Download Resident - UNM Hospitalist Wiki

Resident Version
Acute Renal Failure Module
created by Dr. Chris Delong
Objectives:
By the end of this module, you should be able to:
1. Define acute renal failure (ARF)
2. Identify the main types of acute renal failure by whether they are prerenal,
intrinsic renal (and subtypes) or postrenal.
3. Identify the typical laboratory tests used in working up renal failure and
explain their utility.
4. Understand the Fractional Excretion of Sodium (FENa) equation and its
utility in differentiating causes of ARF.
5. Understand the utility of urine microscopy in differentiating types of acute
renal failure.
References:
1) Singri N, Ahya S, Levin M. Acute Renal Failure. JAMA, February 12, 2003;
289: 747-51.
2) Lameire N, Van Biesen W, Vanholder R. Acute Renal Failure. Lancet 2005;365:
417-30.
Discussion Outline
FIRST STEP: Understanding the definition and types of renal failure
Acute renal failure is generally defined as an increase in serum creatinine of 0.5 mg/dL
over 2 weeks or less when the baseline creatinine is less than 2.5. If the baseline
creatinine is more than 2.5, it is defined as an increase of more than 20% over 2 weeks or
less.
A general understanding of what can cause renal failure will assist you in clinical
evaluation. What follows is a modified figure from the referenced Lancet article entitled
“Acute Renal Failure” that concisely categorizes the major types of renal failure with
their causes.
- The most common causes of acute renal failure are acute tubular necrosis and prerenal
azotemia.
SECOND STEP: History and examination
A thorough history and examination are essential in the assessment of acute renal failure.
A modification of Table 2 from the referenced JAMA article on Acute Renal Failure
follows:
Type of
Renal
Failure
Prerenal
History questions
Medications
Physical Exam
Vomiting
Diarrhea
Bleeding
Fevers
Recent operation
(hypotension) Heart or liver
disease
Diuretics
Chemotherapy
Intrarenal
Pharyngitis or other URI
Sinusitis (Wegner’s)
Hemoptysis (Wegner’s,
Goodpasture’s)
Muscle trauma
Urine color
Decreased Urinary stream
Nocturia
Anuria
Increased frequency
Flank pain
Nephrotoxic
(NSAIDS, etc)
Orthostatic
hypotension
Skin Turgor
Buccal mucosa
Edema
CHF findings
Signs of chronic liver
disease
Edema
Livedo Reticularis
Petechiae
Palpable purpura
Muscle tenderness
Postrenal
IV contrast
exposure
Diphenhydramine
Anticholinergics
Bladder distension
Prostate enlargement
Abdominal or pelvic
mass
THIRD STEP: Imaging and Laboratory studies
Imaging studies:
- A renal ultrasound is an extremely useful diagnostic tool to evaluate patients with
ARF
o Identifies obstruction if present
o Size and echogenicity of kidneys
Laboratory tests: An initial assessment of renal function is an appropriate first step
- Renal function evaluation
o Serum Creatinine
 BUN/Creatinine ratio: If >15-20:1 ratio, it is suggestive of kidney
hypoperfusion
 Keep in mind that patients with cirrhosis, low muscle mass
may not have this finding in the setting of kidney
hypoperfusion
o Additional estimation of glomerular filtration rate (GFR), however these
are more useful in patients with stable renal function
 Cockcroft-Gault equation, Modification of Diet in Renal Disease
(MDRD)
- Urine studies
o Volume
 Oliguria <400 mL/day
 Anuria <100 mL/day
o Urinalysis and culture
 Urinalysis specifics
 Specific gravity (if high, consistent with prerenal etiology)
 If infection may be underlying etiology (LCE, Nitrites)
 Presence of blood (multiple etiologies including intrinsic
renal and postrenal)
 Elevated protein levels:
o If present, obtain 24-hour urine protein to evaluate
quantity
o Urine Sodium and Creatinine
 To assist in evaluation of Fractional Excretion of Sodium (FENa)
 Equation: FENa percent = (Urine Na x Plasma Cr)
x 100
(Plasma Na x Urine Cr)
 What is the utility of calculating the FENa?
o Helps to distinguish prerenal (<1%) from renal
etiology (>2%)
 However a low FENa can also be seen in
acute glomerulonephritis, vasculitis and
obstruction
o Urine Microscopy: Specific findings are helpful in establishing diagnosis






Eosinophils: May be suggestive of Acute Interstitial Nephritis
(AIN); Though sensitivity and specificity of this finding for AIN
are low.
Red blood cell casts: Consistent with glomerular pathology,
nephritic syndrome
Dysmorphic red blood cells: Typically present with glomerular,
nephritic diseases
Granular Casts: observed in numerous disorders, represent
degenerating cellular casts or aggregated proteins; may be part of
an “active sediment” or a non-specific finding
White blood cell casts: Typically present AIN, Pyelonephritis, or a
nephritic syndrome
Muddy brown casts: Typically present with Acute Tubular
Necrosis
Table of Urinalysis and Chemistry findings in different types of renal failure
Urine Test
Prerenal
Acute
Tubular
Necrosis
Muddy
Brown
Casts
Glomerulonephritis Obstruction
>30
Acute
Interstitial
Nephritis
White blood
cells,
eosinophils,
cellular casts
Minimal,
may be
increased
with
NSAIDs
>30
Sediment
Bland
Protein
None or
low
None or
low
Urine
Sodium in
mEq/L
FENa in
percent
<20
<1
>1
Variable
<1
Dysmorphic red
blood cells, red
blood cell casts
Bland or red
blood cells
Increased, >100
mg/dL
Low
<20
Acute <20
After days
>40
Acute <1
After days >1
Adapted from cited JAMA article entitled “Acute Renal Failure”
FOURTH STEP: Additional tests, indications and their meaning
In what circumstances are more tests indicated?
- Typically if there is an “active sediment,” meaning dysmorphic red blood cells or
red blood cell casts, additional tests are indicated to determine the underlying
etiology as treatments differ based on the diagnosis
- Nephritic syndromes: Tests to obtain
o Complements: If low, consistent with lupus, immune complex disease
o Anti-GMB antibody: If positive, consistent with diagnosis of
Goodpasture’s syndrome
o ANCA
 C-ANCA/PR3: If positive, consistent with diagnosis of Wegner’s
 P-ANCA/MPO: If positive, consistent with Microscopic
Polyangitis
 P-ANCA (non-MPO/PR3): Polyarteritis Nodosa
o Biopsy: Indicated in following cases
 Isolated glomerular hematuria with proteinuria
 Nephrotic syndrome
 Acute nephritic syndrome
 Unexplained acute or subacute renal failure
FIFTH STEP: Treatment
- The treatment of renal failure will depend on many variables, among which are the
etiology and severity of the condition.
If the etiology is prerenal, establishing effective renal perfusion is a reasonable first
approach.
- however, this can be very difficult to do in patients with underlying heart or liver
dysfunction
- If the etiology is determined to be autoimmune, immunosuppression will likely be
indicated.
- If the etiology is infectious, antibiotics should be initiated.
If postrenal, correction of obstruction should be the primary initial therapeutic goal.
In all cases, following daily fluid input and output is essential.
In addition, searching for and treating acute complications, specifically electrolyte
abnormalities (Sodium, potassium, acidosis, hyperphosphatemia) is an important aspect
to managing ARF.
- Avoiding nephrotoxic agents such as NSAIDs, IV contrast and certain antibiotics is
indicated in patients with ARF. Also, adjust renally-cleared medications based on the
patient’s GFR.
- Dialysis may be necessary, particularly in cases where patient’s renal function
deteriorates.
- indications for acute dialysis include
o Severe acidosis not responsive to other treatment
o Severe electrolyte abnormalities, particularly elevated potassium with
cardiac conduction effects
o Severe fluid overload unresponsive to diuresis
o Uremia with end-organ effects such as pericardial rubs
Case:
HPI: A 52 year old man presents to you in clinic complaining of “red urine” for the past
week. He has never had this problem before. He has not noted any changes in his
urinary frequency and reports no difficulty with starting a urine stream or incomplete
evacuation. He also states that he recently had a runny nose, sore throat and cough which
resolved about 3 weeks ago. He did not take any antibiotics for this illness. On further
review of systems he reports progressive shortness of breath over the past 6 months
primarily with exertion. He denies any chest pain, rashes, swelling of his extremities or
neurological symptoms.
PMH:
1. Hepatitis C confirmed by PCR, for which patient has not received treatment
2. Hypertension
3. Chronic allergies with sinusitis
4. Osteoarthritis
Medications:
1) Ibuprofen as needed for osteoarthritis pain (approximately 800-1600 mg daily
2) Hydrochlorothiazide 25 mg daily
3) Fluticasone nasal spray, 2 sprays in each nostril daily
FH: Father with MI at age 45, Mother with numerous blood clots and miscarriages
SH: Pt quit smoking 10 years ago, drinks alcohol occasionally and stopped using IV
drugs approximately 10 years ago
PE:
VS: Temperature 36.9 C BP 140/85 HR 95 RR 16 O2 91% on room air
HEENT: Pupils equally round, reactive to light; mucous membranes moist; no nasal
abnormalities; bilateral maxillary sinus tenderness present; no lymphadenopathy or
thyromegaly
Lungs: Bilateral fine crackles throughout both lung fields
CV: Regular rate and rhythm, no m/g/r
Abd: Normal bowel sounds, no tenderness to palpation, no notable bladder distension
Rectal: Normal rectal tone with normally sized prostate, no nodules; guaiac negative
stool
Neuro: Non-focal
Extremities: No cyanosis, edema or clubbing
Labs:
CBC: WBC 9.0 (70% PMNs, 20% Lymphocytes, 7% Monos, 2% Eosinophils), HCT 42,
PLT 200
Chemistries: Sodium 135, Potassium 4.6, Chloride 105, Bicarbonate 18, BUN 20,
Creatinine 2.5 (baseline 1.2), Glucose 96, Calcium 8.2, Phosphorus 3.2, Magnesium 2.5
LFTs: Significant for an AST of 90, ALT 100
Coags: Normal
UA: Specific gravity 1.010 (normal), positive leukocyte esterase, negative nitrites, 3+
RBCs, 2+ protein
Urine microscopy: RBC and WBC casts, dysmorphic RBCs ; no crystals
Imaging:
CXR: Bilateral interstitial abnormalities
Kidney Ultrasound: no hydronephrosis or stranding, kidneys are normal in size and
echogenicity
Case Questions:
1. What is the etiology of this patient’s renal failure: Prerenal, Intrinsic Renal or
Postrenal?
2. What is on your differential?
3. Which additional lab studies would you perform?
4. How does this test change your differential diagnosis?
5. What further tests would you perform to narrow your diagnosis?
6. Now what is your most likely diagnosis?
7. How would you typically confirm this diagnosis prior to instituting therapy?
Review Questions
1. An otherwise healthy 54-year-old man presents to your office with the complaints of
joint pain and swelling of his legs for one week. On exam, his blood pressure is elevated
to 165/95. Other significant findings include bibasilar pulmonary crackles and 2+
bilateral lower extremity edema. You order a urine microscopy in which you find
dysmorphic red blood cells, red blood cell casts and white blood cell casts. You suspect a
rapidly progressive glomerulonephritis and order complement levels.
If they are low, which etiology is least likely?
A. Glomerulonephritis related to SLE
B. Wegener’s granulomatosis
C. Post-infectious glomerulonephropathy
D. Glomerulonephritis related to Hepatitis C (mixed essential cryoglobulinemia)
2. You are called to evaluate a 42 year-old man in the Intensive Care Unit for evaluation
of acute renal failure. The patient was admitted 4 days previously for multilobar
pneumonia that was severe enough to require intubation. In reviewing his records, you
see that he was hypotensive to 85/45 on the day of admission, which improved to 105/52
with fluid boluses and pressor therapy. Upon evaluation, the patient is intubated and
unable to answer questions. His most recent blood pressure is 140/90, with a heart rate of
90, oxygen saturation of 93% on his current ventilator settings and he has been afebrile
for the past 48 hours. His last chemistry panel shows a Sodium on 140, potassium on 5.2,
BUN of 30 and creatinine of 2.5 (baseline on admission was 1.3).
Which of the following results of urinalysis would be consistent with his clinical history?
A. Moderate number of hyaline and granular casts
B. Presence of moderate protein, dysmorphic red blood cells and red blood cell casts
C. Dirty brown granular casts with granular epithelial cells
D. Large amount of white blood cells with bacteria
3. A 48-year-old man is brought into the emergency department by his wife. She states
that he began complaining of arthralgias and fevers about 2 weeks ago, which he
attributed to the “flu.” Within the past 2 days the patient has become confused and has
developed a rash and swelling in his legs. On physical exam, his Temperature is 37.0,
Heart Rate is 89, and Blood pressure is 160/90. He is oriented to time but not to place.
His exam reveals palpable purpuric lesions on his bilateral lower extremities with trace
edema. Labs reveal an elevated white blood cell count to 19,000 with Neutrophil
predominance, a hematocrit of 33 and platelets of 500. His BUN is elevated to 80 and his
creatinine is 3.8. You obtain further tests which show Red blood cell and white blood
cell casts in the urine with a moderate amount of protein. Complement levels are normal
and a p-ANCA is positive with antimyeloperoxidase specificity.
Which of the following conditions is most likely responsible for his condition?
A. Polyarteritis nodosa
B. Wegener granulomatosis
C. IgA Nephropathy
D. Henoch Schonlein Purpura
E. Microscopic Polyangiitis
4. A 40-year-old diabetic woman presents to your office with the complaint of “bloody
urine” that started 2 days after the onset of an upper respiratory infection, from which she
had symptoms of a sore throat, cough and nasal congestion. Her brother has a childhood
history of a similar condition after he had strep throat.
What is the most likely explanation for her hematuria?
A. Poststreptococcal glomerulonephritis
B. Polyarteritis nodosa
C. IgA Nephropathy
D. Glomerulosclerosis
Post Module Evaluation
Please place completed evaluation in an interdepartmental mail envelope and address to
Dr. Wendy Gerstein, Department of Medicine, VAMC (111).
1) Topic of module:__________________________
2) On a scale of 1-5, how effective was this module for learning this topic? _________
(1= not effective at all, 5 = extremely effective)
3) Were there any obvious errors, confusing data, or omissions? Please list/comment
below:
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
4) Was the attending involved in the teaching of this module? Yes/no (please circle).
5) Please provide any further comments/feedback about this module, or the inpatient
curriculum in general:
6) Please circle one:
Attending
Resident (R2/R3)
Intern
Medical student