Acute Tubular Necrosis (ATN) is the most common cause of intrinsic acute kidney injury and results from direct injury to the renal tubular epithelial cells. It is frequently encountered in hospitalized and critically ill patients in the UAE and represents a major contributor to prolonged kidney dysfunction and increased mortality in intensive care settings.

ATN typically develops following prolonged ischemia or exposure to nephrotoxic substances. Ischemic ATN occurs when sustained hypotension, shock, severe blood loss, or sepsis deprives the kidneys of adequate oxygen delivery. Toxic ATN results from exposure to medications, contrast agents, heavy metals, or endogenous toxins such as myoglobin released during rhabdomyolysis.

In ATN, injured tubular cells lose their ability to reabsorb and secrete substances properly. Cellular debris accumulates within the tubules, causing obstruction and back leakage of filtrate. These changes lead to reduced urine output, impaired waste excretion, and significant electrolyte and acid–base disturbances.

Clinically, patients may present with oliguria or non-oliguric kidney failure, fatigue, nausea, confusion, swelling, and shortness of breath due to fluid overload. Laboratory findings include rising serum creatinine, hyperkalemia, metabolic acidosis, and characteristic granular casts on urine microscopy. Unlike prerenal AKI, ATN does not respond rapidly to fluid resuscitation.

Diagnosis is based on clinical context, laboratory evaluation, and urine sediment examination. Imaging studies are typically normal but are useful in excluding obstruction. Kidney biopsy is rarely required unless the diagnosis is uncertain or alternative causes of intrinsic AKI are suspected.

Management of ATN is primarily supportive. Treatment includes optimizing hemodynamic status, avoiding further nephrotoxic exposure, correcting electrolyte imbalances, and carefully managing fluid balance. Renal replacement therapy may be required in cases of severe metabolic derangement, refractory fluid overload, or uremic complications. Recovery from ATN occurs in phases, beginning with stabilization, followed by gradual regeneration of tubular cells and restoration of kidney function. While many patients recover fully, ATN is associated with an increased risk of progression to chronic kidney disease, particularly in older adults and those with pre-existing renal impairment. Early nephrology involvement improves monitoring, complication management, and long-term outcomes.