C H A P T E R
58  
Urinary Tract Obstruction
Kevin P.G. Harris, Jeremy Hughes
DEFINITIONS
Obstructive uropathy refers to the structural or functional
changes in the urinary tract that impede normal urine flow.
Obstructive nephropathy refers to the renal disease caused by
impaired flow of urine or tubular fluid. Hydronephrosis refers to
dilation of the urinary tract. Importantly, hydronephrosis is not
synonymous with obstructive uropathy as it can occur without
functional obstruction to the urinary tract and can be absent in
established obstruction. Obstructive uropathy and nephropathy
frequently coexist, and their management requires close collabo­
ration between nephrologists and urologists. Some surgical
aspects of obstruction to the urinary tract are discussed in
Chapter 59.
Obstructive uropathy is classified according to the site, degree,
and duration of the obstruction. Acute or chronic obstruction
can occur anywhere in the urinary tract and includes intrarenal
causes (casts, crystals) and extrarenal causes. Acute or chronic
obstruction is further subdivided into upper urinary tract obstruc­
tion (usually unilateral obstruction occurring above the vesico­
ureteral junction) and lower urinary tract obstruction (usually
bilateral obstruction located below the vesicoureteral junction).
Complete obstruction of the urinary tract is termed high grade,
whereas partial or incomplete obstruction is termed low grade.
Unilateral obstruction in a patient with two normal kidneys
will not result in significant renal impairment because the con­
tralateral kidney compensates. However, bilateral obstruction or
the obstruction of a single functioning kidney will result in renal
failure. In acute urinary tract obstruction, changes are mainly
functional, whereas structural damage to the kidney results from
more chronic obstruction. The acute functional changes may
recover after the effective release of the obstruction, but struc­
tural changes may be permanent and lead to chronic renal
impairment. Urinary tract obstruction remains a major cause of
renal impairment worldwide.
ETIOLOGY AND PATHOGENESIS
The causes of obstructive uropathy affecting the upper and lower
urinary tracts are summarized in Figures 58.1 and 58.2.
Congenital Urinary Tract Obstruction
Congenital urinary tract obstruction occurs most frequently in
males, most commonly as a result of either posterior urethral
valves or pelviureteral junction obstruction. If obstruction occurs
early during development, the kidney fails to develop and
702
becomes dysplastic. If the obstruction is bilateral, there is a high
mortality rate as a result of severe renal failure. If the obstruction
occurs later in gestation and is low grade or unilateral, hydrone­
phrosis and nephron loss will still occur, but renal function may
be sufficient to allow survival, and such patients may not present
until later in childhood. Pelviureteral junction obstruction, if it
is mild, may not present until adulthood and in some patients
may be an incidental finding (Fig. 58.3). However, with increased
use and improved sensitivity of antenatal scanning, congenital
abnormalities of the urinary tract are now frequently identified
early, allowing prompt postnatal (and in some cases antenatal)
intervention to relieve the obstruction and hence to preserve
renal function. Congenital causes of obstruction are discussed
further in Chapter 50.
Acquired Urinary Tract Obstruction
Acquired urinary tract obstruction may affect either the upper
or lower urinary tract and can result from either intrinsic or
extrinsic causes. Intrinsic causes of obstruction may be intra­
luminal or intramural.
Intrinsic Obstruction
Intraluminal Obstruction  Intraluminal obstruction may result
from tubular intrarenal obstruction, such as the deposition of
uric acid crystals in the tubular lumen after treatment of hema­
tologic malignant neoplasms (tumor lysis syndrome). It may also
occur with the precipitation of Bence Jones protein in myeloma
and with the precipitation or crystal formation of a number of
drugs, including sulfonamides, acyclovir, methotrexate, and indi­
navir (see Chapter 66).
Extrarenal intraluminal obstruction in young adults is most
commonly caused by renal calculi (see Chapter 57). Calcium
oxalate stones are the most common and typically cause intermit­
tent acute unilateral urinary tract obstruction but rarely result
in marked chronic renal impairment. Less common causes of
urinary lithiasis, such as struvite stones, uric acid stones, and
cystinuria, are often bilateral and hence more likely to cause
long-term renal impairment. Renal calculi lodge more com­
monly in the calyx, pelviureteral junction, or vesicoureteral junc­
tion and at the level of the pelvic brim. Surgical management of
stones is discussed in Chapter 59. Intraluminal obstruction can
also result from a sloughed papilla after papillary necrosis or
blood clots after macroscopic hematuria (clot colic). Papillary
necrosis may occur in diabetes mellitus, sickle cell trait or disease,
analgesic nephropathy, renal amyloidosis, and acute pyelone­
phritis. Clot colic can occur with bleeding from renal tumors or
 CHAPTER 58  Urinary Tract Obstruction 703

Causes of Upper Urinary

Tract Obstruction
Intrinsic Causes Extrinsic Causes

Intraluminal Reproductive
Intratubular deposition of crystals system
(uric acid, drugs) Cervix: carcinoma
Stones Uterus: pregnancy, tumors,
Papillary tissue prolapse, endometriosis, pelvic
Blood clots inflammatory disease
Fungal ball Ovary: abscess, tumor, cysts
Prostate: carcinoma
Intramural Vascular system
Functional: pelvic-ureteral or Aneurysms: aorta, iliac vessels
vesicoureteral junction Aberrant arteries: pelviureteral
dysfunction junction
Anatomic: tumors (benign or Venous: ovarian veins, retrocaval
malignant) ureter
Infections, granulomas, strictures
Gastrointestinal
tract
Crohn’s disease
Pancreatitis
Appendicitis
Diverticulitis
Tumors
Retroperitoneal
space Figure 58.3  Intravenous urogram demonstrating pelviureteral
Lymph nodes junction obstruction. The study was performed in a previously asymp-
Fibrosis: idiopathic, drugs, or tomatic adult to investigate nonspecific right loin pain. There is unilateral
inflammatory
Tumors: primary or metastatic
(right side) dilation of the pelvicalyceal system. The ureter has not been
Hematomas visualized.
Radiation therapy

Surgical disruption or ureteral

ligation arteriovenous malformations, after renal trauma, and in patients
with polycystic kidney disease.
Figure 58.1  Causes of upper urinary tract obstruction. The most
common causes are in italics.
Intramural Obstruction  Intramural obstruction can result
from either functional or anatomic changes. Functional disorders
Causes of Lower Urinary include vesicoureteral reflux, adynamic ureteral segments (usually
at the junction of the ureter with the pelvis or bladder), and
Tract Obstruction neurologic disorders. The last may result in a contracted (hyper­
Urethral anatomic causes tonic) bladder or a flaccid (atonic) bladder, depending on whether
Urethal strictures: trauma, postinstrumentation, infections the lesion affects upper or lower motor neurons, and lead to
such as gonococcal urethritis, nongonococcal urethritis, impaired bladder emptying with vesicoureteral reflux. Bladder
tuberculosis
dysfunction is very common in patients with multiple sclerosis
Posterior urethral valves and after spinal cord injury and is also seen in diabetes mellitus,
Stones
Blood clots in Parkinson’s disease, and after cerebrovascular accidents. Some
Periurethral abscess drugs (anticholinergics, levodopa) can alter neuromuscular activ­
Phimosis ity of the bladder and result in functional obstruction, especially
Paraphimosis if there is preexisting bladder outflow obstruction (e.g., prostatic
Meatal stenosis
hypertrophy).
Urethral functional causes Anatomic causes of intramural obstruction of the upper
Anticholinergic drugs, antidepressants, levodopa urinary tract include transitional cell carcinoma of the renal
Prostate pelvis and ureter and ureteral strictures secondary to radio­
Benign prostatic hypertrophy therapy or retroperitoneal surgery. Rarely, obstruction may
Prostatic carcinoma
Prostatic calculi
result from ureteral valve malfunction, polyps, or strictures after
Prostatic infection therapy for tuberculosis. Intramural obstruction of the lower
urinary tract can result from urethral strictures, which are usually
Bladder anatomic causes
Bladder cancer secondary to chronic instrumentation or previous urethritis, or
Schistosomiasis (Schistosoma haematobium infection) malignant and benign tumors of the bladder. Infection with
Bladder calculi Schistosoma haematobium, when the ova lodge in the distal ureter
Bladder trauma, pelvic fracture and bladder, is a common cause of obstructive uropathy world­
Bladder functional causes wide; up to 50% of chronically infected patients develop ureteral
Neurogenic bladder: spinal cord defects or trauma, diabetes, strictures and fibrosis, with contraction of the bladder.
multiple sclerosis, Parkinson’s disease, cerebrovascular
accidents
Extrinsic Obstruction
Figure 58.2  Causes of lower urinary tract obstruction. The most The most common cause of extrinsic compression in women is
common causes are in italics. pressure from a gravid uterus on the pelvic rim; the right ureter
704 SECTION X  Urologic Disorders
is more commonly affected. It is usually asymptomatic, and the
changes resolve rapidly after delivery. Rarely, bilateral obstruc­
tion and acute kidney injury [AKI] may occur. Ureteral dilation
may frequently be seen in pregnancy as a result of hormonal
effects (especially progesterone) on smooth muscle, but this does
not indicate functional obstruction (see Chapter 41, Fig. 41.1).
Carcinoma of the cervix may also cause extrinsic obstruction
because direct extension of the tumor to involve the urinary tract
occurs in up to 30% of patients. Other pelvic pathologic pro­
cesses that can cause ureteral compression include benign and
malignant uterine and ovarian masses, abscesses, endometriosis,
and pelvic inflammatory disease. Compression of the ureters
outside the bladder may also occur with uterine prolapse.
Although rare (<0.5%), inadvertent ureteric ligation may occur
during surgical procedures, particularly those related to obstet­
rics and gynecology. Unilateral ligation may go undetected, but
AKI will result from bilateral ligation.
In men, the most common cause of extrinsic obstruction of
the lower urinary tract is benign prostatic hypertrophy. Carci­
noma of the prostate can also result in obstruction either from
direct tumor extension to the bladder outlet or ureters or from
metastases to the ureter or lymph nodes.
Retroperitoneal disease may also result in extrinsic obstruc­
tion of the ureters, as can metastases or extension of tumors from
the cervix, prostate, bladder, colon, ovary, and uterus. Primary
tumors of the retroperitoneum, such as lymphomas and sarco­
mas, can commonly cause obstruction. Obstruction can also
result from inflammatory conditions affecting the retroperito­
neum, such as Crohn’s disease and large bowel diverticulitis. In
Crohn’s disease, the obstruction is usually right sided as a result
of ileocecal disease. Less common pathologic processes include
retroperitoneal fibrosis, in which thick fibrous tissue extends
out from the aorta to encase the ureters and draw them medially
(Fig. 58.4). Retroperitoneal fibrosis may be idiopathic but can
result from inflammatory aortic aneurysms, certain drugs (e.g.,
Figure 58.4  Retrograde pyelogram showing idiopathic retroperi-
toneal fibrosis. Dilation of the pelvicalyceal system is clearly demon-
strated. The ureters, however, are not dilated, and the left ureter can be
seen being pulled medially as a result of encasement in thick fibrous
tissue.
β-blockers, bromocriptine, and methysergide), previous irradia­
tion, trauma or surgery, and granulomatous disease (e.g., tuber­
culosis, sarcoidosis). Ureteral compression may also be a result
of vascular abnormalities, including aneurysmal dilation of the
aorta or iliac vessels, aberrant vessels, and anatomic variations in
the location of the ureter (retrocaval ureter).
PATHOPHYSIOLOGY
Obstruction to the renal tract causes profound functional and
structural changes of the kidney.1 Initially, changes are predomi­
nantly functional and potentially reversible, but with time,
chronic and irreversible structural changes occur. Our under­
standing of the consequences of urinary tract obstruction stem
mainly from the study of animal models.2 Although many studies
have focused on the effects of complete ureteral obstruction in
rodents, investigators have also examined models of chronic
complete, partial, or reversible obstruction in adult and neonatal
animals.3 Available experimental data show little species to
species variation in the response to acute obstruction, suggesting
that similar changes are likely to occur in humans. The complex
effects of urinary tract obstruction on the kidney affect both
glomerular hemodynamics and tubular function.4
Changes in Glomerular Function
Glomerular filtration rate (GFR) declines progressively after the
onset of complete ureteral obstruction. Glomerular filtration
is determined by the mean hydraulic pressure gradient between
the glomerular capillary lumen and Bowman’s space, the renal
plasma flow, the ultrafiltration coefficient of the glomerular cap­
illary wall, and the mean oncotic pressure difference across the
glomerular wall. Obstruction can affect all of these, and the
effects vary with the duration of the obstruction, the hydration
state, and the presence or absence of a contralateral functioning
kidney.
After complete ureteral obstruction, there is an initial rise in
proximal tubular pressure. At the same time, afferent arteriolar
dilation occurs as a result of the generation of vasodilatory pros­
taglandins (e.g., prostacyclin, prostaglandin E2). Glomerular cap­
illary hydraulic pressure increases, but this does not offset the
rise in tubular pressure, and there is a net decrease in the hydrau­
lic pressure gradient across glomerular capillaries, resulting in an
80% decline in GFR.
About 2 to 5 hours after obstruction, renal blood flow begins
to decline, whereas intratubular pressure continues to increase.
Within 5 hours, proximal tubular pressure begins to decline
toward control values. From this time, the main determinant of
the decrease in GFR is the fall in intraglomerular capillary pres­
sure as a result of an increase in resistance of afferent arterioles.
This results in a progressive fall in renal plasma flow, which
reaches 30% to 50% of control values by 24 hours. Preferential
constriction of the preglomerular blood vessels lowers both
plasma flow and glomerular capillary pressure, resulting in a
greater decrement in GFR than in plasma flow and a fall in
filtration fraction. A falling filtration fraction also results from
diversion of blood to nonfiltering areas of the kidney or a reduc­
tion in the ultrafiltration coefficient. The relative changes in
ureteral pressure, renal plasma flow, and GFR are summarized
in Figure 58.5.
The intrarenal vasoconstriction results from the generation
of angiotensin II and thromboxane A2, the release of vasopressin
(antidiuretic hormone), and the decreased nitric oxide produc­

The Effects of Complete
Ureteral Obstruction
200
180 Ureteral pressure
Percentage of control values
Renal plasma flow
160
Glomerular filtration rate
140
120
100
80
60
40
20
0 tract obstruction often exhibit urinary acidification defects. This
0 2 4 6 8 10 12 14 16
Time postobstruction (hours)
Figure 58.5  The effects of complete ureteral obstruction. The rela-
tive changes in ureteral pressure, renal plasma flow, and glomerular filtra-
tion rate are shown with data from experimental studies of unilateral
ureteral obstruction in rats.
tion. Angiotensin II and thromboxane A2 may also reduce the
ultrafiltration coefficient.4,5 The central role of these two vaso­
constrictors has been demonstrated by studies in rats, in which
pretreatment with angiotensin-converting enzyme inhibitors and
thromboxane synthase inhibitors virtually normalized renal
function after the relief of short-term ureteral obstruction.6
Intrarenal angiotensin II generation occurs secondary to an
increase in renin release either through reduced delivery of
sodium and chloride to the distal nephron (macula densa mecha­
nism) or through a reduction in transmural pressure at the baro­
receptor as a consequence of the prostaglandin-dependent
dilation of the afferent arteriole. Generation of thromboxane A2
occurs in both glomeruli and infiltrating interstitial cells.
An interstitial leukocyte infiltrate, predominantly macro­
phages, develops in response to chemoattractants such as mono­
cyte chemoattractant protein 1 and osteopontin expressed by
tubular cells. This infiltrate plays a key role in the acute func­
tional changes after ureteral obstruction7 and is implicated in the
pathogenesis of the late structural changes that occur after
obstruction as macrophage depletion limits interstitial fibrosis.8
The extent to which glomerular function recovers after the
release of ureteral obstruction depends on the duration of the
obstruction. Whole-kidney GFR may return to normal after
short-term obstruction (days), whereas recovery may be incom­
plete after prolonged obstruction. Evidence from studies in rats
now suggests that even with shorter periods of obstruction
(72 hours), there may be a permanent loss of nephrons, and
whole-kidney GFR returns to normal only at the expense of
hyperfiltration (increase in single-nephron GFR) in the remain­
ing functional nephrons.9
Changes in Tubular Function
Abnormalities in tubular function are common in urinary tract
obstruction and are manifested as altered renal handling of elec­
trolytes and changes in the regulation of water excretion.4 The
degree and nature of the tubular defects after obstruction depend
in part on whether the obstruction is bilateral or unilateral.
These differences could result from the dissimilar hemodynamic
CHAPTER 58  Urinary Tract Obstruction 705
responses, different intrinsic changes within the nephron, differ­
ences in extrinsic factors (e.g., volume expansion and accumula­
tion of natriuretic substances in bilateral obstruction) between
the two states, or a combination of all three.
After ureteral obstruction, the ability to concentrate the urine
is markedly impaired, with maximum values of 350 to 400
mOsm/kg reported in the rat. Causative factors include a loss of
medullary tonicity, an overall decrease in GFR in deep nephrons,
and a reduced expression of sodium transporters.10 Also, the col­
lecting duct is unresponsive to vasopressin because of a reduction
in the expression of renal aquaporins that results from both
cyclooxygenase 2 activity11 and angiotensin II.12
Rats exhibit reduced expression of multiple acid-base trans­
porters after ureteral obstruction,13 and patients with urinary
18 may be detected only by exogenous acid loading, but hyperchlo­
remic acidosis caused by impaired distal acid secretion, hypo­
reninemic hypoaldosteronism (type 4 renal tubular acidosis), and
a combination of these findings have been described. This acidi­
fying defect results from a marked increase in bicarbonate excre­
tion or from a distal acidification defect, possibly as a result of
abnormalities of the H+-ATPase activity of intercalated cells of
the collecting duct after ureteral obstruction.
Obstruction alters renal potassium handling. In the presence
of a normal functioning contralateral kidney, potassium excre­
tion is reduced after relief of obstruction, either in proportion to
or perhaps even greater than the fall in GFR (i.e., fractional
excretion of potassium is unaltered or slightly reduced). There
is a defect in the distal potassium secretory mechanism after
unilateral obstruction that may be secondary to reduced respon­
siveness of that nephron segment to aldosterone. By contrast,
after release of bilateral ureteral obstruction, there is a marked
increase in both net and fractional potassium excretion. The
major mechanism by which potassium losses occur in this setting
is an increased delivery of sodium to the distal tubule, resulting
in an accelerated sodium-potassium exchange.
Recovery of tubular function after release of obstruction is
slow and may remain abnormal even after whole-kidney GFR
has returned to normal. In rats, acidification and potassium han­
dling abnormalities persist for at least 14 days and urinary con­
centrating ability is abnormal for up to 60 days after the release
of 24 hours of unilateral ureteral obstruction. These observations
are consistent with persistent alterations in distal tubular and
collecting duct function or a loss in functioning juxtaglomerular
nephrons after the release of the obstruction.
Histopathologic Changes
The morphologic alterations in renal architecture are similar
irrespective of the cause of the obstruction. Initially, there is
renal enlargement and edema with pelvicalyceal dilation (Fig.
58.6). Tubular dilation that predominantly affects the collecting
duct and distal tubular segments develops microscopically,
although cellular flattening and atrophy of proximal tubular cells
can also occur. Glomerular structures are usually preserved ini­
tially, although Bowman’s space may be dilated and contain
Tamm-Horsfall protein. Ultimately, some periglomerular fibro­
sis may develop.
Inadequately treated obstruction to the urinary tract eventu­
ally causes irreversible structural changes to the renal tract. The
renal pelvis becomes widely dilated, with the renal papillae either
flattened or hollowed out. The cortex and medulla become
grossly thinned, such that the kidney becomes a thin rim of renal
tissue surrounding a large saccular pelvis (Fig. 58.7). Histologic
706 SECTION X  Urologic Disorders
Figure 58.6  Autopsy specimen of a kidney showing the early
effects of ureteral obstruction. The kidney is enlarged and edematous
with pelvicalyceal dilation. There is good preservation of the renal
parenchyma.
Figure 58.7  Chronic ureteral obstruction. Surgical specimen of a
kidney showing gross dilation of the pelvicalyceal system and the reduc-
tion of the renal cortex to a thin fibrotic rim of tissue. There would have
been no prospect for any significant functional recovery in this kidney
after the relief of the obstruction.
examination demonstrates tubulointerstitial fibrosis and oblit­
eration of nephrons. There is tubular proliferation and apoptosis,
epithelial-mesenchymal transition, (myo)fibroblast accumula­
tion, increased extracellular matrix deposition, and tubular
atrophy. Ischemia as a result of the decreased renal blood flow
contributes to the parenchymal damage after obstruction. In
both genetic and interventional studies, an important pathologic
role for angiotensin II and transforming growth factor β (TGF-
β) has been established.14,15
Infiltrating macrophages play a pivotal role in the chronic
tissue injury and fibrosis that result from prolonged ureteral
obstruction (Fig. 58.8).8,16 Interstitial macrophages release profi­
brogenic factors such as TGF-β and galectin-3, which promote
progressive fibrosis. Local angiotensin II generation may also
stimulate the production of TGF-β by tubular cells. Treatments
shown to ameliorate chronic interstitial damage in experimental
obstructive uropathy include angiotensin receptor blockers,
pentoxifylline, simvastatin, and growth factors (such as bone
morphogenetic protein 7, hepatocyte growth factor, and epider­
mal growth factor); beneficial effects include a reduction in tubu­
lointerstitial inflammation and fibrosis, epithelial-mesenchymal
transdifferentiation, and tubular cell apoptosis.3 However, it is
pertinent that differences have been noted in the response of
adult and neonatal rodents to experimental therapeutic interven­
tions, and it is unclear whether such differences might occur in
humans.
EPIDEMIOLOGY
Obstructive uropathy is a common entity and can occur at all
ages. The prevalence of hydronephrosis at autopsy is 3.5% to
3.8%, with about equal distribution between males and females,17
although this underestimates the true incidence as these figures
exclude transient obstruction. The frequency and etiology of
obstruction vary in both sexes with age. Antenatal ultrasound has
significantly increased the detection rate of lower urinary tract
obstruction in the fetus.18 In children younger than 10 years,
obstruction is more common in boys; congenital urinary tract
anomalies, such as urethral valves and pelviureteral junction
obstruction, account for most cases. In North America, obstruc­
tive uropathy remains the most common cause of end-stage renal
disease (ESRD) in pediatric patients registered for renal trans­
plantation, accounting for 16% of cases. In addition, congenital
obstructive uropathy accounts for 0.7% of all patients (median
age, 31 years) maintained with renal replacement therapy, dem­
onstrating the continued impact of this disease into adult life.19
In young adults (<20 years of age), the frequency of urinary tract
obstruction is similar in males and females. Beyond 20 years of
age, obstruction becomes more common in women, mainly as a
result of pregnancy and gynecologic malignant neoplasms. The
peak incidence of renal calculi occurs in the second and third
decades of life with a threefold increased incidence in men. After
the age of 60 years, obstructive uropathy occurs more frequently
in men secondary to benign prostatic hypertrophy and prostatic
carcinoma. About 80% of men older than 60 years have some
symptoms of bladder outflow obstruction, and up to 10% have
hydronephrosis. In Europe, acquired urinary tract obstruction
accounts for 3% to 5% of the cases of ESRD in patients older
than 65 years, with most resulting from prostatic disease.20 In the
United States, the number of patients receiving renal replace­
ment therapy as a result of acquired obstruction continues to
increase, accounting for 1.4% of prevalent patients, although the
rise is not as rapid as with other causes of ESRD.19
CLINICAL MANIFESTATIONS
Obstruction of the urinary tract can present with a wide range
of clinical symptoms, depending on the site, degree, and duration
of obstruction.4 The clinical manifestations of upper and lower
urinary tract obstruction differ. Symptoms can be caused by
mechanical obstruction of the urinary tract (usually pain) or can
result from the complex alterations in glomerular and tubular
function that may occur in obstructive nephropathy. The latter
commonly present as alterations in urine volume and as renal
failure, which can be acute or chronic. For example, patients with
complete obstruction present with anuria and AKI, whereas
those with partial obstruction may present with polyuria and
polydipsia as a result of acquired vasopressin resistance. Alterna­
tively, there may be a fluctuating urine output, alternating from
oliguria to polyuria. However, obstructive uropathy and hence
obstructive nephropathy can occur without symptoms and with
minimal clinical manifestations. Thus, obstruction of the urinary
tract must be considered in the differential diagnosis of any
patient with renal impairment.
 CHAPTER 58  Urinary Tract Obstruction 707

Impairment of Function and Structural

Damage in Obstructive Nephropathy

Obstruction of
urinary tract

Mechanical stimulation Release of

Abrupt fall in GFR
Membrane stretch chemoattractants

Stimulation of Macrophage infiltration

intrinsic renal cells and interstitial
inflammation

Generation of Mediator and

vasoactive substances, cytokine generation,
e.g., Ang II, e.g., nitric oxide,
TXA2 TNF-α, TGF-β

Altered renal Peritubular Tubular cell Myofibroblast

hemodynamics capillary loss apoptosis accumulation and
and ischemia and tubular interstitial fibrosis
atrophy

Acute
kidney injury

Nephron loss

Irreversible renal injury and

scarring with resultant chronic
renal failure

Figure 58.8  Events leading to acute impairment of renal function and chronic structural damage in obstructive nephropathy. Ang II, angio-
tensin II; GFR, glomerular filtration rate; TGF-β, transforming growth factor β; TNF-α, tumor necrosis factor α; TXA2, thromboxane A2.

Pain Lower Urinary Tract Symptoms

Pain is a frequent complaint in patients with obstructive uropa­
thy, particularly in those with ureteral calculi. The pain is
believed to result from stretching of the collecting system or the
renal capsule. Its severity correlates with the degree of distention
and not with the degree of dilation of the urinary tract. On
occasion, the location of the pain helps determine the site of
obstruction. With upper ureteral or pelvic obstruction, flank
pain and tenderness typically occur, whereas lower ureteral
obstruction causes pain that radiates to the groin, the ipsilateral
testicle, or the labia. Acute high-grade ureteral obstruction
may be accompanied by a steady and severe crescendo flank
pain radiating to the labia, the testicles, or the groin (“classic”
renal colic). The acute attack may last less than half an hour
or as long as a day. In contrast, pain radiating into the flank
during micturition is said to be pathognomonic of vesicoureteral
reflux. By comparison, patients with chronic, slowly progressive
obstruction may have no pain or minimal pain during the course
of their disease. In such patients, any pain that does occur is
rarely colicky in nature. In pelviureteral junction obstruction,
pain may occur only after fluid loading to promote a high urine
flow rate.
Obstructive lesions of the bladder neck or bladder disease may
cause a decrease in the force or caliber of the urine stream,
intermittency, post-micturition dribbling, hesitancy, or nocturia.
Urgency, frequency, and urinary incontinence can result from
incomplete bladder emptying. Such symptoms commonly result
from prostatic hypertrophy and are frequently referred to as
prostatism, but they are not pathognomonic of this condition.
Urinary Tract Infections
Urinary stasis resulting from obstruction predisposes to urinary
tract infections, and patients may develop cystitis with dysuria
and frequency or pyelonephritis with loin pain and systemic
symptoms. Infection occurs more often in patients with lower
urinary tract obstruction than in those with upper urinary tract
obstruction.
Urinary tract infection in men or young children of either sex,
recurrent or persistent infections in women, infections with
unusual organisms such as Pseudomonas species, and a single
attack of acute pyelonephritis require further investigation to
exclude obstruction. Also, the presence of obstruction makes
708 SECTION X  Urologic Disorders
effective eradication of the infection difficult. Infections of the
urinary tract with a urease-producing organism such as Proteus
mirabilis predispose to stone formation. These organisms gener­
ate ammonia, which results in urine alkalinization and favors the
development of magnesium ammonium phosphate (struvite)
stones. Struvite calculi can fill the entire renal pelvis to form a
staghorn calculus that eventually leads to loss of the kidney if it
is untreated. Thus, stone formation and papillary necrosis can
also be a consequence of urinary tract obstruction as well as a
cause of obstruction.
Hematuria
Calculi may cause trauma to the urinary tract uroepithelium and
result in either macroscopic or microscopic hematuria. Any neo­
plastic lesion that obstructs the urinary tract, especially uroepi­
thelial malignant neoplasms, may bleed, resulting in macroscopic
hematuria. Urinary tract bleeding may also result in obstruction,
giving rise to clot colic when it is in the ureter or clot retention
when it is in the bladder.
Changes in Urine Output
Complete bilateral obstruction or unilateral obstruction of a
single functioning kidney such as a renal transplant will result in
anuria. However, when the lesion results in partial obstruction,
urine output may be normal or increased (polyuria). A pattern
of alternating oliguria and polyuria or the presence of anuria
strongly suggests obstructive uropathy.
Abnormal Physical Findings
Physical examination findings can be completely normal. Some
patients with upper urinary tract obstruction may have flank
tenderness. Long-standing obstructive uropathy may result in an
enlarged kidney that may be palpable. Hydronephrosis is a
common cause of a palpable abdominal mass in children. Lower
urinary tract obstruction causes a distended, palpable, and occa­
sionally painful bladder. A rectal examination and, in women, a
pelvic examination should be performed because they may reveal
a local malignant neoplasm or prostatic enlargement.
Acute or chronic hydronephrosis, either unilateral or bilat­
eral, may cause hypertension as a result of impaired sodium
excretion with expansion of extracellular fluid volume or from
the abnormal release of renin. On occasion, in patients with
partial urinary tract obstruction, hypotension occurs as a result
of polyuria and volume depletion.
Abnormal Laboratory Findings
Urinalysis may show hematuria, bacteriuria, pyuria, crystalluria,
and low-grade proteinuria, depending on the cause of obstruc­
tion. However, urinalysis may be completely negative despite
advanced obstructive nephropathy. In the acute phase of obstruc­
tion, urinary electrolyte values are similar to those seen in a
“prerenal” state, with a low urinary sodium (<20 mmol/l), a
low fractional excretion of sodium (<1%), and a high urinary
osmolality (>500 mOsm/kg). However, with more prolonged
obstruction, there is a decreased ability to concentrate the urine
and an inability to reabsorb sodium and other solutes. These
changes are particularly marked after the release of chronic
obstruction and give rise to the syndrome commonly referred to
as postobstructive diuresis. Obstructive nephropathy may cause
secondary polycythemia as a result of increased erythropoietin
production.
Increases in serum urea and creatinine are the most significant
laboratory abnormalities in patients with obstructive uropathy.
Electrolyte abnormalities may also occur, including a hyperchlo­
remic hyperkalemic (type 4) metabolic acidosis or hypernatremia
as a result of acquired nephrogenic diabetes insipidus. The devel­
opment of obstruction in patients with underlying chronic kidney
disease may accelerate the rate of progression. ESRD may occa­
sionally be caused by chronic obstructive uropathy that had been
asymptomatic.
Obstruction in Neonates or Infants
With the advent of routine antenatal scanning, the diagnosis
of hydronephrosis and genitourinary abnormalities is now fre­
quently made antenatally; however, unsuspected obstructive
uropathy may present in the postnatal period with failure to
thrive, voiding difficulties, fever, hematuria, or symptoms of
renal failure. Oligohydramnios at the time of delivery should
raise the suspicion of obstructive uropathy, as should the pres­
ence of congenital anomalies of the external genitalia. Nonuro­
logic anomalies, such as ear deformities, a single umbilical artery,
imperforate anus, or a rectourethral or rectovaginal fistula,
should prompt investigation for urinary tract obstruction. Any
infant with neurologic abnormalities may have a neurogenic
bladder with associated obstructive uropathy.
DIAGNOSIS
Prompt diagnosis of urinary tract obstruction is essential to allow
treatment to limit any long-term adverse consequences. Symp­
toms such as “renal colic” may suggest the diagnosis and prompt
appropriate investigation. However, urinary tract obstruction
should be actively considered in any patient with unexplained
acute or chronic kidney impairment. The diagnostic approach
has to be tailored to the clinical presentation (Fig. 58.9), but a
careful history and thorough physical examination are manda­
tory in all patients.
Urinalysis may provide valuable diagnostic information.
Hematuria suggests that the obstructing lesion is a calculus,
sloughed papilla, or tumor. Bacteriuria suggests urinary stasis,
especially in men or in pregnant women, but it may also be a
complication of chronic obstruction. The presence of crystals in
the urine sediment (cystine or uric acid) may be an indication
of the type of stone causing the ureteral obstruction or the intra­
renal obstruction resulting in AKI. Laboratory studies should
include an assessment of renal function (serum creatinine and
urea) and the measurement of serum electrolytes.
Imaging
Because the sites, causes, and consequences of obstruction to the
renal tract are so variable, no single imaging investigation can
diagnose renal tract obstruction with certainty. Thus, no single
imaging investigation should be relied on to definitively exclude
obstruction, especially if the clinical suspicion of obstruction is
high. Therefore, the approach to the patient with suspected
obstruction may require the complementary use of a number of
different imaging techniques.
Ultrasound is the most widely used imaging modality, but
the imaging approach to investigation of obstruction is chang­
ing. Computed tomography (CT) and magnetic resonance (MR)
 CHAPTER 58  Urinary Tract Obstruction 709

Investigation and Management of Suspected Urinary Tract Obstruction

Suspected obstruction

History/examination
Urinalysis and urine
culture
Assessment of renal
function

Lower tract Flank pain Ultrasound scan ±

symptoms ? Renal colic plain abdominal x-ray

Bladder CT scan Nondilated

ultrasound (or IVU) Dilation of PC system
PC system
scan

Obstruction
Large residual Impaired Normal
still suspected
volume renal function renal function

Catheterize Further imaging Consider

Nephrostomy to define lesion retrograde
(CT or MR scan) pyelography

Consider diuresis
Nephrostogram to renogram
define lesion

Plan definitive therapy

Figure 58.9  Investigation and management of suspected urinary tract obstruction. A full history and examination should be performed,
together with urinalysis, urine microscopy and culture, and measurement of renal function and serum electrolytes. Ultrasound is a useful first-line
investigation for any patient with suspected urinary tract obstruction. Helical (spiral) computed tomography (CT) is now the preferred imaging technique
when renal calculi are suspected. Either CT or magnetic resonance (MR) urography can accurately diagnose both the site and the cause of obstruction
in most cases. If there is renal impairment, insertion of a nephrostomy allows the effective relief of the obstruction and time for renal function to
recover while definitive therapy is planned. IVU, intravenous urography; PC, pelvicalyceal.

urography are useful in accurately diagnosing both the site
and the cause of obstruction, but the availability and expertise
in the use of different imaging techniques vary from center to
center, and older imaging techniques, such as intravenous urog­
raphy (IVU), can still be used effectively to evaluate patients
with obstructive uropathy. The role of imaging techniques is
shown in Figure 58.9. Imaging is also discussed further in
Chapter 5.
Ultrasound
Ultrasound can define renal size and demonstrate calyceal dila­
tion21 (Fig. 58.10) but depends on the expertise of the operator.
Although it is sensitive for detection of hydronephrosis, ultra­
sound will often not detect its cause. Pathologic change within
the ureter is difficult to demonstrate, and tiny stones will not
generate acoustic shadows. However, unilateral hydronephrosis
suggests obstruction of the upper urinary tract by stones, blood
clots, or tumors. Bilateral hydronephrosis is more likely to result
from a pelvic problem obstructing both ureters or obstruction of
the bladder outlet, in which case the bladder will also be enlarged.
Ultrasound is often combined with radiographic examination of
the kidneys, ureters, and bladder (often known as KUB) to ensure
that ureteral stones or small renal stones are not overlooked.
Ultrasound produces false-negative results in cases of nondi­
lated obstructive uropathy.21 Immediately after acute obstruction
(<24 hours), the relatively noncompliant collecting system may
not have dilated, such that an ultrasound examination may be
normal. Furthermore, if urine flow is low, as in severe dehydra­
tion or renal failure, there may be little dilation of the urinary
tract. Dilation may also be absent in slowly progressive obstruc­
tion when the ureters are encased by fibrous tissue (as in retro­
peritoneal fibrosis) or by tumor. The acoustic shadow of a
staghorn calculus can also mask dilation of the upper urinary
tract. The sensitivity of ultrasound for diagnosis of obstruction
can be improved by measuring the resistive index with color
Doppler ultrasound. A resistive index above 0.7 reflects the
increased vascular resistance present in obstruction and effec­
tively discriminates between obstructed and nonobstructed
kidneys.21 Such ultrasound techniques are particularly useful
when it is especially important to minimize radiation exposure,
710 SECTION X  Urologic Disorders
Figure 58.10  Renal ultrasound scan of a patient with obstruction
of the urinary tract causing hydronephrosis. The kidney is hydrone-
phrotic with dilation of the pelvicalyceal system; dilation of the upper
ureter is also clearly seen (arrows).
for example, in pregnant women and children, and in the
follow-up of patients requiring repeated imaging, such as after
extracorporeal shock wave lithotripsy.
Even in experienced hands, ultrasound may have a significant
false-positive rate, especially if minimal criteria are adopted to
diagnose obstruction. In addition, the echogenicity produced by
multiple renal cysts may be mistaken for hydronephrosis.
Ultrasound scanning can be used to assess bladder emptying
and should be undertaken in patients with lower urinary tract
symptoms. A large post-micturition residual volume suggests
bladder outflow obstruction, which should prompt further uro­
logic investigation and treatment.
The investigation of neonates with hydronephrosis diagnosed
antenatally depends on the grade of hydronephrosis identified.
Neonates with grade 1 or 2 hydronephrosis (no calyceal dilation)
undergo ultrasound scanning; neonates with grade 3 to 5 hydro­
nephrosis (indicating increasingly severe pelvicalyceal dilation)
require both ultrasound scanning and voiding cystourethrogra­
phy. This combination can distinguish megaureter resulting
from obstruction or reflux and diagnose posterior urethral valves
and ureteropelvic junction obstruction.
Plain Abdominal Radiography
A plain abdominal radiograph (or KUB) allows an assessment of
kidney size and contour and frequently demonstrates renal
calculi because about 90% of calculi are radiopaque.
Intravenous Urography
IVU was formerly the first-choice investigation for suspected
upper urinary tract obstruction. In patients with normal renal
function, it can usually define both the site and the cause of the
obstruction. However, the excretion of contrast material may be
poor or delayed in patients with low GFR because of a decreased
filtered load of the contrast agent, which is potentially nephro­
toxic. IVU is no longer a first-line investigation to diagnose
urinary tract obstruction, especially in patients with impaired
renal function.
Figure 58.11  CT scan of the abdomen showing a grossly hydro-
nephrotic kidney on the left (arrows mark dilated renal pelvis).
Dilated loops of small bowel are seen in the right hypochondrium.
Sequential sections demonstrated that the ureter was dilated along its
length and that there was a pelvic mass, which was responsible for both
bowel and left ureteral obstruction. The mass was subsequently shown
to be arising from a carcinoma of the colon.
Computed Tomography
Non–contrast-enhanced helical (spiral) CT scanning is used
increasingly as the primary imaging modality for the evaluation
of patients with acute flank pain.22 Stones are easily detected
because of their high density, and CT can provide an accurate and
rapid diagnosis of an obstructing ureteral calculus. In addition, it
provides useful information about the site and nature of the
obstructing lesion, especially when this is extrinsic to the urinary
tract (Fig. 58.11; see also Chapter 59, Fig. 59.2). CT demon­
strates retroperitoneal disease, such as para-aortic and paracaval
lymphadenopathy; retroperitoneal fibrosis is evident as increased
attenuation within the retroperitoneal fat, with encasement of
one or both ureters. Hematomas, primary ureteral tumors, and
polyps are also detectable. The diagnostic potential of CT is
enhanced by the administration of contrast material, but this may
limit its use in patients with renal impairment. In addition, it
involves considerable exposure to ionizing radiation.
Magnetic Resonance Urography
MR urography (combined with KUB) can diagnose ureteral
obstruction due to renal calculi with accuracy similar to that of
spiral CT scanning but without exposure to contrast medium or
ionizing radiation. The technique has less observer variability
and is more accurate than CT in detecting indirect evidence of
obstruction, such as perirenal fluid.23 MR urography can rapidly
and accurately depict the morphologic features of dilated urinary
tracts and provide information about the degree and level of
obstruction (Fig. 58.12).24 MR urography is a particularly attrac­
tive imaging modality for the evaluation of hydronephrosis in
children as it provides both anatomic and functional data and can
indicate whether the hydronephrosis is compensated (symmetric
changes of signal intensity of the nephrogram) or decompen­
sated.25 Signs of decompensation (acute on chronic obstruction)
include edema of the renal parenchyma, a delayed and increas­
ingly dense nephrogram, a delayed calyceal transit time, and a
more than 4% difference in the calculated differential renal func­
tion. MR urography is likely to be increasingly used in the future.
Retrograde Pyelography
Retrograde pyelography (Fig. 58.13; see also Fig. 58.4) may be
particularly useful to identify both the site and the cause of the
 CHAPTER 58  Urinary Tract Obstruction 711

Diuretic Isotopic Renography

Normal uptake and excretion of isotope

Renal isotope
activity
Time
Obstruction: delayed excretion

Renal isotope
activity
Furosemide

Time
Dilation without obstruction

Renal isotope
activity
Figure 58.12  MR urography showing obstructive
uropathy. T2-weighted MR image shows a proximal right-sided ureteral Furosemide
obstruction with an associated mild hydronephrosis. The obstruction was
secondary to a ureteral calculus.

Time

Figure 58.14  Diuretic isotopic renography. Idealized tracings for

normal, obstructed, and dilated kidneys without obstruction of the upper
urinary tract. In obstruction, there is delayed excretion of 99mTc-MAG3
despite administration of furosemide. When there is dilation of the upper
urinary tract without obstruction, the isotope is retained but is rapidly
excreted after the administration of furosemide.

obstruction. It is also helpful when nondilated urinary tract

obstruction is suspected or when there is a history of allergic
reactions to contrast material. Urinary tract infection that may
become overwhelming if obstruction is present is a contraindica­
tion to retrograde pyelography.

Diuresis Renography
A diuresis renogram using technetium Tc 99m mercaptoacetyl­
triglycine (99mTc-MAG3), combined with intravenous furose­
mide administered 20 to 30 minutes after injection of the isotope
(diuretic isotopic renography), can be used to distinguish between
simple dilation of the collecting system and true obstruction.26
Normally, there is a rapid washout of the isotope from the
kidney, and persistence of the isotope suggests a degree of
obstruction (Fig. 58.14). Poor renal function significantly limits
the usefulness of renography as the diuretic response to furose­
mide may be absent. Diuresis renography may also be used for
follow up of patients who have undergone surgical procedures
to relieve obstruction, such as a pyeloplasty.

Figure 58.13  Ureteral obstruction by a tumor. A retrograde pyelo-
gram shows that the tumor is within and obstructing the ureter (arrows).
Above the tumor, there is dilation of the ureter; but below it, the ureter
is of a normal caliber.
Pressure-Flow Studies
A pressure-flow study (Whitaker test27) involves puncture of the
collecting system with a fine-gauge needle to perfuse fluid (at
10 ml/min) with concurrent measurement of the differential
712 SECTION X  Urologic Disorders
pressure between the bladder and the collecting system; a pres­
sure above 20 cm H2O indicates obstruction. This test is now
rarely required.
Other Evaluations
Lower urinary tract obstruction may be evaluated by cystoscopy,
which allows a visual inspection of the entire urethra and the
bladder. Urodynamic studies (see Chapter 50, Fig. 50.17) can
assess bladder outlet obstruction, measure the residual urine
volume after voiding, and detect functional bladder abnormali­
ties. Although IVU with oblique films of the bladder and urethra
during voiding (excretory cystography) and after voiding can also
evaluate the site of lower urinary tract obstruction and the
amount of residual urine, this has now largely been superseded
by the use of ultrasound, CT, and MR urography.
DIFFERENTIAL DIAGNOSIS
Diagnostic uncertainty arises with nonobstructive dilation of the
upper urinary tract that may be seen with vesicoureteral reflux,
diuretic administration, diabetes insipidus, congenital megacaly­
ces, chronic pyelonephritis, and postobstructive atrophy. Diure­
sis renography or retrograde pyelography may be required to
exclude obstruction.
NATURAL HISTORY
Obstructive uropathy is potentially curable but will result in
progressive irreversible loss of nephrons and renal scarring if it
is left untreated (Fig. 58.15). ESRD will result if both kidneys
are affected or if there is only a solitary kidney. Outcome data
for obstructive uropathy are limited, but the exact prognosis
will depend on the pathologic process responsible for the
Figure 58.15  Pathology of chronic ureteral obstruction. This is a
section of the rim of renal tissue from the kidney shown in Figure 58.7.
The renal capsule is at the top, the urinary space at the bottom. The
cortex is considerably thinned, and only a few atrophic tubules remain
(arrows) within an interstitium comprising dense fibrous tissue and a
mononuclear cell infiltrate (blue-staining nuclei). No glomeruli can be
seen. This demonstrates why there would be no prospect for any signifi-
cant functional recovery in this kidney even after the relief of the
obstruction.
obstruction, the duration of the obstruction, and the presence or
absence of urosepsis. Relief of short-term obstruction (<1 to 2
weeks) usually results in an adequate return of renal function.
With chronic progressive obstruction (>12 weeks), there is often
irreversible and severe renal damage, and renal functional recov­
ery may be limited even after relief of the obstruction. A single-
center study identified 104 patients who presented with obstruc­
tive nephropathy.28 The mean GFR at presentation and at 3, 12,
and 36 months was 9 ml/min, 28 ml/min, 29 ml/min, and 30 ml/
min (patients on dialysis excluded), demonstrating significant but
nonprogressive renal impairment after relief of obstruction. It is
likely that the prognosis for renal functional recovery is better
the earlier the obstruction is diagnosed and relieved.
TREATMENT
General Considerations
Treatment is dictated by the location of the obstruction, the
underlying cause, and the degree of any renal impairment. If
renal impairment is present, the treatment of obstruction requires
close collaboration between nephrologists and urologists to
reduce the risks associated with the metabolic and electrolyte
consequences of renal failure and to optimize the chances for
long-term recovery of renal function. For example, complete
bilateral ureteral obstruction presenting as AKI is a medical
emergency and requires rapid intervention to salvage renal func­
tion. Prompt intervention to relieve the obstruction should result
in a rapid improvement in renal function. Dialysis should rarely
be required in patients with AKI secondary to obstruction except
to make the patient fit for intervention, for example, by improv­
ing life-threatening hyperkalemia or severe fluid overload. The
rapid relief of obstruction will limit permanent renal damage,
but renal function may not recover immediately if acute tubular
necrosis has resulted from obstruction or any accompanying
sepsis.
Some surgical aspects of the management of obstructive urop­
athy are discussed in Chapter 59. The site of obstruction fre­
quently determines the approach. If the obstruction is distal to
the bladder, a urethral catheter or, if this cannot be passed, a
suprapubic cystostomy will effectively decompress the kidneys.
Placement of nephrostomy tubes or cystoscopy and passage of a
retrograde ureteral catheter will relieve upper urinary tract
obstruction. Percutaneous nephrostomy (PCN) is generally the
appropriate emergency treatment of upper urinary tract obstruc­
tion, especially in the setting of AKI. PCN can be achieved with
local anesthesia and should allow rapid recovery of renal function
in most patients (>70%), avoiding the need for dialysis. After
relief of the obstruction by PCN, the exact site and nature of the
obstructing lesion can be determined by an antegrade study
infusing radiographic contrast material into the nephrostomy
tube (nephrostogram, Fig. 58.16), and time can be taken to plan
definitive therapy. Major complications of nephrostomy inser­
tion (abscess, infection, and hematoma) occur in less than 5% of
patients. If both kidneys are obstructed, the nephrostomy should
initially be placed in the kidney with the most preserved renal
parenchyma, although bilateral nephrostomies may be required
to maximize the potential for the recovery of renal function. If
infection occurs above a ureteral obstruction (pyonephrosis),
drainage of the kidney by PCN can play an important therapeu­
tic role together with appropriate antibiotics.
A nephrostomy can be used to gauge the potential for func­
tional recovery in patients with chronic obstruction. Failure of

A B
Figure 58.16  Nephrostogram. A nephrostomy has been placed percutaneously into the dilated collecting system of the kidney under ultrasound
control (A). After infusion of contrast material down the nephrostomy, the dilated pelvicalyceal system and upper ureter (B) and the lower ureter (C)
are outlined. The ureter is dilated along its length but tapers abruptly at the vesicoureteral junction (arrow). In this case, the obstruction was caused
by a radiolucent stone.
renal recovery after several weeks of nephrostomy drainage
strongly suggests irreversible structural damage and thus no
likely benefit from undertaking a more definitive surgical
correction of the obstructing lesion. Long-term nephrostomy
is increasingly used as a definitive therapy for patients who
are unsuitable for major surgical intervention and those
with incurable malignant disease (see Chapter 59 for further
discussion).
Ureteral obstruction requiring intervention occurs in approx­
imately 3% of renal transplant recipients.29 It can be treated
by nephrostomy and ureteric stenting, percutaneous incision
or balloon dilation of the stricture, or open surgical repair (see
Chapter 99).
Specific Therapies
Calculi are the most common cause of ureteral obstruction, and
their treatment includes relief of pain, elimination of obstruc­
tion, and treatment of infection (see Chapter 59). Ureteral
obstruction by papillary tissue, blood clots, or a fungus ball is
treated by procedures similar to those used for calculi. When
obstruction is caused by neoplastic, inflammatory, or neurologic
disease, there is unlikely to be spontaneous remission of the
obstruction, and some form of urinary diversion, such as an ileal
conduit, should be considered. Some obstructing neoplastic
lesions, such as lymphadenopathy from lymphoma, may respond
to chemotherapy. Management of malignant urinary tract
obstruction is discussed further in Chapter 59.
In idiopathic retroperitoneal fibrosis, ureterolysis (in which
the ureters are surgically freed from their fibrous encasement)
may be beneficial, especially in combination with corticosteroid
therapy to prevent recurrence. A retrospective study demon­
strated the effectiveness of ureteric stent insertion and cortico­
steroids in idiopathic retroperitoneal fibrosis.30
CHAPTER 58  Urinary Tract Obstruction 713
C
Functionally significant pelviureteral junction obstruction
should be corrected surgically by either an open (Anderson-
Hynes) pyeloplasty or a laparoscopic approach. The laparoscopic
approach results in significantly less morbidity and has good
long-term outcomes that are identical to those of the open pro­
cedure. Balloon dilation of the abnormal segment of ureter is
also possible, but the recurrence rate is high.
Benign prostatic hypertrophy is the most common cause of
lower urinary tract obstruction in men and may be mild and
nonprogressive. A patient with minimal symptoms, no infection,
and a normal upper urinary tract can continue with assessment
until he and his physician agree that further treatment is desir­
able. Medical therapy with either α-adrenergic blockers (e.g.,
tamsulosin) or 5α-reductase inhibitors (e.g., finasteride) may be
used in patients with moderate symptoms.31 α-Blockers relax the
smooth muscle of the bladder neck and prostate and decrease
urethral pressure and outflow obstruction. 5α-Reductase inhibi­
tors inhibit the conversion of testosterone to the active metabo­
lite dihydrotestosterone and reduce prostatic hypertrophy.
Combination therapy with these agents may be synergistic. Sur­
gical intervention with transurethral resection of the prostate is
generally required for failed medical treatment, debilitating
symptoms, urinary retention, recurrent infection, or evidence of
renal parenchymal damage. Holmium laser enucleation of the
prostate is a less invasive alternative to transurethral resection of
the prostate with good short-term and long-term outcomes.32
Urethral strictures in men can be treated by dilation or direct-
vision internal urethrotomy. The incidence of bladder neck and
urethral obstruction in women is low and treatment rarely
required. Suprapubic cystostomy may be necessary for bladder
drainage in patients unable to void after injury to the urethra or
in those who have an impassable urethral stricture.
When obstruction results from neuropathic bladder function,
urodynamic studies are essential to determine therapy. The goals
714 SECTION X  Urologic Disorders
of therapy are to establish the bladder as a urine storage organ
without causing renal parenchymal injury and to provide a mech­
anism for bladder emptying that is acceptable to the patient.
Patients may have either a flaccid atonic or an unstable hyper­
tonic bladder. Ureteral reflux and parenchymal damage may
develop in both cases, although it is more common in patients
with a hypertonic bladder. Asking the patient to void at regular
intervals may achieve satisfactory emptying of the bladder.
Patients with an atonic bladder and significant residual urine
retention associated with recurrent urosepsis need to undertake
clean intermittent self-catheterization. The aim should be to
catheterize four or five times per day to ensure that the amount
of urine drained from the bladder on each occasion is less than
400 ml. External sphincterotomy has also been used in men with
an atonic bladder and may relieve outlet obstruction and promote
bladder emptying, but it may cause urinary incontinence and the
need to wear an external collection device. In patients with a
hypertonic bladder, improvement in the storage function of the
bladder may be obtained with anticholinergic agents. On occa­
sion, chronic clean intermittent self-catheterization is necessary.
Whenever possible, chronic indwelling catheters should be
avoided in patients with a neurogenic bladder because they may
lead to the formation of bladder stones, urosepsis, and urethral
erosion, and they predispose to squamous cell carcinoma of the
bladder. Patients who have chronic indwelling catheters for more
than 5 years should have annual cystoscopic examinations. If
deterioration in renal function occurs despite conservative mea­
sures or there is intractable incontinence or a small contracted
bladder, an upper urinary tract diversion procedure such as an
ileal conduit may be required.
Management of Postobstructive Diuresis
Marked polyuria (postobstructive diuresis) is frequently seen
after the release of bilateral obstruction or obstruction of a single
functioning kidney. Release of unilateral obstruction rarely
results in a postobstructive diuresis33 despite the presence of
tubular dysfunction and a concentrating defect. This is due to
intrinsic differences in the tubular response to unilateral and
bilateral obstruction and, more important, the salt and water
retention and renal impairment that occurred in bilateral obstruc­
tion (not evident in unilateral obstruction because of the contra­
lateral normal kidney). The resultant increase in natriuretic
factors (including atrial natriuretic peptide) and substances able
to promote an osmotic diuresis, such as urea,34 promote an
appropriate postobstructive diuresis to excrete water and electro­
lytes that were retained during the period of obstruction.
However, the postobstructive diuresis may also be inappropriate
as a result of tubular dysfunction, and if it is not managed cor­
rectly, this may cause severe volume depletion and electrolyte
imbalance with continued renal dysfunction. Intravenous and
oral fluid replacement is usually required, with careful and
regular clinical assessment of fluid balance and serum electrolytes
to tailor the fluid replacement regimen appropriately. Once the
patient is deemed euvolemic, urine losses plus an allowance for
insensible losses should be replaced. Urine volume should be
measured regularly (hourly) to facilitate fluid administration, and
serum electrolytes should be measured at least daily and as fre­
quently as every 6 hours when there is a massive diuresis. Daily
weighing of the patient is also helpful. Replacement fluid regi­
mens should include sodium chloride, a source of bicarbonate,
and potassium. Calcium, phosphate, and magnesium replace­
ment may also be necessary.
If fluid administration is overzealous, the kidney will not
recover its concentrating ability, and a continued “driven” diure­
sis will result. It may then be necessary to decrease fluid replace­
ment to levels below those of the urine output and to observe
the patient carefully for signs of volume depletion.
Future Prospects
Understanding of the pathophysiologic changes that follow ure­
teral obstruction has allowed the development of rational inter­
ventional therapies to hasten the recovery of renal function and
to limit permanent renal damage. Although the best treatment
option in humans remains the prompt and effective relief of
the obstruction, the development and implementation of
improved imaging modalities that provide more sophisticated
anatomic and functional information (including intrarenal
oxygen content35) will undoubtedly refine management and
increase the data available for making key clinical decisions, such
as whether and when surgical intervention is required.
REFERENCES
1. Wen JG, Frøkiaer J, Jørgensen TM, et al. Obstructive nephropathy: An
update of the experimental research. Urol Res. 1999;27:29-39.
2. Harris KPG. Models of obstructive nephropathy. In: Gretz N, Strauch
M, eds. Experimental and Genetic Rat Models of Chronic Renal Failure.
Basel: Switzerland; 1993:156-168.
3. Chevalier RL, Forbes MS, Thornhill BA. Ureteral obstruction as a
model of renal interstitial fibrosis and obstructive nephropathy. Kidney
Int. 2009;75:1145-1152.
4. Klahr S, Harris KPG. Obstructive uropathy. In: Seldin D, Giebisch G,
eds. The Kidney: Physiology and Pathophysiology. 2nd ed. New York: Raven
Press; 1992:3327-3369.
5. Klahr S, Harris K, Purkerson ML. Effects of obstruction on renal func­
tions. Pediatr Nephrol. 1988;2:34-42.
6. Purkerson ML, Klahr S. Prior inhibition of vasoconstrictors normalizes
GFR in postobstructed kidneys. Kidney Int. 1989;35:1305-1314.
7. Harris KP, Schreiner GF, Klahr S. Effect of leukocyte depletion on the
function of the postobstructed kidney in the rat. Kidney Int. 1989;36:
210-215.
8. Henderson NC, Mackinnon AC, Farnworth SL, et al. Galectin-3 expres­
sion and secretion links macrophages to the promotion of renal fibrosis.
Am J Pathol. 2008;172:288-298.
9. Bander SJ, Buerkert JE, Martin D, et al. Long-term effects of 24-hr
unilateral ureteral obstruction on renal function in the rat. Kidney Int.
1985;28:614-620.
10. Li C, Wang W, Kwon TH, et al. Altered expression of major renal Na
transporters in rats with bilateral ureteral obstruction and release of
obstruction. Am J Physiol Renal Physiol. 2003;285:F889-F901.
11. Nørregaard R, Jensen BL, Li C, et al. COX-2 inhibition prevents down­
regulation of key renal water and sodium transport proteins in response
to bilateral ureteral obstruction. Am J Physiol Renal Physiol. 2005;289:
F322-F333.
12. Jensen AM, Li C, Praetorius HA, et al. Angiotensin II mediates down­
regulation of aquaporin water channels and key renal sodium transport­
ers in response to urinary tract obstruction. Am J Physiol Renal Physiol.
2006;291:F1021-F1032.
13. Wang G, Li C, Kim SW, et al. Ureter obstruction alters expression of
renal acid-base transport proteins in rat kidney. Am J Physiol Renal
Physiol. 2008;295:F497-F506.
14. Misseri R, Meldrum KK. Mediators of fibrosis and apoptosis in obstruc­
tive uropathies. Curr Urol Rep. 2005;6:140-145.
15. Bascands JL, Schanstra JP. Obstructive nephropathy: Insights from
genetically engineered animals. Kidney Int. 2005;68:925-937.
16. Ricardo SD, Diamond JR. The role of macrophages and reactive
oxygen species in experimental hydronephrosis. Semin Nephrol. 1998;18:
612-621.
17. Bell ET. Renal Diseases. Philadelphia: Lea & Febiger; 1946.
18. Lissauer D, Morris RK, Kilby MD. Fetal lower urinary tract obstruction.
Semin Fetal Neonatal Med. 2007;12:464-470.
19. U.S. Renal Data System, USRDS 2005. Annual Data Report: Atlas of
End-Stage Renal Disease in the United States. Bethesda, Md: National

Institutes of Health, National Institute of Diabetes and Digestive and
Kidney Diseases; 2005.
20. Sacks SH, Aparicio SA, Bevan A, et al. Late renal failure due to prostatic
outflow obstruction: A preventable disease. BMJ. 1989;298:156-159.
21. Mostbeck GH, Zontsich T, Turetschek K. Ultrasound of the kidney:
Obstruction and medical diseases. Eur Radiol. 2001;11:1878-1889.
22. Pfister SA, Deckart A, Laschke S, et al. Unenhanced helical computed
tomography vs intravenous urography in patients with acute flank pain:
Accuracy and economic impact in a randomized prospective trial. Eur
Radiol. 2003;13:2513-2520.
23. Regan F, Kuszyk B, Bohlman ME, et al. Acute ureteric calculus obstruc­
tion: Unenhanced spiral CT versus HASTE MR urography and abdomi­
nal radiograph. Br J Radiol. 2005;78:506-511.
24. Blandino A, Gaeta M, Minutoli F, et al. MR pyelography in 115 patients
with a dilated renal collecting system. Acta Radiol. 2001;42:532-536.
25. Grattan-Smith JD, Little SB, Jones RA. MR urography evaluation of
obstructive uropathy. Pediatr Radiol. 2008;38(Suppl 1):S49-S69.
26. O’Reilly PH. Diuresis renography 8 years later: An update. J Urol.
1986;136:993-999.
27. Whitaker RH, Buxton-Thomas MS. A comparison of pressure flow
studies and renography in equivocal upper urinary tract obstruction.
J Urol. 1984;131:446-449.
28. Ravanan R, Tomson CR. Natural history of postobstructive nephropa­
thy: A single-center retrospective study. Nephron Clin Pract. 2007;105:
c165-c170.
CHAPTER 58  Urinary Tract Obstruction 715
29. Faenza A, Nardo B, Catena F, et al. Ureteral stenosis after kidney trans­
plantation. A study on 869 consecutive transplants. Transplant Int. 1999;
12:334-340.
30. Fry AC, Singh S, Gunda SS, et al. Successful use of steroids and ureteric
stents in 24 patients with idiopathic retroperitoneal fibrosis: A retrospec­
tive study. Nephron Clin Pract. 2008;108:c213-c220.
31. Beckman TJ, Mynderse LA. Evaluation and medical management of
benign prostatic hyperplasia. Mayo Clin Proc. 2005;80:1356-1362.
32. Suardi N, Gallina A, Salonia A, et al. Holmium laser enucleation of the
prostate and holmium laser ablation of the prostate: Indications and
outcome. Curr Opin Urol. 2009;19:38-43.
33. Gillenwater JY, Westervelt FBJ, Vaughan EDJ, et al. Renal function after
release of chronic unilateral hydronephrosis in man. Kidney Int.
1975;7:179-186.
34. Harris RH, Yarger WE. The pathogenesis of post-obstructive diuresis.
The role of circulating natriuretic and diuretic factors, including urea.
J Clin Invest. 1975;56:880-887.
35. Thoeny HC, Kessler TM, Simon-Zoula S, et al. Renal oxygenation
changes during acute unilateral ureteral obstruction: Assessment with
blood oxygen level–dependent MR imaging—initial experience. Radiol-
ogy. 2008;247:754-761.