A 58-year-old man with type 2 diabetes mellitus and stage 3b chronic kidney disease (eGFR 35 mL/min/1.73m²) presents to the radiology department for contrast-enhanced CT abdomen to evaluate recurrent abdominal pain. During the procedure, he receives iohexol (non-ionic, low-osmolar contrast medium) intravenously. Six hours post-procedure, his serum creatinine rises from baseline 2.1 mg/dL to 3.8 mg/dL, with no urine output changes. Which of the following is the most appropriate immediate management?

Explanation

## Contrast-Induced Nephropathy (CIN) Management **Key Point:** The patient has developed contrast-induced acute kidney injury (CI-AKI), defined as a rise in serum creatinine ≥0.5 mg/dL or ≥25% above baseline within 48–72 hours of contrast exposure. In a diabetic patient with pre-existing CKD, this is a recognized complication despite use of low-osmolar contrast. **High-Yield:** Management of CI-AKI is primarily **supportive and preventive**: - Aggressive IV hydration with isotonic saline (0.9% NaCl) is the cornerstone of therapy - Maintains intravascular volume, reduces renal vasoconstriction, and dilutes contrast in tubular fluid - Most cases of CI-AKI resolve spontaneously within 5–7 days with adequate hydration - Monitor renal function (creatinine, urine output) daily until stabilization **Clinical Pearl:** N-acetylcysteine (NAC) has fallen out of favor as a routine preventive agent; meta-analyses show no consistent benefit over hydration alone. It may be considered as adjunctive therapy in high-risk patients, but is NOT first-line acute management. **Warning:** Do NOT use high-osmolar contrast in future imaging—this would worsen the risk of recurrent CI-AKI. Low-osmolar or iso-osmolar agents are preferred in high-risk patients. **Mnemonic: HYDRATE** — **H**ypertonic saline (0.9%), **Y**ield time for renal recovery, **D**aily monitoring, **R**enal function tracking, **A**void nephrotoxins, **T**emperance with contrast volume, **E**nsure adequate urine output. | Intervention | Role in CI-AKI | Evidence | |---|---|---| | IV isotonic saline | First-line; reduces vasoconstriction | Strong | | N-acetylcysteine | Adjunctive; antioxidant | Weak/inconsistent | | Hemodialysis | Only if acute renal failure develops | Supportive only | | Contrast type change | Prevention for future studies | Standard practice | ## Pathophysiology CI-AKI results from: 1. Direct tubular toxicity from contrast osmolarity 2. Renal vasoconstriction and hypoxia 3. Oxidative stress in diabetics and CKD patients Early recognition and aggressive hydration prevent progression to dialysis-requiring acute kidney injury in most cases.