Acute kidney injury: SAQ

This boy presents septic shock with acute kidney injury. The creatinine has risen to 2.3 times the baseline of 48 micromoles per litre, placing him in KDIGO stage 2, and the oliguria for 12 hours confirms the staging. The potassium of 6.8 mmol per litre with peaked T waves is immediately life-threatening, the metabolic acidosis with a pH of 7.22 reflects the accumulating acid and the failing clearance, 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 with the diagnostic workup. [1]

Question 1 (10 marks)

Outline the immediate management of this child, including the staged treatment of his hyperkalaemia and the resuscitation of his shock. [2]

The first priority is the hyperkalaemia with ECG changes, which is an immediate threat of cardiac arrest. I would give intravenous calcium gluconate at 0.5 mL per kg of the 10 percent solution over 5 to 10 minutes with cardiac monitoring to stabilise the myocardial cell membrane. Calcium does not lower the potassium, so I would immediately follow it with agents that shift potassium into the cells: intravenous insulin with glucose, nebulised salbutamol, and sodium bicarbonate given his acidosis. I would recheck the potassium after each intervention because the effect is transient, and I would arrange for renal replacement therapy if the hyperkalaemia is refractory. [2]

In parallel I would resuscitate the shock. I would establish intravenous access and give an isotonic crystalloid bolus of 10 to 20 mL per kg, with reassessment after each bolus, because restoring the perfusion may reverse a pre-renal component of his injury. The PRoMPT BOLUS trial showed no difference between balanced crystalloids and 0.9 percent saline in children with septic shock, so either is acceptable. I would send blood cultures, commence broad-spectrum antibiotics within the first hour, and identify and control the source of the sepsis. I would be cautious with further fluid boluses once he is no longer shocked, because fluid overload has an independent and synergistic effect with AKI on mortality in critically ill children. [2]

I would stop all nephrotoxic drugs and adjust every drug dose to the current estimated GFR. I would monitor him in a high-dependency or intensive care setting with hourly urine output, continuous cardiac monitoring, and serial creatinine, electrolytes, and blood gases. I would involve the paediatric nephrologist and the intensivist early, and I would establish the indications for renal replacement therapy, which include refractory hyperkalaemia, severe metabolic acidosis, fluid overload causing pulmonary oedema, and uraemic complications. [2]

Question 2 (10 marks)

Describe the KDIGO definition and staging of acute kidney injury, and explain the long-term implications of this child's AKI episode for his follow-up. [1]

Acute kidney injury is defined by the KDIGO criteria as a rise in serum creatinine of 0.3 mg per dL or more within 48 hours, or a rise to 1.5 times the baseline value or more within seven days, or a urine output below 0.5 mL per kg per hour for six hours. The staging is into three grades by the magnitude of the change. Stage 1 is a creatinine of 1.5 to 1.9 times baseline or a 0.3 mg per dL rise, with a urine output below 0.5 mL per kg per hour for 6 to 12 hours. Stage 2 is a creatinine of 2.0 to 2.9 times baseline with a urine output below 0.5 mL per kg per hour for 12 hours or more. Stage 3 is a creatinine of 3.0 times baseline or more, or a rise to 4.0 mg per dL or more, or the initiation of renal replacement therapy, or in a patient under 18 years an estimated GFR below 35 mL per min per 1.73 m2, with a urine output below 0.3 mL per kg per hour for 24 hours or more or anuria for 12 hours or more. This boy is in stage 2 on the basis of a creatinine of 2.3 times baseline and 12 hours of oliguria. [1]

The long-term implications have changed the practice. The AWARE study established that AKI independently increases the mortality and the length of stay in critically ill children, with the risk rising through the stages. The meta-analysis by Meena and colleagues showed that children who survive an AKI episode have a higher long-term risk of chronic kidney disease, hypertension, and recurrent AKI, which challenges the older belief that paediatric AKI is fully reversible. This means that this boy needs structured nephrology follow-up after discharge, with blood pressure monitoring, serial creatinine to confirm recovery, urinalysis to exclude residual disease, and the avoidance of nephrotoxic medications. The family should be counselled on the likelihood of recovery in the acute setting and on the importance of the long-term surveillance, because the risk persists even after the apparent renal recovery. [4]