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ACUTE RENAL FAILURE CASE
Patient and Setting: CM is a 35-year-old African-American man; emergency
department
Chief Complaint: Nausea/vomiting, seizure
History of Present Illness: CM was discharged from the hospital 5 days earlier after a serious motor vehicle accident (MVA) that resulted in multiple injuries. During his 10-day hospitalization, a CT with contrast was performed to rule out intracranial bleeds (negative). He experienced an episode of rhabdomyolysis from bodily crush injuries and developed a community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) cellulitis; all illnesses were treated appropriately. Since discharge from the hospital, CM reports that his feet are swelling, (+) fatigue, (+) nausea and vomiting, and (+) SOB. He has also noticed a decrease in urine output, although he reports he has not been eating or drinking much at home. Today, CM experienced a seizure and was subsequently brought to the emergency department.
Medical History: Hypertension (× 5 yrs), MVA, cellulitis (CA-MRSA),
contrast-induced nephropathy during recent hospitalization (serum creatinine returned to baseline prior to discharge)
Surgical History: N/A
Family History: Mother: ESRD, DM; Father: died at age 45 due to MI Social History: Ethanol intake: Nil; tobacco: once/month Medications: Lisinopril 40 mg PO BID for 5 years (restarted prior to
discharge after being withheld for 1 week during previous hospitalization)
Hydrochlorothiazide 25 mg PO QD for 5 years Amlodipine 10 mg PO QD for 2 years Septra DS 2 tabs PO BID for cellulitis Ibuprofen 800 mg PO TID for back pain Centrum One 1 tab PO QD Allergies: Morphine (tongue swelling, itching, rash, SOB)
Physical Examination: GEN: Well-developed, nourished African-American man VS: BP 190/100, HR 83, RR 26, T 37.3°C, Wt 80 kg, Ht 182 cm HEENT: WNL COR: RRR CHEST: Small crackles, rales, and wheezing ABD: WNL GU: Deferred RECT: Deferred EXT: Bilateral LE swollen with fluid, 3+ pitting edema NEURO: A & O × 2 (place, time)
Results of Pertinent Laboratory Tests, Serum Drug Concentrations, and Diagnostic Tests: Na 132 (132) HCO3 18 (18) Hct 0.39 (39) Plts 250 × 109 (250 × 103) K 5.9 (5.9) BUN 54 (150) Hgb 140 (14) Glucose 7 (126) Cl 100 (100) SCr 442 (5) Alb 31 (3.1) A1c 5% Lkcs 10 × 109 (10 × 103) Eosinophils 1% Blood Gas: pH 7.3 (7.3); pCO2 5.3 (40); HCO3 18 (18); pO2 12.9 (97) Blood Cultures: negative Urine Output: 300 mL/24 hr Urinalysis: WBC: 2+ Protein: 3+ RBC: 4+ Albumin: 2+ Color: cloudy LE: (−) Nitrite: (−) Blood: large Eosinophils: 0% Spec. Gravity: 1.011 Na: 65 Osmolality: 300 mOsm/kg Urine Cast: coarse granular pH: 8 FENA 3% PROBLEM LIST Identify principal problems from the scenario in priority order (see Answers for correct list of problems). SOAP NOTE To be completed by student (see Answers for correct SOAP Note)
CASE QUESTIONS
1. Identify agents in CM’s medication profile with the potential to cause acute renal failure and describe the mechanism for kidney damage.
2. List signs and symptoms of acute renal failure. 3. List the physical assessment and laboratory findings in CM consistent with
acute renal failure.
4. Identify the goals of therapy for treatment of acute renal failure in CM.
5. Describe pharmacologic and nonpharmacologic treatment options for acute
renal failure in CM including dosing regimens, route, dosing interval, and duration of therapy. Justify your choice.
6. Classify CM’s acute renal failure as prerenal, intrinsic, or postrenal and justify
your answer.
7. Which of the following radiographic examinations would be beneficial in determining whether CM’s acute renal failure is due to obstruction?
A) Computed tomography (CT) B) Ultrasound C) Magnetic resonance imaging D) Positron emission tomography (PET) scan
8. If oral furosemide is used, what is one reason a high dose may be required to
overcome diuretic resistance? A) Decreased conversion of furosemide to its active metabolite B) Decreased efficacy due to inactivation of furosemide by uremic toxins C) Decreased efficacy from altered regulation of sodium-potassium ATPase pump D) Decreased bioavailability of furosemide due to gastrointestinal edema
9. Discuss the limitations in using the Cockcroft-Gault method to assess kidney
function in patients with ARF.
10. What are potential therapies for CM’s hyperkalemia?
11. Interpret the clinical significance of a (+) urine eosinophilia?
12. Based on the available data on prevention of contrast-induced nephropathy, which of the following agents should not be recommended?
A) Fenoldopam B) Normal saline solutions C) Sodium bicarbonate solutions D) N-acetylcysteine
13. What is the mostly likely cause of CM’s recent seizure? 14. Summarize therapeutic, pathophysiologic, and disease management concepts
for acute renal failure using a key points format.
Model Answer
Problem List
1. Acute renal failure
2. Hyperkalemia
3. Hypertension
4. Metabolic Acidosis
5. Hypervolemia
6. Seizure
7. Cellulitis
SOAP Note
S: “I can’t pee, and when I do, my urine is a very dusty looking color. My ankles
and legs are swollen, and I have a lower back pain. My sister told me I had a
seizure.”
O: Lower back flank pain, decreased urine output with dingy colored urine;
crackles and rales on chest exam
Laboratory:
BP 190/100, K 5.9, BUN 54 (150), SCr 442 (5)
pH 7.3 (7.3), HCO3 18 (18)
Urine: WBC 2+, RBC 4+, Na 65, coarse granular casts
A: Problem 1: Acute renal failure, possibly drug-induced
Problem 2: Hyperkalemia due to acute renal failure
Problem 3: Hypertension secondary to acute renal failure and fluid
accumulation
Problem 4: Metabolic acidosis due to acute renal failure
Problem 5: Hypervolemia due to acute renal failure
Problem 6: Seizure secondary to uremia
Problem 7: Completion of therapy for CA-MRSA
P: Problem 1: Acute renal failure, possibly drug-induced
• Discontinue ACEI (lisinopril), NSAID (ibuprofen), diuretic (HCTZ),
and Septra, which are all potential drug-induced causes of acute renal
failure.
• Start a 500–1000 mL NS bolus. Repeat fluid boluses as patient can
tolerate.
• Start furosemide 80 mg IV over 30 minutes if no response to fluid
challenge, and increase dose if no response after 1 hour; if still no
response after 2 hours, consider adding thiazide diuretic (metolazone);
if no response, consider RRT based on indications for dialysis.
• Monitor urine output hourly.
• Monitor vital signs every shift.
• Monitor blood chemistries daily.
• Sepsis is a known cause of acute renal failure. Consider drawing blood
cultures to evaluate for infectious etiology.
Problem 2: Acute renal failure–induced hyperkalemia
• Address underlying causes of acute renal failure (decreased renal
perfusion, drug induced).
• Monitor EKG readings for hyperkalemia-induced dysrhythmia (peaked
T waves).
• Monitor serum potassium daily.
• Consider starting alternative antibiotic for treating CA-MRSA
(clindamycin, fluoroquinolone, pending susceptibilities) because
Septra can cause hyperkalemia.
Problem 3: Hypertension secondary to acute renal failure and fluid
accumulation
• Address underlying causes of ARF (decreased renal perfusion, drug
induced).
• The use of furosemide for fluid mobilization and renal perfusion may
decrease blood pressure as a result of normalizing blood volume.
• If blood pressure does not decrease with fluid removal, consider
starting antihypertensive therapy for hypertensive emergency (labetalol
20 mg by slow injection over 2 minutes with repeat injections of 40 or
80 mg given at 10-minute intervals) until the desired blood pressure is
achieved.
• Monitor blood pressure hourly for reduction in blood pressure and
prevention of hypotension.
• Monitor for end-organ damage from increased blood pressure.
• Educate patient on importance of blood pressure control, goals, and
blood pressure monitoring.
Problem 4: Metabolic acidosis due to acute renal failure
• Acidosis should correct with the improvements in renal function and
fluid administration.
• If acidosis is not corrected as renal function improves, consider
treatment with sodium bicarbonate.
• If RRT is initiated, the bicarbonate in the dialysate solution will treat
the metabolic acidosis.
Problem 5: Hypervolemia due to acute renal failure
• The use of furosemide for fluid mobilization should improve CM’s
symptoms of fluid overload (shortness of breath, edema).
• Monitor for improvement in breathing and edema.
• Perform chest exam after fluid mobilization to assess lung function.
• If fluid mobilization is not effective for edema, consider the use of
albumin to pull fluid from the interstitial space, if indicated.
Problem 6: Seizure secondary to uremia
• Address underlying causes of acute renal failure (decreased renal
perfusion, drug induced) to improve solute control and lower urea
concentration.
• Monitor blood urea nitrogen levels.
• Pharmacologic therapy with antiepileptic agents is not warranted at
this time.
• Monitor CM for further seizure activity.
• If renal function does not improve and urea levels do not decrease,
consider initiation of RRT for fluid and solute control.
Problem 7: Completion of therapy for CA-MRSA
• An alternative antibiotic to Septra should be chosen for the patient
based on sensitivities. (Septra is known to cause acute renal failure
from crystal formation and can cause allergic interstitial nephritis,
although this was ruled out in CM.)
• CM should receive the full course of treatment for CA-MRSA and be
scheduled for follow-up to evaluate for resolution of infection.
Answers to Case Questions
1. Agents in CM’s medication profile with the potential to cause ARF are as
follows:
a. Lisinopril (ACEI): Decreases glomerular filtration (GFR) rate by
preventing compensatory vasoconstriction of the efferent arteriole, an
angiotensin-mediated mechanism beneficial in conditions of decreased
renal perfusion (e.g., dehydration). Preventing constriction of the
efferent arteriole in these conditions decreases intraglomerular pressure
and, thus, GFR.
b. Ibuprofen (NSAID): Decreases glomerular perfusion by preventing the
dilation of the afferent artery, a prostaglandin-mediated mechanism
beneficial in conditions of decreased renal perfusion. This inhibition
results in decreased blood flow to the glomerulus and a decrease in
GFR.
c. Hydrochlorothiazide (diuretics): Diuretics may lead to a decrease in
circulating blood volume (and prerenal acute renal failure) if excessive
diuresis occurs. Overdiuresis is common in individuals with decreased
fluid intake or excessive losses and in the elderly.
Note: If the effects of ACEIs and NSAIDs and concomitant causes of
prerenal acute renal failure (e.g., conditions that decrease renal
perfusion) are not reversed, structural damage to the kidney or intrinsic
renal failure may result from prolonged ischemia.
d. Sulfamethoxazole-trimethoprim (Septra): May cause acute renal failure
by two mechanisms.
i. Formation of crystals in the urine (from the sulfamethoxazole
component) that may deposit in the tubules and cause
intratubular obstruction. Patients with a decrease in circulating
volume (e.g., dehydration, heart failure) and chronic kidney
disease are a greater risk for this type of drug-induced effect.
ii. Can cause interstitial nephritis and tubular necrosis, classified
as intrinsic renal failure. These types of acute renal failure have
been attributed, in part, to hypersensitivity to the
sulfamethoxazole component. (Note: Creatinine is primarily
filtrated by the glomerulus; however, as much as 10% is
secreted by the tubules. The trimethoprim component of Septra
inhibits the tubular secretion of creatinine, leading to a small
increase in serum creatinine, without a true change in kidney
function.)
2. Community patients that develop acute renal failure can present with
decreased urine output, weight gain, flank pain, edema, symptoms of uremia
(confusion, fatigue, bleeding, and decreased appetite), and cloudy or foamy
urine.
3. Physical findings consistent with fluid overload: Edematous ankles and legs
(3+ pitting edema), rales and crackles on lung exam; elevated BP 190/100
Laboratory tests: BUN 54 (150), SCr 442 (5), K 5.9, HCO3 18 (18)
Urine: Proteinuria, Na 65, coarse granular casts, RBC 4+, WBC 2+, osmolality
300 mOsm/kg
4. Goals for therapy include:
• Address underlying cause of acute renal failure
• Correct fluid and electrolyte disturbances
• Slow or reverse kidney damage
• Avoid further insults that would delay recovery (e.g., nephrotoxins)
• Provide supportive measures until kidney function returns
5. Pharmacologic and nonpharmacologic treatment options include the
following:
• Acute renal failure is commonly caused by medications. Removing
nephrotoxic drugs, specifically the ACEI (lisinopril), the NSAID
(ibuprofen), and Septra is the first step to treating acute renal failure in
CM.
• Fluid management is the mainstay of therapy in treating acute renal
failure. CM has signs of fluid overload and oliguric acute renal failure
(urine output < 400 mL/d); therefore, a cautious fluid challenge
regimen of 500–1000 mL intravenous bolus of normal saline over 30
minutes to an hour may be attempted to provide adequate extracellular
volume and maintain renal perfusion, yet minimize the risk of
worsening his volume status if urine output does not increase.
• Initiation of a loop diuretic such as furosemide should be considered if
CM fails to response to repeated fluid challenges. Furosemide 80 mg
intravenous should be initiated, and the dose should be adjusted based
on urine output. If no increase in urine output is observed in an hour,
the dose should be doubled. Consider adding metolazone, the thiazide-
like diuretic that retains its effect at GFRs of less than 30 mL/min, if a
loop diuretic alone does not increase urine output. Diuretic-resistant
acute renal failure may need to be treated by renal replacement therapy
(i.e., dialysis) depending on the patient’s clinical status and indications
for dialysis.
6. CM’s acute renal failure likely began as prerenal as a result of his poor intake
of fluids (decreasing effective circulating volume) in conjunction with use of
agents that prevent autoregulation by the kidney to maintain adequate
intraglomerular pressure (e.g., ACEI, NSAIDs). Although prerenal causes are
usually reversible, if not addressed, they lead to intrinsic renal failure as a
result of prolonged ischemic conditions. The structural damage associated
with intrinsic renal failure alters transport of solutes and water and urinary
concentrating ability. This damage may or may not be reversible. CM has
evidence of intrinsic renal failure: presence of granular casts in the urine, a
FENA >1%, urine sodium >40, urine + WBC and RBCs, and urine osmolality
<300 mOsm/kg. Postrenal ARF is not likely in CM because he does not have
evidence of obstruction.
7. B. Ultrasound
8. D. Decreased bioavailability of furosemide due to gastrointestinal edema
9. The Cockcroft-Gault (CG) equation is commonly used for estimating kidney
function in clinical practice; however, use of this equation is most appropriate
for patients with stable kidney function. This is not the case in acute renal
failure since serum creatinine values fluctuate in this patient population. For
example, CM’s serum creatinine could have been 3.5 yesterday, but today is 5.
Since CM’s kidney function may not be stable, the CG equation is not
recommended to assess his kidney function. Other methods that account for
changes in serum creatinine, such as the Jelliffe equation, are more appropriate
in acute renal failure. A measured creatinine clearance may also be calculated
using urine creatinine from a timed collection, along with the patient’s serum
creatinine.
10. Hyperkalemia is commonly associated with acute and chronic renal failure.
Once CM’s acute renal failure resolves, the potassium will likely correct. If a
loop diuretic such as furosemide is administered, it will assist in decreasing
serum potassium. If the potassium level is life threatening (>6.5, risk of
arrhythmias), agents that can rapidly lower serum potassium concentrations or
shift potassium intracellularly should be used (i.e., insulin/glucose, kayexalate)
in conjunction with a cardioprotective agent (e.g., 1 g IV calcium gluconate).
Treatment of CM’s metabolic acidosis will also address hyperkalemia.
11. A test that is positive for eosinophils in the urine is indicative of an allergic
process in the kidney, interstitial nephritis. A urine eosinophilia of >5% would
be significant for an acute allergic process. Urine eosinophilia is commonly
associated with a fever, arthralgia, and rash. Septra, NSAIDs, and diuretics
have been associated with allergic interstitial nephritis. The absence of
eosinophils in CM’s urine is a pertinent negative to help rule out allergic
interstitial nephritis.
12. A. Fenoldopam
13. Acute and severe elevations in serum urea nitrogen can have a neurotoxic
effect. Neurotoxicities include: depression, seizure, and psychosis.
14. Key Points
• Prevention is the best intervention for acute renal failure (ARF).
Conventional therapy offers little benefit to patients with established
ARF.
• Early recognition and management of prerenal ARF is important to
prevent intrinsic renal failure.
• Drug-induced causes of ARF should be evaluated in all cases of ARF.
• Patients with nonoliguric ARF have a significantly lower mortality rate
than anuric or oliguric patients; however, conversion from anuria or
oliguria to nonoliguria does not decrease mortality.
• Attempts to increase urine output may prevent complications of fluid
overload and facilitate patient management.
• In patients with ARF, a complete and regular review of drug therapy is
necessary to make appropriate dose adjustments for drugs that are
renally eliminated.
• Potential nephrotoxic agents should be avoided and alternative agents
should be used whenever possible. If potential nephrotoxins must be
administered, consider hydration to improve renal perfusion and
reduce tubular workload.
• RRT may be required to support the patient awaiting renal function
recovery based on the indications for dialysis.
• The potential for drug removal during dialysis must be considered
when designing drug regimens for patients with ARF.