive and associated with vasculitis
Can present with viral-like prodrome
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IgA nephropathy
Postinfectious glomerulonephritis
Lupus nephritis
Mixed cryoglobulinemia
Myalgias, arthralgias, back pain, fever, malaise
Kidney biopsy : Extensive cellular crescents with or without immune
complexes
Can develop ESRD in days to weeks
Treat with glucocorticoids and cyclophosphamide
Postinfectious Proliferative
Glomerulonephritis

Usually after strep infection of upper respiratory
tract or skin after a 8-14 day latent period
 Can
also occur in subacute bacterial endocarditis,
visceral abscesses, osteomyelitis, bacterial sepsis
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Hematuria, hypertension, edema, proteinuria
Positive antistreptolysin O titer (90% upper
respiratory and 50% skin)
Treatment is supportive
 Screen
family members with throat culture and treat
with antibiotics if necessary
A 19yo woman with Breast Cancer s/p
chemo in the ER has weakness, fever, rash.
WBC=15.4, Hct 24, Cr 2.9, LDH 600, CK
600. UA=3+ protein, 3+blood, 20 RBC.
What next test do you order? What’s her
likely diagnosis?
A.
B.
C.
D.
E.
Nephrotic
Syndrome
ATN
Acute
Glomerulonephritis
Thrombotic
Thromboctyopenic
Purpura
Rhabdomyolysis
TTP
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Order blood smear to rule out TTP
TTP associated with malignancy and
chemotherapy
TTP may mimic Glomerulonephritis on UA
(RBCs, WBCs)
Thrombocytopenia and anemia not consistent
with nephrotic or nephritic syndrome
Need CK in the thousands to cause ARF
Microvascular ARF
TTP/HUS
 HELLP syndrome
 Platelets form thrombi and deposit in
kidneys leading to glomerular capillary
occlusion or thrombosis
 Plasma exchange, steroids, IVIG, and
splenectomy are possible treatments

Macrovascular ARF
Aortic Aneurysm
 Renal artery dissection or thrombosis
 Renal vein thrombus
 Atheroembolic disease

 New
onset or accelerated HTN?
 Abdominal bruits, reduced femoral pulses?
 Vascular disease?
 Embolic source?
Your 68yo male inpatient with baseline
Cr=1.2 had negative cardiac cath 4 days
ago, now Cr=1.8 and blanching rash.
Renal Artery
Stenosis
B. Contrast-Induced
Nephropathy
C. Abdominal Aortic
Aneurysm
D. Cholesterol
Atheroemboli
A.
Why do his toes look like this?
Renal Atheroembolic Disease
1% of cardiac caths can cause atheromatous debris
scraped from the aortic wall will embolize
 Retinal
 Cerebral
 Skin (Livedo Reticularis, Purple toes)
 Renal (ARF)
 Gut (Mesenteric ischemia)
 Unlike in Contrast-Induced Nephropathy, Serum Cr will
NOT improve with IVF
 Diagnosis of exclusion: will NOT show up on MRI or
Renal U/S; WILL show up on renal biopsy
 Treatment is supportive
Post-Renal ARF
• Urethral obstruction: prostate or urethral
stricture
• Bladder calculi or neoplasm
• Pelvic or retroperitoneal neoplams
• Bilateral ureteral obstruction
• Retroperitoneal fibrosis
“Doc, your patient has not peed
in 5 hrs....what do you want to
do?”
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Examine patient: Dry? Septic?
Flush foley: sediment can obstruct outflow
Check I/Os: Has she been drinking?
Give IV BOLUS (250-500cc IVF), see if patient
has urine output in next 30-60 min
 If
yes, then patient was dry
 If no, then patient is either REALLY dry or in renal
failure
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Check UA, Labs
Consider Renal U/S if reasonable
You are called to the ER to
see...
A 35yo woman with previously normal
renal function now with BUN=60, Cr=3.5.
Do you call the Renal fellow to dialyze this
pt?
 What if her K=5.9?
 What if her K=7.8?

Indications for acute dialysis
AEIOU
 Acidosis
(metabolic)
 Electrolytes (hyperkalemia)
 Ingestion of drugs/Ischemia
 Overload (fluid)
 Uremia
You admit this patient to telemetry and
aggressively hydrate her
 You recheck labs 6h later and BUN=85,
Cr=4.2. Suddenly the patient starts to
seize.
 Now what?
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Patient is Uremic
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General
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Mental status change
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Uremic encephalopathy
Seizures
Asterixis
GI disturbance
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Fatigue, weakness
Pruritis
Anorexia, early satiety, nausea and emesis
Uremic Pericarditis
Platlet dysfunction and bleeding
A patient with chronic lung disease has
acute pleuritic pain and O2 saturation of
87%. You want to rule out PE but her Cr
is 1.4. Can you get a CT with IV
contrast?
Send her for Stat CT with IV contrast
B. Send her for Stat CT without IV
contrast
C. Just give her heparin
D. Begin IV hydration
E. Begin pre-procedure Mannitol
F. Get a VQ scan instead
A.
Contrast-Induced Nephrotoxicity
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Cr increases by 25% post-procedure
Contrast causes renal vasoconstriction
leading to renal hypoxia
Iodine itself may be nephrotoxic
If Cr>1.4, use pre-procedure prophylaxis
Pre-Procedure Prophylaxis
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IVF 0.9NS
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Mucomyst (N-acetylcysteine)
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1-1.5 mg/kg/hour x 12 hours prior to procedure and 612 hours after
Free radical scavenger; prevents oxidative tissue
damage
600mg po BID x 4 doses (2 before procedure, 2 after)
Bicarbonate (JAMA 2004)
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Alkalinizing urine should reduce renal medullary damage
D5W with 3 amps HCO3; bolus 3.5 mL/kg 1 hour
preprocedure, then 1mL/kg/hour for 6 hours
postprocedure
Small study and not reduplicated in larger trial
thereafter
Chronic Renal Failure

Definitions
•
•
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Chronic Renal Failure (CRF) - irreversible kidney
dysfunction with azotemia >3 months
Creatinine Clearance (CCr) - the rate of filtration of
creatinine by the kidney (GFR marker)
Glomerular Filtration Rate (GFR) - the total rate of
filtration of blood by the kidney
Etiology

Episodes of ARF (usually acute tubular
necrosis) often lead, eventually, to CRF
•
Over time, combinations of acute renal
insults are additive and lead to CRF
• The definition of CRF requires that at least
3 months of renal failure have occurred

Causes of Acute Renal Failure (ARF)
•
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Prerenal azotemia - renal hypoperfusion, usually with
acute tubular necrosis
Intrinsic Renal Disease, usually glomerular disease
Postrenal azotemia - obstruction of some type
Common Underlying Causes of
CRF
Causes of CRF
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There are about 50,000 cases of ESRD per year
Diabetes: most common cause ESRD
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Over 30% cases ESRD are primarily to diabetes
CRF associated HTN causes about 23% ESRD cases
Glomerulonephritis accounts for ~10% cases
Polycystic Kidney Disease - about 5% of cases
Rapidly progressive glomerulonephritis (vasculitis) - about 2%
of cases
Renal (glomerular) deposition diseases
Renal Vascular Disease - renal artery stenosis, atherosclerotic
vs. fibromuscular
Causes of CRF
Additional Causes of CRF

•
•
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Medications - especially causing
tubulointerstitial diseases (common ARF,
rare CRF)
Analgesic Nephropathy over many years
Pregnancy - high incidence of increased
creatinine and HTN during pregnancy in
CRF
Analgesic Nephropathy
Analgesic Nephropathy

•
•
•
•
•
•
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Slow progression of disease due to chronic daily
ingestion of analgesics
Drugs associated with this entity usually contain two
antipyretic agents and either caffeine or codeine
More common in Europe and Australia than USA
Polyuria is most common earliest symptom
Macroscopic hematuria and papillary necrosis
Chronic interstitial nephritis, renal papillary necrosis,
renal calcifications
Associated with long-term use of non-steroid antiinflammatory drugs
Analgesic Nephropathy
Patients at risk include DM, CHF, Hepatic
disease, and the elderly
 Pathophysiology: nonselective NSAIDS
inhibit synthesis vasodilatory prostaglandin
in the kidney inducing a prerenal state
ARF

Electrolyte Abnormalities

Excretion of sodium is initially increased,
probably due to natriuretic factors
•
•
•
•
•
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As glomerular filtration rate (GFR) falls, FeNa rises
Maintain urine volume until GFR <10-20mL/min and
then edema begins
Cannot conserve sodium when GFR <25mL/min,
and FeNa rises with falling GFR
Tubular potassium secretion is decreased
Cannot handle bolus potassium
Do not use potassium sparing diuretics
Acid Base Balance
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Normally, produce ~1mEq/kg/day of Hydrogen ions
When GFR <40mL/min, there is a decrease in NH4
excretion which adds to metabolic acidosis
When GFR <30mL/min, then urinary phosphate
buffers decline and acidosis worsens
Bone CaCO3 begins to act as the buffer and bone
lesions result (renal osteodystrophy)
Usually will not have wide anion gap acidosis if patient
can still make urine
Defect in renal generation of HCO3 as well as
retention of nonvolatile acids
Bone Metabolism
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Low GFR leads to increased phosphate, low calcium, and an
acidosis
Other defects include decreased dihydroxy-vitamin D
production
Bone acts as a buffer for acidosis, leading to chronic bone
loss in renal failure
Low vitamin D causes poor calcium absorption and
secondary hyperparathyroidism
Increased PTH maintains normal serum Calcium and
Phosphorus until GFR <30mL/min
Chronic hyperparathyroidism and bone buffering of acids
leads to severe osteoporosis
Other Abnormalities
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Slight hypermagnesemia with inability to
excrete high magnesium loads
Uric acid retention occurs with GFR
<40mL/min
Vitamin D conversion to dihydroxy-Vitamin
D is severely decreased
Erythropoietin (EPO) levels fall and anemia
develops
Accumulation of normally excreted
substances
Complications

Immunosuppression
•
•
•
•
•
Patients with CRF are at increased risk for
infection
Cell mediated immunity is particularly impaired
Hemodialysis seems to increase immune
compromise
Complement system is activated during
hemodialysis
Patients with CRF should be vaccinated
aggressively
Anemia



Due to reduced erythropoietin production
by kidney
Occurs when creatinine rises to >2.53mg/dL
Anemia management with Procrit and
Arensp
Phosphorus
Hyperphosphatemia

•
•
•
•
•
Decreased excretion by kidney
Increased phosphate load from bone metabolism
Increased PTH levels leads to renal bone disease
Eventually, parathyroid gland hyperplasia occurs
Danger of calciphylaxis
Treatment
PREVENTION
Treat the underlying cause
Chronic Hemodialysis Medications
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•
•
•
•
•
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Anti-hypertensives - Labetolol, CCB, ACE inhibitors
Eythropoietin (Epogen®) for anemia in ~80% dialysis pts
Vitamin D Analogs - calcitriol given intravenously
Calcium carbonate
RenaGel, a non-adsorbed phosphate binder
DDAVP may be effective for patients with symptomatic platelet
problems