Adverse reactions to iodinated contrast media (ICM) are more likely to develop in patients with asthma, a history of allergy or contrast reaction and in those who are debilitated or medically unstable. These reactions can be divided into renal and general, and the latter are subdivided into acute and delayed. Acute general reactions can be minor, intermediate or severe. Fatal reactions are rare. The introduction of low-osmolality agents has caused an overall reduction in the number of non-fatal contrast reactions. Prompt recognition and treatment of acute adverse side effects to ICM is invaluable and may prevent a reaction from becoming severe. Familiarity with cardiopulmonary resuscitation is essential for successful management of life-threatening reactions. Contrast-media-induced renal impairment can be reduced with the use of low-osmolality contrast media and extracellular volume expansion. The use of ICM in diabetic patients receiving metformin should be carried out with care to avoid metformin-induced lactic acidosis. However, this problem is mainly observed in patients with diabetic nephropathy.

The effect of increased intrapelvic pressure on renal perfusion was examined by simple magnified angiography of freshly excised artificially perfused kidneys of adult Danish Landrace pigs. In all kidneys control angiography was performed at normal intrapelvic pressure (0-5 mmHg). Intrapelvic pressure was raised by retrograde ureteral perfusion of saline in 9 kidneys. Repeat angiography was performed at an intrapelvic pressure of 30-35 mmHg (4 kidneys), 50-55 mmHg (5 kidneys) or 0-5 mmHg (4 kidneys). Angiography demonstrated a delay in arterial filling in kidneys with increased intrapelvic pressure. Perfusate flow measurements showed a corresponding fall in perfusion flow. Retrograde ureteral perfusion was repeated at similar pressures using contrast medium. Intrarenal backflow (IRB) was demonstrated in all 9 kidneys with elevated intrapelvic pressure. IRB localized to 84 per cent of the compound papillae and to 40 per cent of the simple papillae, and was independent of the level of elevated intrapelvic pressure. One-third of the papillae with IRB had absent or markedly decreased arterial filling in the corresponding lobe at angiography. A third retrograde ureteral perfusion was done with a mixture of barium sulphate and gelatin in 4 kidneys. Light microscopy demonstrated that the primary pathway for IRB was canalicular. The contrast medium entered the interstice by three routes: (1) Tubular leakage in the papilla and the corticomedullary region, (2) tears originating in the papilla itself and (3) tears in the calyceal fornix with extension into the parenchyma.

Using mp-MRI, even without previous experience, can improve the detection rate of significant PCa at repeated biopsy and allows more accurate Gleason grading.

Retrograde pyelography was carried out in rabbits during and following temporary clamping of either the renal artery and vein together or the main renal vein alone. Pyelosinous backflow was observed in all kidneys and pyelovenous backflow in 16 of the 18 kidneys, occurring at intrapelvic pressures between 50 and 100 mmHg. During simultaneous complete renal artery and vein occlusion intrarenal backflow occurred in all 3 kidneys examined while it was observed in 3 of 6 kidneys when the pyelography was performed 5 min after removal of the clamp. During complete renal vein occlusion filling with contrast medium of the central intrarenal veins occurred in all 3 kidneys but only in 3 of 6 kidneys examined after the clamp had been removed. Microscopically, pyelosinous backflow was explained by vital tears in the fornix of the pelvic cavity. Tears extending into the kidney parenchyma were only observed in kidneys with intrarenal backflow at pyelography.