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Ovid: Oxford Handbook of Urology

Authors: Reynard, John; Brewster, Simon; Biers, Suzanne Title: Oxford Handbook of Urology, 1st Edition Copyright ©2006 Oxford University Press > Table of Contents > Chapter 10 – Upper tract obstruction, loin pain, hydronephrosis Chapter 10 Upper tract obstruction, loin pain, hydronephrosis P.402
Hydronephrosis Dilatation of the renal pelvis and calyces (Fig. 10.1). When combined with dilatation of the ureters known as hydroureteronephrosis. Obstructive nephropathy is damage to the renal parenchyma resulting from an obstruction to the flow of urine anywhere along the urinary tract. Dilatation of the renal pelvis and calyces can occur without obstruction and therefore hydronephrosis should not be taken to necessarily imply the presence of obstructive uropathy. Ultrasound

  • False -ve (i.e. obstruction present, no hydronephrosis)—acute onset of obstruction; in the presence of an intrarenal collecting system; with dehydration; misdiagnosis of dilatation of the calyces as renal cortical cysts (in acute ureteric colic, ultrasonography fails to detect hydro-nephrosis in up to 35% of patients with proven acute obstruction on IVU).
  • False +ve (i.e. hydronephrosis, no obstruction)—capacious extrarenal pelvis; parapelvic cysts; vesicoureteric reflux; high urine flow.

Diagnostic approach to the patient with hydronephrosis Patients with hydronephrosis may present either as an incidental finding of hydronephrosis on an ultrasound or CT done because of non-specific symptoms or it may be identified in a patient with a raised creatinine or presenting with loin pain. Symptoms, if present, will depend on the rapidity of onset of obstruction of the kidney (if that is the cause of the hydronephrosis), whether the obstruction is complete or partial, unilateral or bilateral, and whether the obstruction to the ureter is extrinsic to the ureter or is within its lumen. History

  • Severe flank pain suggests a more acute onset of obstruction and, if very sudden in onset, a ureteric stone may well be the cause. Pain induced by a diuresis (e.g. following consumption of alcohol) suggests a possible PUJO.
  • Anuria (the symptom of bilateral ureteric obstruction or complete obstruction of a solitary kidney).
  • If renal function is impaired, symptoms of renal failure may be present (e.g. nausea, lethargy, anorexia).
  • Extrinsic causes of obstruction (e.g. compression of the ureters by retroperitoneal malignancy) usually have a more insidious onset, whereas intrinsic obstruction (ureteric stone) is often present with severe pain of very sudden onset.
  • An increase in urine output may be reported by the patient due to poor renal concentrating ability.
  • Obstruction in the presence of bacterial urinary tract infection—signs and symptoms of pyelonephritis (flank pain and tenderness, fever) or sepsis.
Fig. 10.1 Hydronephrosis as seen on renal ultrasonography


  • Measure blood pressure—elevated in high pressure chronic retention (HPCR) due to benign prostatic obstruction (caused by fluid overload).
  • Bilateral oedema (due to fluid overload).
  • Abdominal examination—percuss and palpate for an enlarged bladder.
  • DRE (?prostate or rectal cancer) and in women, vaginal examination (?cervical cancer).
  • Check serum creatinine to determine the functional effect of the hydronephrosis.
  • Renal ultrasonography (if not already done).

IVU findings in renal obstruction

  • An obstructive (dense) nephrogram.
  • A delay in filling of the collecting system with contrast material.
  • Dilatation of the collecting system.
  • An increase in renal size.
  • Rupture of fornices (junction between renal papilla and its calyx) with urinary extravasation.
  • Ureteric dilatation and tortuosity.
  • A standing column of contrast material in the ureter.

Unilateral hydronephrosis KUB X-ray (a ureteric stone may be seen); CTU (or IVU) if stone suspected.

  • If no stone seen, but hydronephrosis is confirmed and ureter is non-dilated, the obstruction must be at the PUJ. In the absence of a ureteric stone visible on CTU, the diagnosis must be PUJO.
  • If no stone seen and ureter is dilated as well as kidney, ureteric TCC is likely. Arrange retrograde ureterography to identify site of obstruction, and ureteroscopy/ureteric biopsy.

Bilateral hydronephrosis

  • If the patient is in retention or has a substantial post-void residual urine volume, pass a catheter. If the elevated creatinine falls (and the hydronephrosis improves), the diagnosis is BOO, due, for example, to BPH, prostate cancer, urethral stricture, detrusor-sphincter dyssynergia. If the creatinine remains elevated, the obstruction affecting both ureters is higher ‘up stream’.
  • TRUS and prostatic biopsy if prostate cancer suspected on DRE, CT scan—looking for malignant bilateral ureteric obstruction, AAA.

Causes of hydronephrosis Unilateral

  • Obstructing ureteric stone
  • PUJO
  • Obstructing clot in ureter
  • Obstructing ureteric TCC
  • (Any of the causes listed below where the pathologic process has not yet extended to involve both ureters)


  • Bladder outlet obstruction (BOO)
    • BPH
    • Prostate cancer
    • Urethral stricture
    • Detrusor-sphincter dyssynergia
    • Posterior urethral valve
  • Bilateral ureteric obstruction at their level of entry into the bladder
    • Locally advanced cervical cancer
    • Locally advanced prostate cancer
    • Locally advanced rectal cancer
    • Poor bladder compliance (often combined with detrusor-sphincter dyssynergia): neuropathic bladder (spinal cord injury, spina bifida); post-pelvic radiotherapy
  • Periureteric inflammation
    • From adjacent bowel involved with inflammatory bowel disease (e.g. Crohn’s, ulcerative colitis) or diverticular disease
  • Retroperitoneal fibrosis
    • Idiopathic (diagnosed following exclusion of other causes)
    • Periarteritis—aortic aneurysm, iliac artery aneurysm
    • Post irradiation
    • Drugs—methysergide, hydralazine, haloperidol, LSD, methyldopa, beta blockers, phenacetin, amphetamines
    • Malignant—retroperitoneal malignancy (lymphoma, metastatic disease from e.g. breast cancer), post chemotherapy
    • Chemicals—talcum powder
    • Infection—TB, syphilis, gonorrhoea, chronic UTI
    • Sarcoidosis
  • Bilateral PUJO (uncommon)
  • Hydronephrosis of pregnancy (partly due to smooth muscle relaxant effect of progesterone, partly obstruction of ureters by fetus)
  • Hydronephrosis in association with an ileal conduit (a substantial proportion of patients with ileal conduit urinary diversion have bilateral hydronephrosis, in the absence of obstruction)
  • Bilateral ureteric stones (rare)

Management of ureteric strictures (other than PUJO) Definition A normal ureter undergoes peristalsis and therefore at any one moment at least one area of the ureter will be physiologically narrowed. A ureteric stricture is a segment of ureter which is narrowed and remains so on several images (i.e. it is a length of ureter which is constantly narrow). Causes Most ureteric strictures are benign and iatrogenic. Some follow impaction of ureteric stone for a prolonged period; malignant strictures—within wall of ureter (e.g. TCC ureter), extrinsic compression from outside wall of ureter (e.g. lymphoma, malignant retroperitoneal lymphadenopathy); retroperitoneal fibrosis (RPF) which may be benign (idiopathic, aortic aneurysm, post irradiation, analgesic abuse) or malignant (retroperitoneal malignancy, post chemotherapy). Mechanism of iatrogenic ureteric stricture formation Normally ischaemic:

  • Usually injury at time of open or endoscopic surgery (e.g. damage to ureteric blood supply or direct damage to ureter at time of colorectal resection, AAA graft, hysterectomy); at ureteroscopy—mucosal trauma (from ureteroscope or electrohydraulic lithotripsy), perforation of ureter (urine extravasation leading to fibrosis)
  • Radiotherapy in the vicinity of the ureter
  • Stricture of ureteroneocystostomy of renal transplant

Investigations The stricture may be diagnosed following investigation for symptoms (loin pain, upper tract infection) or may be an incidental finding on an investigation done for some other reason. The stricture may be diagnosed on a renal ultrasound (hydronephrosis), an IVU or CTU. A MAG3 renogram will confirm the presence of obstruction (some minor strictures may cause no renal obstruction) and establish split renal function. Where ureteric TCC is possible proceed with ureteroscopy and biopsy. ‘Treatment’ options

  • Nothing (symptomless stricture in an old patient with significant comorbidity or <25% function in an otherwise healthy patient with a normally functioning contralateral kidney).
  • Permanent JJ stent or nephrostomy, changed at regular intervals (symptomatic stricture in an old patient with significant comorbidity or <25% function in affected kidney with compromised overall renal function).
  • Dilatation (balloon or graduated dilator) (Figs. 10.2 and 10.3).
  • Incision + balloon dilatation (endoureterotomy by Acucise balloon; ureteroscopy or nephrostomy and incision e.g. by laser). Leave a 12Ch stent for 4 weeks.
Fig. 10.2 Balloon dilatation of a lower ureteric stricture
Fig. 10.3 The catheter used for balloon dilatation


  • Excision of stricture and repair of ureter (open or laparoscopic approach).
  • Nephrectomy.

Factors associated with reduced likelihood of a good outcome after endoureterotomy:

  • <25% function in kidney
  • Stricture length >1cm
  • Ischaemic stricture
  • Mid-ureteric stricture (compared with upper and lower)—tenuous blood supply
  • JJ stent size <12Ch

Ureteroenteric strictures (ileal conduits, ureteric implantation into neobladder) These are due to ischaemia and/or periureteral urine leak in the immediate post-operative period, which leads to fibrosis in the tissues around the ureter. In ileal conduits, the left ureter is affected more than right because greater mobilization is required to bring it to the right side and it may be compressed under the sigmoid mesocolon, both of which impair blood flow to the distal end of the ureter. P.409
Pathophysiology of urinary tract obstruction Effects of obstruction on renal blood flow and ureteric pressure Acute unilateral obstruction of a ureter (UUO) Leads to a triphasic relationship between renal blood flow (RBF) and ureteric pressure.

  • Phase 1 (up to 1.5h post obstruction): ureteric pressure rises, RBF rises (afferent arteriole dilatation).
  • Phase 2 (from 1.5–5h post obstruction): ureteric pressure continues to rise, RBF falls (efferent arteriole vasoconstriction).
  • Phase 3 (beyond 5h): ureteric pressure falls, RBF continues to fall (afferent arteriole vasoconstriction).

Acute bilateral obstruction of a ureter (BUO) or obstruction of a solitary kidney

  • Phase 1 (up to 1.5h post obstruction): ureteric pressure rises, RBF rises (afferent arteriole dilatation).
  • Phase 2 (from 1.5–5h post obstruction): ureteric pressure continues to rise, RBF is significantly lower than that during unilateral ureteric obstruction.
  • Phase 3 (beyond 5h): ureteric pressure remains elevated (in contrast to UUO). By 24 hours RBF has declined to the same level for both unilateral and bilateral ureteric obstruction.

In UUO, the decrease in urine flow through the nephron results in a greater degree of Na absorption, so Na excretion falls. Water loss from the obstructed kidney increases. Release of BUO is followed by a marked natriuresis, increased K excretion, and a diuresis (a solute diuresis). This is due to:

  • an appropriate (physiological) natriuresis, to excrete excessive Na which is a consequence of BUO
  • a solute diuresis from the accumulation of urea in extracellular fluid
  • a diminution of the corticomedullary concentration gradient, which is normally established by the countercurrent mechanism of the loop of Henle, and is dependent on maintenance of flow through the nephron—reduction of flow, as occurs in BUO, reduces the efficiency of the countercurrent mechanism (effectively, the corticomedullary concentration gradient is ‘washed out’).

There may also be accumulation of natriuretic peptides (e.g. ANP) during BUO which contributes to the natriuresis following release of the obstruction. P.411
Likelihood of recovery of renal function after release of obstruction In dogs with completely obstructed kidneys, full recovery of renal function after 7 days of UUO occurs within 2 weeks of relief of obstruction. 14 days of obstruction leads to a permanent reduction in renal function to 70% of control levels (recovery to this level taking 3–6 months after reversal of obstruction). There is some recovery of function after 4 weeks of obstruction, but after 6 weeks of complete obstruction there is no recovery. In humans, there is no clear relationship between the duration of BUO and the degree of recovery of renal function after relief of obstruction. P.412
Physiology of urine flow from kidneys to bladder Urine production by the kidneys is a continuous process. Its transport from the kidneys, down the ureter, and into the bladder occurs intermittently, by waves of peristaltic contraction of the renal pelvis and ureter (peristalsis = wavelike contractions and relaxations). The renal pelvis delivers urine to the proximal ureter. As the proximal ureter receives a bolus of urine it is stretched and this stimulates it to contract, while the segment of ureter just distal to the bolus of urine relaxes. Thus the bolus of urine is projected distally. The origin of the peristaltic wave is from collections of pacemaker cells in the proximal most regions of the renal calyces. In species with multiple calyces, such as humans, there are multiple pacemaker sites in the proximal calyces. The frequency of contraction of the calyces is independent of urine flow rate (it is the same at high and low flow rates) and it occurs at a higher rate than that of the renal pelvis. Precisely how frequency of contraction of each calyx is integrated into a single contraction of the renal pelvis is not known. All areas of the ureter are capable of acting as a pacemaker. Stimulation of the ureter at any site produces a contraction wave that propagates proximally and distally from the site of stimulation, but under normal conditions, electrical activity arises proximally and is conducted distally from one muscle cell to another (the proximal most pacemakers are dominant over these latent pacemakers). Peristalsis persists after renal transplantation and denervation and does not therefore appear to require innervation. The ureter does, however, receive both parasympathetic and sympathetic innervation, and stimulation of these systems can influence the frequency of peristalsis and the volume of urine bolus transmitted. At normal urine flow, the frequency of calyceal and renal pelvic contractions is greater than that in the upper ureter, and there is a relative block of electrical activity at the PUJ. The renal pelvis fills; the ureter below it is collapsed and empty. As renal pelvic pressure rises, urine is extruded into the upper ureter. The ureteric contractile pressures that move the bolus of urine are higher than renal pelvic pressures. A closed PUJ may prevent back-pressure on the kidney. At higher urine flow rates every pacemaker-induced renal pelvic contraction is transmitted to the ureter. To propel a bolus of urine the walls of the ureter must coapt (touch). Resting ureteric pressure is ~0–5cmH2O and ureteric contraction pressures range from 20 to 80cmH2O. Ureteric peristaltic waves occur 2–6 times per minute. The VUJ acts as a one-way valve under normal conditions, allowing urine transport into the bladder and preventing reflux back into the ureter. P.413
Ureter innervation Autonomic the ureter has a rich autonomic innervation.

  • Sympathetic—preganglionic fibres from spinal segments T10 to L2; post-ganglionic fibres arise from the coeliac, aorticorenal, mesenteric, superior and inferior hypogastric (pelvic) autonomic plexuses.
  • Parasympathetic—vagal fibres via coeliac to upper ureter; fibres from S2–4 to lower ureter.

Role of ureteric autonomic innervation is unclear. It is not required for ureteric peristalsis (though it may modulate this). Peristaltic waves originate from intrinsic smooth muscle pacemakers located in minor calyces of renal collecting system. Afferent upper ureter—afferents pass (alongside sympathetic nerves) to T10–L2; lower ureter—afferents pass (alongside sympathetic nerves and by way of pelvic plexus) to S2–4. Afferents subserve stretch sensation from renal capsule, collecting system of kidney (renal pelvis and calyces), and ureter. Stimulation of the mucosa of the renal pelvis, calcyes, and ureter also stimulates nociceptors, the pain so felt being referred in a somatic distribution to T8–L2 (kidney T8–L1, ureter T10–L2), in the distribution of the subcostal, iliohypogastric, ilioinguinal, or genitofemoral nerves. Thus, ureteric pain can be felt in the flank, groin, scrotum or labia, and upper thigh depending on the precise site in the ureter from which the pain arises.

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