A 68-year-old man with no previous history of renal disease is evaluated in the postoperative unit due to decreased urine output. The patient was admitted due to severe abdominal pain, fever, and vomiting. Evaluation revealed perforated sigmoid diverticulitis, and the patient underwent urgent sigmoid resection. Postoperatively, he has received maintenance intravenous fluids and piperacillin/tazobactam. In the day since surgery, the patient has had 200 mL of urine output. Temperature is 37.1 C (98.8 F), blood pressure is 100/70 mm Hg, and pulse is 96/min. The lungs are clear to auscultation, and heart sounds are normal. The abdomen shows postoperative changes with sluggish bowel sounds. The patient has no skin rash. Laboratory results are as follows:
| Hemoglobin | 10.5 g/dL |
| Leukocytes | 13,000/mm3 |
| Sodium | 138 mg/dL |
| Potassium | 5.1 mg/dL |
| Glucose | 108 mg/dL |
| Creatinine | 1.9 mg/dL |
| Blood urea nitrogen | 82 mg/dL |
Urinalysis reveals no sediment, and bladder scanning reveals no urine. Which of the following is the best next step in management of this patient?
Prerenal acute kidney injury | |
Etiology |
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Clinical features |
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Treatment |
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EABV = effective arterial blood volume; NSAID = nonsteroidal anti-inflammatory drug. | |
This patient with elevated serum creatinine and no underlying renal disease likely has prerenal acute kidney injury (AKI) due to intravascular volume depletion. Preoperative infection and intraoperative blood loss predispose patients to volume depletion, and volume depletion is further suggested by tachycardia. There is no intrinsic damage to the kidneys in prerenal AKI, but decreased renal perfusion leads to a decreased glomerular filtration rate and increased serum creatinine. The kidneys increase tubular sodium and water resorption, resulting in markedly increased passive resorption of urea. Therefore, a blood urea nitrogen/creatinine ratio >20:1 (43:1 in this patient) is highly suggestive of a prerenal state. Oliguria (<500 mL of urine/24 hours) is often present, as is unremarkable urine sediment (absence of casts, cells, or protein).
Although heart failure can lead to prerenal AKI in the setting of hypervolemia (due to decreased effective arterial blood volume), most prerenal AKI is due to a volume-depleted state. In the absence of clear signs of volume overload (eg, elevated jugular venous pressure, lung crackles), patients with suspected prerenal AKI should be treated with intravenous isotonic fluid (eg, normal saline) to restore renal perfusion.
(Choice B) Beta-lactam antibiotics (eg, piperacillin/tazobactam) are a common cause of intrinsic AKI due to acute interstitial nephritis (AIN). AIN necessitates discontinuation of the offending drug; however, no leukocytes on urinalysis and absence of skin rash make AIN unlikely.
(Choice C) Low-dose dopamine acts primarily as a dopamine-1 receptor agonist, resulting in renal arteriole dilation and increased renal blood flow. However, fluid bolus is the best treatment in this patient with evidence of hypovolemia.
(Choices D and E) Loop diuretics (eg, furosemide) or osmotic diuretics (eg, mannitol) would worsen this patient's volume depletion and possibly lead to intrinsic renal injury (eg, acute tubular necrosis) due to a further decrease in renal perfusion.
(Choice F) Intravenous urography visualizes radiopaque contrast filling the urinary tract and is useful in diagnosing ureteral injury. Iatrogenic ureteral injury can occur following abdominal surgery; however, unilateral injury does not result in AKI, and bilateral injury (a potential cause of postrenal AKI) is extremely unlikely.
Educational objective:
Intravascular volume depletion is a common cause of prerenal acute kidney injury (AKI). Patients typically have an elevated blood urea nitrogen/creatinine ratio (>20:1), oliguria, and unremarkable urine sediment. Administration of intravenous fluid restores renal perfusion and corrects the AKI.