Stones may be present without producing symptoms or significant renal damage. This is particularly true with large stones lodged in the renal pelvis. Smaller stones may pass into the ureter, where they may lodge and produce intense pain, known as renal or ureteral colic, characterized by paroxysms of flank pain radiating toward the groin. Often at this time there is gross hematuria. The clinical significance of stones lies in their capacity to obstruct urine flow or to produce sufficient trauma to cause ulceration and bleeding. In either case, they predispose the sufferer to bacterial infection. In most cases, the diagnosis is readily made radiologically.
Hydronephrosis refers to dilation of the renal pelvis and calyces, with accompanying atrophy of the parenchyma, caused by obstruction to the outflow of urine. The obstruction may be sudden or insidious, and it may occur at any level of the urinary tract, from the urethra to the renal pelvis. The most common causes are categorized as follows:
Congenital, such as atresia of the urethra, valve formations in either the ureter or urethra, an aberrant renal artery compressing the ureter, renal ptosis with torsion, or kinking of the ureter
Foreign bodies, such as calculi or sloughed necrotic papillae
Proliferative lesions, such as benign prostatic hyperplasia, carcinoma of the prostate, bladder tumors (papilloma and carcinoma), contiguous malignant disease (retroperitoneal lymphoma, and carcinoma of the cervix or uterus)
Inflammatory lesions, such as prostatitis, ureteritis, urethritis, and retroperitoneal fibrosis
Neurogenic, such as paralysis of the bladder following spinal cord damage
Normal pregnancy, in which hydronephrosis is mild and reversible
Bilateral hydronephrosis occurs only when the obstruction is below the level of the ureters. If blockage is at the ureters or above, the lesion is unilateral. Sometimes obstruction is complete, allowing no urine to pass; usually it is only partial.
Even with complete obstruction, glomerular filtration persists for some time, and the filtrate subsequently diffuses back into the renal interstitium and perirenal spaces, from where it ultimately returns to the lymphatic and venous systems. Because of the continued filtration, the affected calyces and pelvis become dilated, often markedly so. The unusually high pressure thus generated in the renal pelvis, as well as that transmitted back through the collecting ducts, causes compression of the renal vasculature. Both arterial insufficiency and venous stasis result, although the latter probably is more important. The most severe effects are seen in the papillae, because they are subjected to the greatest increases in pressure. Accordingly, the initial functional disturbances are largely tubular, manifested primarily by impaired concentrating ability. Only later does glomerular filtration begin to diminish. Experimental studies indicate that serious irreversible damage occurs in about 3 weeks with complete obstruction, and in 3 months with incomplete obstruction. In addition to functional changes, the obstruction also triggers an interstitial inflammatory reaction, leading eventually to interstitial fibrosis.