Contrast induced nephropathy

Contrast-Induced Nephropathy (CIN), also known as contrast-induced acute kidney injury (CI-AKI), is a form of acute kidney injury (AKI) that occurs following the administration of intravascular radiographic contrast media. The condition is characterized by a sudden deterioration in renal function, typically within 48-72 hours after exposure to contrast material. CIN is a significant cause of hospital-acquired renal impairment and is associated with increased morbidity and mortality rates.

Etiology and Pathophysiology[edit | edit source]

The exact mechanism of CIN is not fully understood, but it is believed to involve a combination of reduced renal blood flow and direct toxicity to the renal tubules. Contrast media can cause vasoconstriction, leading to hypoxia in the renal medulla. Additionally, the osmotic effects of contrast agents can result in tubular cell damage. Patients with pre-existing chronic kidney disease (CKD), diabetes mellitus, dehydration, or those receiving high volumes of contrast material are at increased risk.

Clinical Presentation[edit | edit source]

Symptoms of CIN may include a decrease in urine output and an increase in serum creatinine levels. However, many cases are asymptomatic and are identified through laboratory monitoring. It is important to differentiate CIN from other causes of AKI, such as nephrotoxic medications or acute tubular necrosis.

Diagnosis[edit | edit source]

The diagnosis of CIN is primarily based on the temporal relationship between contrast exposure and the development of AKI, in the absence of an alternative explanation for renal impairment. An increase in serum creatinine by ≥0.5 mg/dL or a 25% increase from baseline within 48-72 hours after contrast exposure is diagnostic.

Prevention and Management[edit | edit source]

Preventive measures are key in managing CIN. These include adequate hydration before and after contrast exposure, using the lowest possible dose of contrast, and choosing non-ionic, low-osmolality contrast agents. In high-risk patients, prophylactic administration of N-acetylcysteine or sodium bicarbonate may be considered. Once CIN occurs, management is supportive, focusing on maintaining fluid and electrolyte balance and avoiding further nephrotoxic insults.

Prognosis[edit | edit source]

The prognosis of CIN varies. While many cases are transient and resolve with supportive care, CIN can lead to persistent renal dysfunction or progress to end-stage renal disease (ESRD) in severe cases. The risk of adverse outcomes is higher in patients with pre-existing renal impairment or other comorbid conditions.

Epidemiology[edit | edit source]

The incidence of CIN varies widely, depending on the definition used and the population studied. It is more common in patients with risk factors such as CKD, diabetes, and dehydration.