A 68-year-old male, Mr. Arthur Jenkins, presented to the emergency department with a three-day history of progressively worsening fatigue, decreased urine output, and mild nausea. He reported no fever, chest pain, or abdominal pain. His past medical history included hypertension managed with lisinopril and type 2 diabetes mellitus controlled with metformin. He denied any recent illnesses, travel, or new medications. On examination, Mr. Jenkins appeared fatigued but well-hydrated, with normal vital signs except for a slightly elevated blood pressure of 155/90 mmHg. His abdomen was soft and non-tender. Laboratory investigations revealed a serum creatinine of 3.2 mg/dL (baseline 1.1 mg/dL), a blood urea nitrogen (BUN) of 55 mg/dL, and a potassium of 5.8 mEq/L. Urinalysis showed trace protein and no red blood cells or white blood cells. A renal ultrasound revealed normal-sized kidneys with no hydronephrosis.
The constellation of symptoms, elevated creatinine and BUN, and hyperkalemia, in the absence of overt signs of infection or obstruction, strongly suggested an acute kidney injury (AKI). Given his medical history and medication list, both prerenal and intrinsic causes were considered. The elevated BUN:creatinine ratio (approximately 17:1) could point towards a prerenal component, suggesting reduced renal perfusion. However, the absence of hypotension on presentation and the relatively normal physical examination made severe prerenal azotemia less likely as the sole cause. The normal kidney size and lack of hydronephrosis on ultrasound effectively ruled out chronic kidney disease as the primary driver and chronic obstruction.
Initial management focused on stabilizing Mr. Jenkins' electrolyte imbalance and addressing potential contributing factors. Intravenous fluids were initiated with normal saline to improve renal perfusion, and his antihypertensive medication, lisinopril, a known nephrotoxin in the setting of AKI, was discontinued. Metformin was also held due to the risk of lactic acidosis in the context of impaired renal function. His hyperkalemia was treated with oral potassium binder (e.g., sodium polystyrene sulfonate) and a low-potassium diet. Continuous cardiac monitoring was implemented due to the risk of arrhythmias associated with hyperkalemia.
Over the next 48 hours, Mr. Jenkins' urine output gradually increased, and his serum creatinine trended downwards to 2.5 mg/dL, with BUN improving to 45 mg/dL and potassium normalizing to 4.2 mEq/L. This improvement in renal function, following fluid resuscitation and discontinuation of offending medications, indicated a significant prerenal component to his AKI, likely exacerbated by dehydration and the vasodilatory effects of his lisinopril on the afferent arteriole, further compromising glomerular filtration under a suboptimal hemodynamic state. The mild nausea was attributed to the uremic state.
Further investigation into the underlying cause of the initial dehydration and potential subclinical illness was pursued. Mr. Jenkins recalled a mild gastroenteritis two weeks prior, which he had largely dismissed, experiencing a few days of decreased oral intake. This history, combined with the initial presentation, solidified the diagnosis of acute tubular necrosis (ATN) secondary to prolonged prerenal azotemia from that episode. ATN is a common cause of AKI in hospitalized patients, often triggered by prolonged periods of inadequate renal perfusion.
Mr. Jenkins was discharged on hospital day five with instructions to maintain adequate hydration, follow a low-sodium diet, and monitor his blood pressure. His medications were re-evaluated, and his hypertension was managed with a calcium channel blocker. He was scheduled for a follow-up appointment with his primary care physician and a nephrologist to monitor his renal recovery and assess for any long-term sequelae. This case highlights the importance of a thorough history, prompt laboratory assessment, and targeted management in addressing acute kidney injury.