Intrinsic Acute Kidney Injury (Intrinsic AKI) results from direct structural damage to kidney tissue, affecting the renal tubules, glomeruli, interstitium, or blood vessels. It represents a more severe form of AKI and often requires specialized nephrology care. Intrinsic AKI is commonly seen in critically ill patients in the UAE, particularly those exposed to prolonged ischemia, severe infection, toxins, or immune-mediated diseases.

The most frequent cause of intrinsic AKI is acute tubular injury, which develops when renal tubular cells are damaged by oxygen deprivation or nephrotoxic substances. Other causes include glomerulonephritis, interstitial nephritis, vasculitis, and microvascular injury. Unlike prerenal AKI, intrinsic AKI does not improve rapidly with fluid resuscitation alone.

Patients may present with reduced urine output, swelling, fatigue, nausea, confusion, or symptoms of uremia. Laboratory findings typically include rising creatinine, electrolyte imbalances, and abnormal urine sediment such as granular casts or cellular debris. These findings indicate direct renal injury.

Diagnosis involves comprehensive laboratory evaluation, urine microscopy, imaging studies, and in selected cases, kidney biopsy to identify the underlying pathology. Differentiating intrinsic AKI from prerenal and postrenal causes is essential for appropriate management.

Management focuses on removing the inciting cause, discontinuing nephrotoxic medications, optimizing hemodynamic status, correcting metabolic abnormalities, and providing renal replacement therapy when indicated. In immune-mediated conditions, immunosuppressive therapy may be required. Recovery depends on the extent of injury and timeliness of treatment. Some patients recover fully, while others may experience incomplete recovery and progression to chronic kidney disease.