Left kidney on arterial phase demonstrates decreased perfusion, prolongation of the cortical nephrographic phase and persistent corticomedullary differentiation on venous phase and persistence of the generalized nephrogram on delayed image.

There is also seen vicarious excretion of contrast in gall bladder.

 

Contrast material progressing from the renal arterial beds through glomeruli, nephrons, and finally the renal collecting systems should be evident in temporally synchronous and symmetric nephrographic phases at CT and therefore is a process that should be critically evaluated. Abnormalities in this evolutionary process are generally detected as unilateral alterations in the progression of the nephrographic sequence. Temporal delay may be attributed to a unilateral decrease in renal blood flow, with a corresponding decline in glomerular filtration and tubular transit rates of contrast material.   

Quantitative reduction in renal blood flow secondary to renal artery stenosis is classically associated with a delayed, dense nephrogram at urography. The direct CT correlate of this finding is asymmetric progression of the CT nephrogram, with prolongation of the cortical nephrographic phase and persistent corticomedullary differentiation on the involved side. A similar CT appearance can be seen with acute renal vein thrombosis, since intravenous clot opposes the arterial perfusion gradient, slowing filtration and decreasing tubular transit. Developing interstitial edema associated with renal vein thrombosis also decreases the forward flow of contrast material by increasing the parenchymal pulp pressure, which leads to compression of tubular lumina (24). Characteristic imaging features of renal vein thrombosis, such as an enlarged renal vein containing a filling defect (thrombus), enlargement of the affected kidney caused by interstitial edema, and possibly retroperitoneal hemorrhage, should easily allow differentiation of this process from the characteristic small, smooth kidney of chronic renal ischemia.  

The most common cause of asymmetric delay in the development of the nephrographic pattern is some form of obstructive uropathy. Obstruction to urine flow anywhere along the outflow tract increases internal pressure within the collecting system proximal to the blockage. Increased pressure in the static urine column is transmitted in a retrograde manner to the level of the nephron opposing the forward perfusion gradient of normal arterial pressure. Eventually, the rates of both glomerular filtration and tubular transit decrease. This delay is demonstrated at CT examinations by slowed progression of nephrographic phases in the obstructed Kidney and persistence of the generalized nephrogram on delayed images. 

When temporal abnormalities of the CT nephrogram are assessed, common causes of unilateral temporal delay, such as renal artery stenosis, renal vein thrombosis, and urinary tract obstruction, should he considered. These entities, although obviously different in cause, relate to similar underlying pathophysiologic principles.