Patient and Setting:

CM is a 35-year-old African-American man; emergency department Nausea/vomiting, seizure

Chief Complaint:

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 (CAMRSA) 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) N/A Mother: ESRD, DM; Father: died at age 45 due to MI Ethanol intake: Nil; tobacco: once/month 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 Morphine (tongue swelling, itching, rash, SOB)

Surgical History: Family History: Social History: Medications:


and Diagnostic Tests: Na 132 (132) HCO3 18 (18) Hct 0. HCO3 18 (18).011 pH: 8 Albumin: PROBLEM LIST Identify principal problems from the scenario in priority order (see Answers for correct list of problems).9 (97) Blood Cultures: negative Urine Output: 300 mL/24 hr Urinalysis: WBC: 2+ Protein: 3+ 2+ Color: cloudy LE: (−) Blood: large Eosinophils: 0% Na: 65 Osmolality: 300 mOsm/kg Urine Cast: coarse granular FENA 3% RBC: 4+ Nitrite: (−) Spec. nourished African-American man VS: BP 190/100.3°C.3 (40).3 (7. Wt 80 kg. pO2 12. and wheezing ABD: WNL GU: Deferred RECT: Deferred EXT: Bilateral LE swollen with fluid.9 (5. T 37. pCO2 5. HR 83. rales.39 (39) Plts 250 × 109 (250 × 103) K 5.1) A1c 5% 9 3 Lkcs 10 × 10 (10 × 10 ) Eosinophils 1% Blood Gas: pH 7. Gravity: 1. Ht 182 cm HEENT: WNL COR: RRR CHEST: Small crackles. Serum Drug Concentrations.9) BUN 54 (150) Hgb 140 (14) Glucose 7 (126) Cl 100 (100) SCr 442 (5) Alb 31 (3. SOAP NOTE To be completed by student (see Answers for correct SOAP Note) .3).Physical Examination: GEN: Well-developed. 3+ pitting edema NEURO: A & O × 2 (place. time) Results of Pertinent Laboratory Tests. RR 26.

Discuss the limitations in using the Cockcroft-Gault method to assess kidney function in patients with ARF. 5. List the physical assessment and laboratory findings in CM consistent with acute renal failure. 2. 3. which of the following agents should not be recommended? A) Fenoldopam B) Normal saline solutions C) Sodium bicarbonate solutions D) N-acetylcysteine . 10. 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. 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. What are potential therapies for CM’s hyperkalemia? 11. Identify agents in CM’s medication profile with the potential to cause acute renal failure and describe the mechanism for kidney damage. and duration of therapy. Describe pharmacologic and nonpharmacologic treatment options for acute renal failure in CM including dosing regimens. dosing interval. or postrenal and justify your answer. 4. Classify CM’s acute renal failure as prerenal. List signs and symptoms of acute renal failure. Interpret the clinical significance of a (+) urine eosinophilia? 12. route. Based on the available data on prevention of contrast-induced nephropathy.CASE QUESTIONS 1. 7. Justify your choice. If oral furosemide is used. intrinsic. Identify the goals of therapy for treatment of acute renal failure in CM. 6.

13. . Summarize therapeutic. pathophysiologic. and disease management concepts for acute renal failure using a key points format. What is the mostly likely cause of CM’s recent seizure? 14.

Seizure 7. Cellulitis SOAP Note S: “I can’t pee. Acute renal failure 2.3).Model Answer Problem List 1.3 (7. K 5. and when I do. decreased urine output with dingy colored urine. my urine is a very dusty looking color. Hypervolemia 6. crackles and rales on chest exam Laboratory: BP 190/100. My ankles and legs are swollen. Hyperkalemia 3. and I have a lower back pain.” O: Lower back flank pain. RBC 4+. Metabolic Acidosis 5. BUN 54 (150). My sister told me I had a seizure. Na 65. HCO3 18 (18) Urine: WBC 2+. SCr 442 (5) pH 7. coarse granular casts . Hypertension 4.9.

and Septra. Repeat fluid boluses as patient can tolerate. consider RRT based on indications for dialysis. possibly drug-induced • Discontinue ACEI (lisinopril). Consider drawing blood cultures to evaluate for infectious etiology.A: Problem 1: Problem 2: Problem 3: Acute renal failure. and increase dose if no response after 1 hour. Sepsis is a known cause of acute renal failure. Monitor vital signs every shift. Monitor blood chemistries daily. • Start furosemide 80 mg IV over 30 minutes if no response to fluid challenge. if still no response after 2 hours. possibly drug-induced Hyperkalemia due to acute renal failure Hypertension secondary to acute renal failure and fluid accumulation Problem 4: Problem 5: Problem 6: Problem 7: Metabolic acidosis due to acute renal failure Hypervolemia due to acute renal failure Seizure secondary to uremia Completion of therapy for CA-MRSA P: Problem 1: Acute renal failure. • • • • Monitor urine output hourly. if no response. diuretic (HCTZ). NSAID (ibuprofen). . which are all potential drug-induced causes of acute renal failure. consider adding thiazide diuretic (metolazone). • Start a 500–1000 mL NS bolus.

pending susceptibilities) because Septra can cause hyperkalemia. • Monitor for end-organ damage from increased blood pressure. • • Monitor serum potassium daily.Problem 2: Acute renal failure–induced hyperkalemia • Address underlying causes of acute renal failure (decreased renal perfusion. drug induced). fluoroquinolone. • Monitor blood pressure hourly for reduction in blood pressure and prevention of hypotension. drug induced). Consider starting alternative antibiotic for treating CA-MRSA (clindamycin. 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. • If blood pressure does not decrease with fluid removal. • Monitor EKG readings for hyperkalemia-induced dysrhythmia (peaked T waves). • The use of furosemide for fluid mobilization and renal perfusion may decrease blood pressure as a result of normalizing blood volume. . Problem 3: Hypertension secondary to acute renal failure and fluid accumulation • Address underlying causes of ARF (decreased renal perfusion.

• If acidosis is not corrected as renal function improves. consider the use of albumin to pull fluid from the interstitial space. edema). Problem 6: Seizure secondary to uremia • Address underlying causes of acute renal failure (decreased renal perfusion. goals. the bicarbonate in the dialysate solution will treat the metabolic acidosis. drug induced) to improve solute control and lower urea concentration. . • • • Monitor for improvement in breathing and edema. • If RRT is initiated. if indicated. Perform chest exam after fluid mobilization to assess lung function. Problem 4: Metabolic acidosis due to acute renal failure • Acidosis should correct with the improvements in renal function and fluid administration. • Monitor blood urea nitrogen levels. If fluid mobilization is not effective for edema. and blood pressure monitoring.• Educate patient on importance of blood pressure control. 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. consider treatment with sodium bicarbonate.

GFR. Agents in CM’s medication profile with the potential to cause ARF are as follows: a. Answers to Case Questions 1.. Problem 7: Completion of therapy for CA-MRSA • An alternative antibiotic to Septra should be chosen for the patient based on sensitivities. dehydration). (Septra is known to cause acute renal failure from crystal formation and can cause allergic interstitial nephritis.) • CM should receive the full course of treatment for CA-MRSA and be scheduled for follow-up to evaluate for resolution of infection. . • • Monitor CM for further seizure activity. although this was ruled out in CM. thus. If renal function does not improve and urea levels do not decrease. Lisinopril (ACEI): Decreases glomerular filtration (GFR) rate by preventing compensatory vasoconstriction of the efferent arteriole.g. consider initiation of RRT for fluid and solute control. an angiotensin-mediated mechanism beneficial in conditions of decreased renal perfusion (e.• Pharmacologic therapy with antiepileptic agents is not warranted at this time. Preventing constriction of the efferent arteriole in these conditions decreases intraglomerular pressure and.

classified as intrinsic renal failure. Note: If the effects of ACEIs and NSAIDs and concomitant causes of prerenal acute renal failure (e. Patients with a decrease in circulating volume (e. d. heart failure) and chronic kidney disease are a greater risk for this type of drug-induced effect. Hydrochlorothiazide (diuretics): Diuretics may lead to a decrease in circulating blood volume (and prerenal acute renal failure) if excessive diuresis occurs. c.g..b. conditions that decrease renal perfusion) are not reversed. Formation of crystals in the urine (from the sulfamethoxazole component) that may deposit in the tubules and cause intratubular obstruction.. These types of acute renal failure have . Overdiuresis is common in individuals with decreased fluid intake or excessive losses and in the elderly. Sulfamethoxazole-trimethoprim (Septra): May cause acute renal failure by two mechanisms. structural damage to the kidney or intrinsic renal failure may result from prolonged ischemia. a prostaglandin-mediated mechanism beneficial in conditions of decreased renal perfusion. ii.g. i. Can cause interstitial nephritis and tubular necrosis. dehydration. Ibuprofen (NSAID): Decreases glomerular perfusion by preventing the dilation of the afferent artery. This inhibition results in decreased blood flow to the glomerulus and a decrease in GFR.

in part. to hypersensitivity to the sulfamethoxazole component. 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. osmolality 300 mOsm/kg 4. (Note: Creatinine is primarily filtrated by the glomerulus. bleeding. Community patients that develop acute renal failure can present with decreased urine output. as much as 10% is secreted by the tubules. WBC 2+. rales and crackles on lung exam. The trimethoprim component of Septra inhibits the tubular secretion of creatinine. and cloudy or foamy urine. symptoms of uremia (confusion. leading to a small increase in serum creatinine. elevated BP 190/100 Laboratory tests: BUN 54 (150). K 5.g. Na 65. coarse granular casts. RBC 4+.9.. and decreased appetite). flank pain.been attributed. fatigue. however. edema. SCr 442 (5). nephrotoxins) Provide supportive measures until kidney function returns . weight gain. HCO3 18 (18) Urine: Proteinuria.) 2. without a true change in kidney function. Physical findings consistent with fluid overload: Edematous ankles and legs (3+ pitting edema). 3.

Furosemide 80 mg intravenous should be initiated.e. the thiazidelike diuretic that retains its effect at GFRs of less than 30 mL/min. specifically the ACEI (lisinopril). 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. the dose should be doubled. the NSAID (ibuprofen). Removing nephrotoxic drugs. if a loop diuretic alone does not increase urine output. Pharmacologic and nonpharmacologic treatment options include the following: • Acute renal failure is commonly caused by medications. and Septra is the first step to treating acute renal failure in CM. and the dose should be adjusted based on urine output. yet minimize the risk of worsening his volume status if urine output does not increase. dialysis) depending on the patient’s clinical status and indications for dialysis.5. therefore. Diuretic-resistant acute renal failure may need to be treated by renal replacement therapy (i. . If no increase in urine output is observed in an hour. CM has signs of fluid overload and oliguric acute renal failure (urine output < 400 mL/d). Consider adding metolazone.. • Fluid management is the mainstay of therapy in treating acute renal failure. • Initiation of a loop diuretic such as furosemide should be considered if CM fails to response to repeated fluid challenges.

This damage may or may not be reversible. urine + WBC and RBCs. B. The structural damage associated with intrinsic renal failure alters transport of solutes and water and urinary concentrating ability. use of this equation is most appropriate for patients with stable kidney function. they lead to intrinsic renal failure as a result of prolonged ischemic conditions. 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. Postrenal ARF is not likely in CM because he does not have evidence of obstruction. urine sodium >40. NSAIDs).g. Although prerenal causes are usually reversible. Other methods that account for changes in serum creatinine.. D. Decreased bioavailability of furosemide due to gastrointestinal edema 9. CM has evidence of intrinsic renal failure: presence of granular casts in the urine. ACEI. are more appropriate . For example. Ultrasound 8. but today is 5. Since CM’s kidney function may not be stable. if not addressed. however.6. This is not the case in acute renal failure since serum creatinine values fluctuate in this patient population. a FENA >1%. 7. CM’s serum creatinine could have been 3. The Cockcroft-Gault (CG) equation is commonly used for estimating kidney function in clinical practice. and urine osmolality <300 mOsm/kg.5 yesterday. the CG equation is not recommended to assess his kidney function. such as the Jelliffe equation.

and diuretics have been associated with allergic interstitial nephritis. . Septra.g.5. interstitial nephritis. 10. agents that can rapidly lower serum potassium concentrations or shift potassium intracellularly should be used (i. The absence of eosinophils in CM’s urine is a pertinent negative to help rule out allergic interstitial nephritis. Urine eosinophilia is commonly associated with a fever. 12. arthralgia.. Once CM’s acute renal failure resolves. Acute and severe elevations in serum urea nitrogen can have a neurotoxic effect.e. NSAIDs. A.. A urine eosinophilia of >5% would be significant for an acute allergic process. Neurotoxicities include: depression. it will assist in decreasing serum potassium. 11. and psychosis. risk of arrhythmias). along with the patient’s serum creatinine. A measured creatinine clearance may also be calculated using urine creatinine from a timed collection. Hyperkalemia is commonly associated with acute and chronic renal failure. 1 g IV calcium gluconate). A test that is positive for eosinophils in the urine is indicative of an allergic process in the kidney. Treatment of CM’s metabolic acidosis will also address hyperkalemia. kayexalate) in conjunction with a cardioprotective agent (e. If a loop diuretic such as furosemide is acute renal failure. insulin/glucose. Fenoldopam 13. seizure. the potassium will likely correct. and rash. If the potassium level is life threatening (>6.

14. • Potential nephrotoxic agents should be avoided and alternative agents should be used whenever possible. • RRT may be required to support the patient awaiting renal function recovery based on the indications for dialysis. If potential nephrotoxins must be administered. . however. • • Drug-induced causes of ARF should be evaluated in all cases of ARF. • Attempts to increase urine output may prevent complications of fluid overload and facilitate patient management. Key Points • Prevention is the best intervention for acute renal failure (ARF). a complete and regular review of drug therapy is necessary to make appropriate dose adjustments for drugs that are renally eliminated. Patients with nonoliguric ARF have a significantly lower mortality rate than anuric or oliguric patients. • Early recognition and management of prerenal ARF is important to prevent intrinsic renal failure. Conventional therapy offers little benefit to patients with established ARF. • The potential for drug removal during dialysis must be considered when designing drug regimens for patients with ARF. • In patients with ARF. consider hydration to improve renal perfusion and reduce tubular workload. conversion from anuria or oliguria to nonoliguria does not decrease mortality.

Sign up to vote on this title
UsefulNot useful