Drug-Induced Acute Kidney Injury: Assessment and Diagnosis

QUESTION

“My doctor wanted me to come into the hospital to be admitted.”

HPI

Wilbur Elliott is a 79-year-old man who originally presented to the hospital 1 month ago with

symptoms of heart failure that culminated in mitral valve replacement surgery. His surgery was

complicated by a 1-hour hypotensive episode, with BP of 70/50 mm Hg during surgery.

At three days post-op, purulent drainage was noted from the surgical site and he was subsequently

diagnosed with mediastinitis. At that time, he was also found to have Serratia bacteremia (blood

cultures × 4 positive for Serratia marcescens, sensitive to gentamicin, piperacillin, ceftazidime,

ceftriaxone, and ciprofloxacin; resistance was noted to ampicillin). Therapy was initiated with

gentamicin and ceftazidime.

Thus far, he has completed day 21 of a 6-week course of antibiotics. A gradual increase in his BUN

and serum creatinine concentrations from baseline were noted and signs of volume overload are

present.

PMHx

• Type 2 DM

• CKD

• Dyslipidemia

• Osteoarthritis

• HTN

• Heart failure

• Depression

PSHx

Mechanical mitral valve replacement surgery 28 days ago

CHP/LSN/DGS 1

Allergies

NKDA, NKFA

FamilyHx

Father had type 2 DM

SocHx

Lives at home with wife; has six children, all living out of state. Retired 11 years ago, coal miner.

Denied nicotine/ETOH/illicit substances.

ROS

Currently complains of trouble breathing, weakness, general malaise, and pain in right hand. No fever

or chills

Physical Examination

Constitutional

Confused-appearing man in mild distress

VS

BP 152/90 mm Hg, P 80 bpm, RR 26, T 37.7°C; current Wt 80 kg (admission Wt 75 kg), Ht 5′9′′

Skin

Turgor intact, surgical incision site healing with no drainage

3

HEENT

Head/face: normocephalic/atraumatic.

Eyes: eyebrows/lashes evenly distributed, no lesions noted, sclera white, conjunctiva pink, no

discharge noted, PERRLA present 4 mm to 3 mm, bilaterally, EOMs intact, fundoscopic exam without

arteriolar narrowing, nicking, hemorrhages, exudates or papilledema, bilaterally.

Sinus/nose: no palpable sinus tenderness, nares patent, no edema/discharge/polyps.

Ears: external ears skin intact, skin color similar to facial skin tone, no discharge noted from auditory

canal.

Oropharynx: tongue midline, pink, moist, no lesions noted ventral/dorsal surface, poor dentition

pharynx: uvula midline, tonsils +1, bilaterally, without erythema or exudates.

Neck: trachea midline, JVD, neck supple, mild tenderness with palpation over trapezius bilaterally,

thyroid not palpable, no lymphadenopathy, carotid pulses palpable +2, bilaterally, no carotid bruits

auscultated.

Lungs

Symmetrical rise/fall of thorax; no tenderness with palpation; increased tactile fremitus noted to bases,

bilaterally; inspiratory wheezes and bibasilar crackles noted.

Cardiac

S1, S2, irregular, no m/r/g

Abdomen

Rounded abdomen, no scars/lesions, non-distended, hypoactive BS x4 quadrants, no bruits

appreciated, general tympany with percussion, no organomegaly or masses

Genit/Rect

No stool noted. No masses noted.

MS/Ext

2+ ankle/sacral edema; some tenderness and limited motion in right hand.

Neuro

A & O to person and place, but not to time.

 

Labs

Na 139 mEq/L Hgb 9.7 g/dL Ca 8.6 mg/dL

K 3.7 mEq/L Hct 29.5% Mg 2.1 mg/dL

Cl 103 mEq/L Plt 303 × 103/mm3 Phos 4.4 mg/dL

CO2 24 mEq/L WBC 8.6 × 103/mm3 INR 2.7

BUN 50 mg/dL (BUN 19 mg/dL on admission)

SCr 3.2 mg/dL (SCr 1.5 mg/dL on admission)

Glu 119 mg/dL

UA

Color, yellow; character, hazy; glucose (-); ketones (-); SG 1.010; pH 5.0; protein 30 mg/dL; coarse

granular casts 5-10/lpf; WBC 0-3/hpf; RBC 0-2/hpf; no bacteria; nitrite (-); osmolality 325 mOsm;

urinary sodium 45 mEq/L; creatinine 33 mg/dL, FENA 3.1%.

Repeat Blood Cultures Today

Negative

Fluid Intake/Output and Daily Weights

Day I/O Weight (kg)

3 days ago 3200 mL/900 mL N/A

2 days ago 2600 mL/1000 mL 76

Yesterday 2800 mL/1300 mL N/A

Today N/A 80

ASSESSMENT AND DIAGNOSIS

1. Drug Induced Acute Kidney Injury

 

1. What are some initial differential diagnoses for the chief complaint? Support each response with

clinical reasoning & judgement.

2. What is the diagnosis? How is the patient’s presentation consistent with the diagnosis? Include,

objective & subjective findings (signs, symptoms, pertinent labs & diagnostic testing, when

applicable).

3. Explain the underlying pathophysiology for the diagnosis. Include etiology & risk factors in your

response.

4. Assess the severity of the condition. What are the potential complications & prognosis for the

diagnosis?

ANSWER

Drug-Induced Acute Kidney Injury: Assessment and Diagnosis

Introduction

Wilbur Elliott, a 79-year-old male, presents with symptoms of heart failure, mitral valve replacement surgery, and subsequent complications leading to drug-induced acute kidney injury (AKI). This essay will discuss the initial differential diagnoses, the confirmed diagnosis of drug-induced AKI, the underlying pathophysiology, and the severity, potential complications, and prognosis for the condition.

Initial Differential Diagnoses

Acute Decompensated Heart Failure (ADHF): ADHF could present with symptoms of trouble breathing, fluid overload, and altered mental status, similar to Wilbur’s presentation. However, Wilbur’s surgical history and blood work indicate other underlying issues.

Sepsis: Sepsis can manifest with systemic inflammation, hypotension, and organ dysfunction, including AKI. Although Wilbur had a post-operative infection, his stable vital signs and lack of fever suggest otherwise.

Acute Myocardial Infarction (AMI): AMI may cause hypotension, chest pain, and ST-segment changes on an ECG. However, the absence of chest pain and specific ECG findings does not align with this diagnosis.

Diagnosis of Drug-Induced Acute Kidney Injury

Wilbur’s presentation is consistent with drug-induced AKI due to his recent exposure to gentamicin and ceftazidime therapy for mediastinitis and Serratia bacteremia. The acute onset of increased serum creatinine and BUN levels, along with purulent drainage from the surgical site, raises suspicion for nephrotoxicity from the antibiotics.

Objective & Subjective Findings:
Increased serum creatinine (3.2 mg/dL) and BUN (50 mg/dL)
Decreased urine output
Ankle/sacral edema and bibasilar crackles on lung examination
Limited motion and tenderness in the right hand

Underlying Pathophysiology

The nephrotoxicity associated with aminoglycoside antibiotics like gentamicin is primarily mediated by oxidative stress, leading to renal tubular cell damage. Ceftazidime can also cause nephrotoxicity, albeit less frequently. The combination of these antibiotics may have contributed to the development of drug-induced AKI in Wilbur, especially given his pre-existing risk factors like age, previous heart failure, and kidney disease.

Severity, Potential Complications & Prognosis

Wilbur’s drug-induced AKI is considered severe due to the significant rise in serum creatinine and BUN levels. Potential complications include fluid overload, electrolyte imbalances, and uremia. The prognosis for drug-induced AKI depends on early recognition and prompt cessation of the offending medications. With appropriate management, recovery is possible, but there may be a risk of residual renal impairment.

Conclusion

Wilbur Elliott’s presentation is consistent with drug-induced acute kidney injury caused by nephrotoxic antibiotics he received post-mitral valve replacement surgery. Understanding the underlying pathophysiology and promptly discontinuing the offending medications are critical to managing the condition effectively. As an EMR, recognizing the severity and potential complications of drug-induced AKI will aid in providing appropriate care and facilitating a positive outcome for the patient.