RATIONALE AND OBJECTIVES. Contrast-induced changes produced in normal renal function are discussed, and possible mechanisms by which such changes may occur are described. Animal experiments are reviewed, with the dog model providing results most closely approximating observations in humans.
METHODS. In the previous studies considered, standard clearance techniques were used to assess glomerulo-vascular changes, while urinary enzyme and protein excretions, along with changes in tubular reabsorption of electrolytes, were examined as indirect measures of contrast-induced tubular effects. The selection of papers for review was based primarily on studies conducted in large animals and humans. To be incorporated, traditional studies regarding accepted methods of analyzing renal function that did not involve extensive surgical preparation were reviewed.
RESULTS. Renal vascular effects of contrast media induce a biphasic change in renal blood flow—a brief increase followed by a more prolonged decline—the magnitude of which varies by dose and route of administration. Tubular effects include increased excretion of cytosolic enzymes plus changes in tubular reabsorption of sodium, potassium, and chloride. A transient osmotic diuresis also occurs.
CONCLUSIONS. Changes in renal blood flow, glomerular filtration rate, urinary electrolyte and solute excretion, and modification of the urinary concentrating-diluting mechanisms have yielded insights into the tubulo-glomerular actions of contrast media. The link between acute renal effects and subsequent contrast-associated nephropathy, while not absolutely defined, is becoming better understood as new information is gained using experimental models that more closely approximate high-risk states, including states of volume depletion, circulatory insufficiency, and pre-existing renal damage. Current attention is focused on the tubulo-glomerular feedback mechanism as accounting for the renal effects of contrast media.