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.

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