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]

Investigations and diagnosis

The diagnosis is stage 3 acute kidney injury in septic shock. The creatinine of 3.1 times baseline confirms the stage 3 classification, and the urine output below 0.3 mL per kg per hour adds to the staging. A full workup seeks the source and the severity: blood cultures, a venous gas, the lactate, the full blood count, the coagulation, the liver function, and the C-reactive protein. A renal ultrasound assesses the kidney size, excludes obstruction, and looks for the small, echogenic kidneys of chronic disease, which would change the diagnosis to acute-on-chronic kidney injury. The urinalysis and the urine microscopy, once a sample is obtained, look for the casts and the cells that distinguish the intrinsic causes. The urine electrolytes allow the calculation of the fractional excretion of sodium, which separates the pre-renal from the intrinsic cause. [1]

Management and outcome

Management begins with the immediate treatment of the hyperkalaemia. Intravenous calcium gluconate at 0.5 mL per kg of the 10 percent solution is given over 5 to 10 minutes with cardiac monitoring for the myocardial membrane stabilisation, followed by the insulin with glucose, the nebulised salbutamol, and the sodium bicarbonate to shift the potassium into the cells. In parallel, the shock is resuscitated with an isotonic crystalloid bolus of 10 to 20 mL per kg with reassessment, and the broad-spectrum antibiotics are commenced within the first hour. [2]

The team is cautious with the further fluid once the shock has resolved, because the fluid overload has an independent and synergistic effect with the AKI on the mortality, as shown by Gist and colleagues. The percentage fluid overload is tracked, and the severe overload causing pulmonary oedema is an indication for the renal replacement therapy. Over the next 12 hours, the boy's potassium responds partially to the staged therapy but recurs, and the fluid overload rises, which prompts the initiation of the continuous kidney replacement therapy, the preferred modality for the haemodynamically unstable child. [3]

Over the following week, with the continuous therapy, the antibiotics, and the supportive intensive care, the boy's sepsis resolves, his creatinine falls, his urine output returns, and he is weaned from the dialysis. The discharge plan addresses the cause, the avoidance of the nephrotoxins, and the structured nephrology follow-up. The family is counselled on the likelihood of the recovery and on the importance of the long-term surveillance, because the meta-analysis by Meena and colleagues showed that the children who survive an AKI episode have a higher long-term risk of the chronic kidney disease, the hypertension, and the recurrent AKI. The follow-up includes the blood pressure monitoring, the serial creatinine, and the urinalysis, because the long-term risk persists even after the apparent renal recovery. [4]