CLINICAL PHARMACOLOGY
Following intravascular injection, RenoCal-76 is rapidly transported through the bloodstream to the kidneys and is excreted unchanged in the urine by glomerular filtration. When urinary tract obstruction is severe enough to block glomerular filtration, the agent appears to be excreted by the tubular epithelium.
Renal accumulation is sufficiently rapid so that the period of maximal opacification of the renal passages may begin as early as five minutes after injection. In infants and small children excretion takes place somewhat more promptly than in adults, so that maximal opacification occurs more rapidly and is less sustained. The normal kidney eliminates the contrast medium almost immediately. In nephropathic conditions, particularly when excretory capacity has been altered, the rate of excretion varies unpredictably, and opacification may be delayed for 30 minutes or more after injection; with severe impairment opacification may not occur. Generally, however, the medium is concentrated in sufficient amounts and promptly enough to permit a thorough evaluation of the anatomy and physiology of the urinary tract. After intramuscular injection, the contrast agent is promptly absorbed and normally reaches the renal passages within 20 to 60 minutes.
Intravascular injection of diatrizoate also opacifies those vessels in the path of flow of the medium, permitting visualization until the circulating blood dilutes the concentration of the medium. Thus selective angiography may be performed following injection directly into veins or arteries.
Computed Tomography
RenoCal-76 enhances computed tomographic brain scanning through augmentation of radiographic efficiency. The degree of enhancement of visualization of tissue density is directly related to the iodine content in an administered dose; peak iodine blood levels occur immediately following rapid injection of the dose. These levels fall rapidly within five to ten minutes. This can be accounted for by the dilution in the vascular and extracellular fluid compartments which causes an initial sharp fall in plasma concentration. Equilibration with the extracellular compartments is reached in about ten minutes; thereafter, the fall becomes exponential. Maximum contrast enhancement frequently occurs after peak blood iodine levels are reached. The delay in maximum contrast enhancement can range from five to forty minutes, depending on the peak iodine levels achieved and the cell type of the lesion. This lag suggests that radiographic contrast enhancement is at least in part dependent on the accumulation of iodine within the lesion and outside the blood pool, although the mechanism by which this occurs is not clear. The radiographic enhancement of nontumoral lesions, such as arteriovenous malformations and aneurysms is probably dependent on the iodine content of the circulating blood pool.
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