Acute kidney injury: Case

This boy presents septic shock with stage 3 acute kidney injury. The creatinine has risen to 3.1 times the baseline of 56 micromoles per litre, which alone places him in stage 3, and the severe oliguria and the anuria risk confirm the staging. The potassium of 7.1 mmol per litre with peaked T waves and a widened QRS is immediately life-threatening, the metabolic acidosis with a pH of 7.18 and a lactate of 4.2 mmol per litre reflects the accumulating acid and the tissue hypoperfusion, and the shock from the presumed sepsis is the precipitating cause. The immediate priority is to treat the hyperkalaemia and to resuscitate the shock in parallel. ^[1]

Clinical findings

The pattern is that of severe septic shock with established intrinsic acute kidney injury. The prolonged capillary refill, the hypotension, and the high lactate confirm the shock, and the oliguria and the 3.1-fold rise in creatinine confirm the stage 3 AKI. The ECG changes from the hyperkalaemia mark an immediate risk of cardiac arrest, and the metabolic acidosis both worsens the hyperkalaemia and depresses the myocardium. The sepsis is the precipitating cause, and the kidney has suffered the combined inflammatory and haemodynamic injury that characterises sepsis-associated AKI, the most common intrinsic AKI in the paediatric intensive care unit. ^[1]

The differential at presentation includes a pre-renal component from the volume depletion, which would respond to the fluid resuscitation, and an established acute tubular necrosis from the septic shock, which would not respond rapidly and would need supportive care over days to weeks. The fractional excretion of sodium, once a urine sample is obtained, would help separate the two, with a value above 1 percent indicating the intrinsic injury. ^[2]