Ureteral Stricture

Updated: Mar 11, 2021
  • Author: Benjamin Newell Breyer, MD, MS; Chief Editor: Bradley Fields Schwartz, DO, FACS  more...
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Practice Essentials

A ureteral stricture is characterized by a narrowing of the ureteral lumen, causing functional obstruction. The most common form of ureteral stricture is ureteropelvic junction (UPJ) obstruction, which is a congenital or acquired narrowing at the level of the UPJ (see Ureteropelvic Junction Obstruction).


Relevant Anatomy

The ureter is a muscular tube lined by transitional epithelium that courses from the renal pelvis to the bladder in the retroperitoneum.

The length of the ureter is 20-30 cm, depending on the individual's height. The lumen size is 4-10 mm in circumference, depending on its location. The narrowest areas include the UPJ, the overpass by the ureter where it crosses over the bifurcation of the iliac arteries, and the ureterovesical junction (UVJ).

In both men and women, the ureter courses posterior to the gonadal vessels and anterior to the iliopsoas muscles, crosses the common iliac artery and vein, and enters inferiorly into the pelvis. In men, the vas deferens loops anterior to the ureter, prior to the ureter entering the bladder. In women, the ureter courses posterior to the uterine arteries (hence, the "water under the bridge" analogy) and close to the uterine cervix prior to reaching the intramural bladder.

The ureteral blood supply is provided from multiple sources. Superiorly, branches from the renal and gonadal arteries may contribute. As the ureter courses through the retroperitoneum, the aorta contributes numerous small branches. In the pelvis, the iliac, vesical, uterine, and hemorrhoidal arteries also contribute to the ureteral blood supply.



Ureteral strictures are typically due to ischemia, resulting in fibrosis. Wolf and colleagues define a stricture as ischemic when it follows open surgery or radiation therapy, whereas the stricture is considered nonischemic if it is caused by spontaneous stone passage or a congenital abnormality. [1] Less commonly, the etiology is mechanical, such as from a poorly placed permanent suture or surgical clip.

Pathologic analysis of the strictures reveals disordered collagen deposition, fibrosis, and varying levels of inflammation, depending on factors such as etiology and interval since the causative insult.

The resulting ureteral obstruction may vary widely from mild, causing only asymptomatic proximal ureteral dilation and hydronephrosis, to severe, causing complete obstruction and subsequent loss of renal function.

Some patients with ureteral strictures are asymptomatic; others are symptomatic only during periods of diuresis or develop severe renal colic. The degree of symptoms correlates poorly with the degree of obstruction; at times, severe obstruction is asymptomatic or silent. Renal failure and azotemia may be due to bilateral strictures, such as in cases of bilateral ureteroenteric strictures, external compression due to retroperitoneal malignancy, or retroperitoneal fibrosis; recovery depends on the duration of ureteral obstruction.



Ureteral strictures may be classified as follows:

  • Extrinsic or intrinsic
  • Benign or malignant
  • Iatrogenic or noniatrogenic

Extrinsic malignant strictures include those caused by primary or metastatic cancer. Primary pelvic malignancies, particularly cancers of the cervix, prostate, bladder, and colon, frequently cause extrinsic compression of the distal ureter. Retroperitoneal lymphadenopathy, caused by a wide range of malignancies, particularly lymphoma, testicular carcinoma, breast cancer, or prostate cancer, may cause proximal to midureteral obstruction.

Extrinsic benign compression due to idiopathic retroperitoneal fibrosis may also cause unilateral or bilateral ureteral obstruction, leading to azotemia.

Transitional cell carcinoma (TCC) may cause malignant intrinsic obstruction.

Malignant ureteral obstruction is differentiated from benign ureteral obstruction by (1) the presence of an extrinsic mass on a CT scan or sonogram and (2) the appearance of the ureter on contrast-study images.

Ureteral TCC may manifest as ureteral obstruction. Ureteral TCCs typically have an irregular mucosal pattern and are associated with dilatation of the ureter below the lesion (goblet sign). Benign strictures are usually smooth, without distal dilatation. In some cases, biopsy may be required to differentiate benign from malignant strictures. Biopsy samples can usually be collected ureteroscopically or with a fluoroscopically directed ureteral brush. Ureteral tumors can also be diagnosed during transureteral resection of the tumor with specialized ureteral resectoscopes.

Benign intrinsic strictures, which are the focus of this article, may be congenital (eg, congenital obstructing megaureter), iatrogenic, or noniatrogenic (eg, those that follow passage of calculi or chronic inflammatory ureteral involvement [eg, tuberculosis and schistosomiasis]).

Iatrogenic benign strictures may result from various causes, including the following:



The widespread use of upper tract endoscopy has led to an increased frequency of iatrogenic ureteral stricture. Early ureteroscopy studies reported ureteral stricture rates of 3%-11% in patients undergoing ureteroscopy for calculus management. More recent studies using smaller fiberoptic endoscopes; laser lithotripsy; and smaller, less traumatic instruments report a ureteral stricture rate of less than 1%.

In a review of 24 patients with highly impacted ureteral stones that were impacted for an average of 11 months, 24% of the patients developed postoperative ureteral strictures; therefore, impaction is a major risk factor. Ureteral perforation during these procedures has also been identified as a risk factor for stricture disease. [3, 4]

Factors associated with ureteral stricture development during ureteroscopy include the following:

  • Large scope size
  • Prolonged case duration
  • Stone impaction
  • Stone size
  • Proximal location
  • Perforation
  • Use of intracorporeal lithotripsy

Ureteral strictures occur in approximately 3-8% of kidney transplant recipients. [5]  Ureteral strictures may complicate urinary diversions. The frequency of ureterointestinal anastomotic strictures during urinary diversion is 3%-5%. Ureteral injuries may result from any pelvic or retroperitoneal surgery, particularly abdominal hysterectomy and sigmoid colectomy. Gynecologic surgery is responsible for up to 75% of iatrogenic ureteral injuries.

Vakili et al performed a prospective analysis of 479 patients undergoing hysterectomy for benign disease. [6] Iatrogenic ureteral injury occurred in 8 patients (1.7%), comparable with previous ranges reported in the literature (0.02%-2.5%). Risk factors for urinary tract injury during hysterectomy include malignancy, pelvic radiation, endometriosis, prior surgery, and surgery for prolapse, although at least half of all ureteral injuries have no identifiable risk factors. Ureteral injuries or injury repairs may also result in strictures, although strictures of these etiologies are less common than strictures caused during endoscopy or anastomosis.