Her skin is red as if sunburnt. Her blood pressure is 75/50 mm Hg. She has been vomiting and had diarrhea this morning. She has not peed for about 6 hours. On exam, she is tachycardic with brisk capillary refill. Her skin is diffusely red and her eyes are injected. There is no hepatosplenomegaly. Her BUN is 29 mg/dL and creatinine is 1.9 mg/dL. Her urinalysis has a specific gravity greater than 1.030. She received fluid resuscitation, requiring multiple normal saline boluses, and has been started on a vasopressor continuous infusion. You suspect toxic shock syndrome with acute kidney injury.
Major microvascular changes and inflammatory pathways induced by acute kidney injury. The release of cytokines and chemokines from infiltrating cells and injured tubules can amplify the destructive process. Strategies that modulate the inflammatory response may prove beneficial in human acute renal failure.
How would you classify her acute kidney injury?
A. Stage 1.
B. Stage 2.
C. Stage 3.
D. Stage 4.
The correct answer is “B.” Acute kidney injury (AKI) is an abrupt decrease in GFR and renal function that is reversible in the majority of cases. It is highly prevalent in the pediatric population, occurring in one of three hospital admissions for children. AKI is an independent risk factor for intensive care unit admissions with prolonged length of stay and ventilation days, and increased mortality. AKI can be oliguric or nonoliguric, and the presence of urine output does not exclude the presence of AKI. There are also only three stages of acute kidney injury. Standardized definitions of AKI are based on changes in serum creatinine and presence of oliguria. This patient’s creatinine is elevated approximately two times her expected baseline, and she has been oliguric for not more than 12 hours, which fits the criteria for stage 2 AKI.
Photo & Caption: Kline MW. Rudolph's Pediatrics, 23e; 2018.