Advanced Clinical Scenario for Multi-Level Learning
Learning Objectives: Upon completion of this interactive case, learners will be able to systematically evaluate patients presenting with acute kidney injury, apply KDIGO staging criteria accurately, implement evidence-based management strategies, recognize complications and their management, and demonstrate appropriate consultation and follow-up planning.
Case Presentation – Initial Encounter:
Mrs. Sarah Chen, a 67-year-old woman with a medical history significant for type 2 diabetes mellitus, hypertension, and osteoarthritis, presents to the emergency department with a chief complaint of decreased urine output and generalized weakness over the past three days. Her daughter, who accompanies her, reports that her mother has been “not herself” lately, appearing more confused and lethargic than usual. The patient herself complains of nausea and has had minimal oral intake over the past 48 hours.
The patient’s medical history reveals that she was diagnosed with diabetes fifteen years ago and has been managed with metformin and insulin glargine. Her hypertension has been controlled with lisinopril 10 mg daily and amlodipine 5 mg daily. For her osteoarthritis, she has been taking ibuprofen 600 mg three times daily for the past two weeks due to increased joint pain following a fall at home. She denies any recent illnesses, fever, or urinary symptoms such as dysuria or frequency.
Interactive Decision Point 1: Initial Assessment Priorities
1- What are the most important initial steps in evaluating this patient’s presentation?
2- Based on the history provided, what are your primary differential diagnoses for this patient’s acute kidney injury, and what additional history would you obtain?
3- What specific risk factors and medication interactions should be prioritized in your assessment, and how would you approach the initial management while awaiting laboratory results?
Physical Examination Findings:
The patient appears ill and lethargic but is oriented to person and place, though somewhat confused about the date. Vital signs reveal a blood pressure of 95/60 mmHg (baseline typically 130-140/80-85 mmHg according to her daughter), heart rate of 105 beats per minute, respiratory rate of 20 breaths per minute, temperature of 98.6°F (37°C), and oxygen saturation of 96% on room air.
Physical examination reveals dry mucous membranes and decreased skin turgor, suggesting volume depletion. Cardiovascular examination shows regular rhythm with no murmurs, rubs, or gallops, but jugular venous pressure is not visible with the patient sitting upright. Pulmonary examination is clear to auscultation bilaterally with no evidence of pulmonary edema. Abdominal examination reveals mild diffuse tenderness without organomegaly or masses. Extremity examination shows trace pedal edema bilaterally, which the daughter reports is new, and no evidence of rash or joint inflammation despite her osteoarthritis complaints.
Laboratory Results – Initial Panel:
The emergency department obtains comprehensive laboratory studies that reveal several concerning abnormalities. Serum creatinine is elevated at 3.2 mg/dL, representing a significant increase from her baseline of 1.1 mg/dL documented six months ago during routine follow-up. Blood urea nitrogen is 65 mg/dL, giving a BUN-to-creatinine ratio of approximately 20:1. Estimated glomerular filtration rate using the CKD-EPI equation is 15 mL/min/1.73m², representing a dramatic decline from her previous eGFR of 55 mL/min/1.73m².
Electrolyte abnormalities include serum sodium of 132 mEq/L, potassium of 5.8 mEq/L, chloride of 105 mEq/L, and bicarbonate of 18 mEq/L, suggesting metabolic acidosis with an anion gap of 15. Glucose is elevated at 245 mg/dL, likely reflecting poor glycemic control in the setting of acute illness and decreased oral intake. Complete blood count shows hemoglobin of 10.2 g/dL (baseline 11.5 g/dL), hematocrit of 30.5%, and white blood cell count of 8,500/μL with normal differential.
Interactive Decision Point 2: KDIGO Staging and Etiology Assessment
1- Using the KDIGO criteria, what stage of acute kidney injury does this patient have, and what does this staging tell us about prognosis?
2- What additional laboratory studies would you order to help determine the etiology of AKI, and what imaging studies might be indicated?
3- How would you differentiate between prerenal azotemia and acute tubular necrosis in this case, and what specific interventions would you implement immediately?
Additional Diagnostic Studies:
Urinalysis reveals specific gravity of 1.025, protein 2+, glucose 3+, ketones negative, blood 1+, leukocyte esterase negative, and nitrites negative. Microscopic examination shows 5-10 red blood cells per high-power field, 2-5 white blood cells per high-power field, and occasional hyaline casts with rare granular casts. No bacteria or crystals are observed. Urine sodium concentration is 15 mEq/L, and fractional excretion of sodium calculates to 0.8%.
Renal ultrasound performed in the emergency department demonstrates normal-sized kidneys bilaterally (right kidney 11.2 cm, left kidney 10.8 cm) with normal echogenicity and no evidence of hydronephrosis or masses. Doppler studies show normal arterial flow patterns bilaterally. Bladder appears normal with minimal post-void residual volume.
Case Evolution – Hour 4:
Despite initial fluid resuscitation with 1 liter of normal saline over two hours, the patient’s clinical status shows minimal improvement. Repeat vital signs show blood pressure of 100/65 mmHg and heart rate of 98 beats per minute. Urine output has been 15 mL over the past two hours despite Foley catheter placement. The patient remains lethargic and now reports mild nausea.
Interactive Decision Point 3: Management Strategy
1- What are the key components of supportive care for acute kidney injury, and what medications should be avoided or dose-adjusted?
2- Given the limited response to initial fluid resuscitation, what are your next management steps, and when would you consider nephrology consultation?
3- How would you approach fluid management in this patient, and what are the indications for renal replacement therapy consideration?
Advanced Management Considerations:
The nephrology consultant evaluates the patient and determines that this represents acute kidney injury likely due to a combination of prerenal azotemia from volume depletion and acute tubular necrosis from NSAID use in the setting of underlying chronic kidney disease. The consultant recommends discontinuation of lisinopril and metformin, careful fluid management with close monitoring of volume status, and aggressive management of hyperkalemia.
Hyperkalemia Management Protocol:
Given the serum potassium of 5.8 mEq/L, immediate treatment is initiated with calcium gluconate 1 gram intravenously for cardiac membrane stabilization, followed by insulin 10 units regular with 25 grams of dextrose to promote intracellular potassium shift. Sodium polystyrene sulfonate 30 grams orally is administered for potassium removal. Electrocardiogram shows peaked T waves in leads V2-V4, confirming the need for aggressive treatment.
Interactive Decision Point 4: Monitoring and Follow-up
1- What parameters should be monitored closely in hospitalized patients with AKI, and how frequently should laboratory studies be repeated?
2- What are the criteria for nephrology consultation in AKI, and how would you counsel the patient and family about prognosis?
3- What are the long-term implications of this AKI episode, and how would you structure follow-up care?
Case Resolution and Learning Points:
Over the next 48 hours, with careful fluid management, medication adjustments, and supportive care, the patient’s kidney function begins to improve. Serum creatinine decreases to 2.1 mg/dL by hospital day 3, and urine output increases to 1,200 mL over 24 hours. The patient’s mental status clears, and she tolerates oral intake well.
Key Teaching Points: This case illustrates the multifactorial nature of acute kidney injury in elderly patients with multiple comorbidities. The combination of volume depletion from poor oral intake and NSAID use in a patient with underlying diabetic nephropathy created a perfect storm for AKI development. Early recognition, appropriate staging using KDIGO criteria, and prompt intervention with fluid management and medication adjustments led to recovery of kidney function.
Expert Commentary: The case demonstrates the importance of medication reconciliation in AKI evaluation, particularly the role of NSAIDs in precipitating kidney injury in vulnerable patients. The fractional excretion of sodium helped differentiate prerenal azotemia from intrinsic kidney disease, though the mixed picture suggested elements of both. The prompt recognition and treatment of hyperkalemia prevented potentially life-threatening cardiac complications.