PART II PATHOLOGY

SUMMARY Observations on the structural changes in experimental hydronephrosis due to complete obstruction of the lower ureter of pigs have suggested that the mechanism of renal substance loss is primarily due to a direct pressure effect on and within the papillae. As a consequence of extensive tubular rupture, disintegration or atrophy, there is a progressive loss of pyramid tissue. Initial cortical changes are secondary to changes in the papillae because of interference with segments of individual nephron units, and consist predominantly of tubular atrophy, although tubulorrhexis also occurs. The distribution of the early cortical changes is related to an anatomical fact frequently overlooked—‐Henle loops are distributed within pyramids according to glomerular zones. Compression of the pelvic renal vein branches by the distending pelvis increases abnormal intra–renal pressure gradients as does focal thrombosis of peritubular capillaries and veins, and may be a contributory factor to furthering and maintaining tubular damage. There is no evidence of a major segmental ischasmic effect. Although compression of the interlobar arteries would be expected to produce general ischaemia in obstructed kidneys, the best preserved cortical areas are furthest from the blood supply, and in post–obstructed kidneys there is no evidence of a previous general ischaemic effect. During the fourth week the rate of cortical atrophy is increased, for with dilatation of the pelvis an increased effective compression force is exerted upon the lateral portions of renal lobules. When ureteric obstruction is relieved and the kidneys are allowed to repair for six months, there is a progressive reduction in kidney size in proportion to the period of obstruction. One kidney became contracted with surface scars, but there is no evidence of chronic pyelonephritis. The histological appearances of these kidneys are of amazing reconstruction of the cortex with minimal fibrosis. One incompletely obstructed kidney became larger than the contralateral kidney in the six–month post–obstructive period, although of reduced mass. Further studies on back pressure atrophy due to incomplete ureteric obstruction are required to resolve conflicting views on pathogenesis.