In mammalian kidneys both inner and outer medulla of the kidney are surrounded by a urinary space, the renal pelvic space. Elaborate renal pelvic spaces surround the entire renal medulla. During rising urine flow, urine is swept up on the outside of the papilla and reaches through the pelvic fornices as far as the outer stripe of the outer medulla where it comes into close contact with capillaries and vasa recta bundles. Physiological findings show that the full refluxes cause a more rapid decrease in the osmolality of the medullary tissue than if urine is not refluxing. The effect upon the papilla and the concentration of the urine is currently the subject of some controversy.
The renal pelvic wall with its muscular coat exhibits peristaltic contractions (about 30/min in the hamster and 50/min in the rat). All structures in the renal papilla including papillary epithelium, collecting ducts, loops of Henle, capillaries and vasa recta, interstitium, and interstitial cells are affected by the peristaltic contractions. In the collecting ducts the flow of urine is intermittent as urine is pushed out in front of each peristaltic wave at the same linear velocity as the propagation of the wave over the papilla (1.6 mm/sec). The collecting ducts remain closed (up to 90% of the time) until urine flows into them from more proximal collecting ducts. At low urine flow rates short boli of urine move through the papillary collecting duct; at higher urine flows the boli are longer. In the loops of Henle and blood vessels the fluid movement is first stopped then partly reversedd as the content of these structures moves toward the outer medulla in both ascending and descending limbs. As a result the capillaries are empty 30% of the time. In spite of the rapid movement of urine through the collecting ducts at low urine flow rate, about half of the fluid entering the last millimeter of ducts is reabsorbed. Measurements of fluidd compartments in papillae with contracted or relaxed renal pelvic wall indicate that the reabsorbed fluid enters the collecting duct cells during the contraction and moves immedi-ately into the interstitium during relaxation. The functional significance of these findings is not yet clear.

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The pathogenic mechanisms in the group of diseases referred to as the tubulointerstitial nephropathies are diverse and several mechanisms may play a role in the initiation and evolution of the lesions at various times in their development. In reflex nephropathy, for example, the coarse renal cortical scars are caused by the bacterial infection, vesicoureteral reflux, and intrarenal reflux. Extravasation of Tamm-Horsfall protein may induce tubulo-interstitial inflammation and fibrosis, perhaps by immune mechanisms in the absence of infection and the presence of high pressure reflux. Progression to chronic renal failure in reflux nephropathy, occurs, in the absence of obstruction, infection, or persistent vesico-ureteral reflux due to the development of secondary progressive glomerulosclerosis. The most likely explanation for the glomerulosclerosis is the hemodynamic adaptive response that occurs in the renal glomerulus as the result of reductions in renal mass and function.

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