Renal arteriography can provide considerable assistance in the diagnosis and management of hydronephrosis. A hydronephrotic kidney which eludes definitive diagnosis by other methods can be recognized by its distinctive arteriographic appearance. Renal arteriography also adds information on renal function and renal blood supply useful in planning a surgical approach to the hydronephrotic kidney. The purpose of this report is to summarize the renal arteriographic findings in hydronephrosis and to present several cases illustrating the efficacy of performing renal arteriography in this entity. Arteriography in Hydronephrosis Knowledge of the effects of hydronephrosis on the renal vasculature is based upon experimental studies by Hinman and Morison (1), Herdman and Jaco (2), Idbohrn (3), and Widen (4). Olsson (5, 6) has verified that the conclusions from animal experimentation are applicable to man. The arteriographic findings in hydronephrosis depend upon the degree and duration of obstruction to the kidney. There may be no detectable abnormality on the renal arteriogram in acute hydronephrosis or in long-standing, but compensated, hydronephrosis. In some cases of acute hydronephrosis there is a delay in the filling of the secondary and tertiary arterial branches of the involved kidney. This delay can be seen by comparing the speed of filling of these vessels with the corresponding vessels of the opposite side. (See Case I, Fig. 1.) The delay in filling has been experimentally studied and is presumably due to increased intrarenal pressure secondary to obstruction of the urinary tract. Persistent hydronephrosis produces atrophic change in the renal vasculature. The atrophy begins with tapering and diminished branching of the peripheral arterial vessels and progresses proximally to involve the main renal artery. In longstanding hydronephrosis, when severe renal damage has occurred, the lumen of the main renal artery is markedly decreased in size. The secondary and tertiary vessels are separated and stretched over the dilated pelvis and calyces and are narrowed and have fewer and smaller branches (Figs. 2–5). We have noted in cases of long-standing, tight pelviureteral junction obstruction a characteristic marked spreading of the branches of the atrophic main renal artery at its bifurcation (Figs. 2–4). This roentgen finding is presumably due to a greatly dilated pelvis.