Sepsis-Induced Acute Kidney Injury (AKI) is a severe complication of systemic infection in which kidney function deteriorates rapidly as part of a broader, dysregulated inflammatory response. It is among the most common causes of AKI in intensive care units across the UAE and carries a high risk of morbidity and mortality if not recognized and treated promptly. Unlike simple hypoperfusion, sepsis-related AKI reflects complex microvascular, inflammatory, and metabolic disturbances that impair renal function even when blood pressure appears adequate.

The pathophysiology of sepsis-induced AKI involves widespread immune activation, endothelial dysfunction, and alterations in renal microcirculation. Inflammatory mediators disrupt capillary blood flow, increase vascular permeability, and impair oxygen delivery to renal tissues. At the cellular level, mitochondrial dysfunction and oxidative stress reduce tubular cell energy production, leading to impaired filtration and tubular handling of electrolytes and water. These mechanisms explain why kidney injury may develop early in sepsis and progress despite aggressive fluid resuscitation.

Clinically, patients may present with reduced urine output, rising serum creatinine, electrolyte disturbances, metabolic acidosis, and fluid overload. These renal findings often occur alongside systemic signs of sepsis such as fever or hypothermia, hypotension, tachycardia, confusion, and evidence of multi-organ dysfunction. In some patients, AKI may be the first manifestation of worsening sepsis.

Diagnosis relies on close monitoring of urine output and serial kidney function tests in patients with suspected or confirmed infection. Laboratory evaluation assesses creatinine trends, electrolyte balance, and acid–base status. Imaging is used selectively to exclude obstructive causes. Early identification is critical, as even mild AKI significantly worsens outcomes in septic patients.

Management focuses on rapid control of infection and kidney-protective supportive care. Early administration of appropriate antibiotics, timely source control, and careful hemodynamic optimization are central to treatment. Fluid therapy must be individualized to restore perfusion without causing harmful fluid overload. Nephrotoxic medications are avoided whenever possible, and drug dosing is adjusted to renal function.

In severe cases, renal replacement therapy may be required to manage refractory metabolic acidosis, hyperkalemia, or fluid overload. Continuous dialysis modalities are often preferred in hemodynamically unstable patients. Early nephrology involvement improves decision-making regarding timing and modality of renal support.
Recovery depends on the severity of sepsis, underlying comorbidities, and speed of intervention. Survivors of sepsis-induced AKI have a higher risk of developing chronic kidney disease and require long-term follow-up to monitor renal recovery and prevent progression.