Expansion
Medullary vasoconstriction and direct tubular toxicity
Expansion
Two mechanisms combine:
- Haemodynamic: contrast triggers renal vasoconstriction, notably in the medulla, worsening the already marginal medullary oxygen supply. Adenosine and endothelin are implicated, with reduced nitric oxide
- Direct tubular toxicity: contrast generates reactive oxygen species and injures tubular cells. The osmotic and viscosity load adds further stress
Creatinine typically rises at 48 to 72 hours and recovers within 7 to 10 days.
Risk factors: pre-existing chronic kidney disease (the most important), diabetic nephropathy, hypovolaemia, heart failure, myeloma, high contrast volume, intra-arterial administration, and concurrent NSAIDs or diuretics.
Prevention rests on volume expansion with isotonic saline before and after, using the lowest volume of low or iso-osmolar contrast, and withholding nephrotoxins. N-acetylcysteine and bicarbonate have not held up in large trials.
Metformin is withheld not because it causes the injury but because it accumulates if injury occurs, risking lactic acidosis.