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.
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George A. Porter (1993) studied this question.
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