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5 .3
C urriculum in Urology
Renal Failure and Androlo-
gy
Obstructive Nephropathy:
Causes and Management
Patrick O’Boyle, Tim Porter
Department of Urology, Taunton and Somerset Hospital, Taunton, UK
Obstructive nephropathy is the end result
of a variety of diseases which cause partial or
complete blockage of drainage from both
kidneys, or a single kidney, or part of one kid-
ney.
Potentially the deterioration in renal
function can be halted or reversed by relief
of the obstruction.
The end result for the individual patient
depends on the duration and degree of
obstruction and in particular the presence of
infection. The relative function of the con-
tralateral kidney is important when a single
unit is involved. The administration of cer-
tain medications, particularly non-steroidal
anti-inflammatory drugs, angiotensin-con-
verting enzyme (ACE) inhibitors and antibi-
otics during the period of obstruction, may
accelerate the decline in renal function.
Sudden onset, bilateral, complete ob-
struction leads to acute renal failure with
Patrick O’Boyle
Department of Urology, Taunton and Somerset Hospital,
Musgrove Park Hospital, Taunton, Somerset, TA1 5DA (UK)
Tel. +44 1823 342 103, Fax +44 1823 343 571
associated metabolic sequelae of acidosis
and hyperkalaemia. More frequently in uro-
logical practice there is gradual onset with
the clinical findings of chronic renal impair-
ment.
The pathophysiological changes which
occur in the kidney have been extensively
studied in both humans and animal experi-
ments. The latter have the benefit of provid-
ing conditions which can be controlled effec-
tively and models of partial or complete
renal obstruction are readily simulated.
Unfortunately many of the observations can-
not be applied directly to the human situa-
tion, for example the length of time follow-
ing obstruction after which the renal effects
will become irreversible.
This article reviews the pertinent knowl-
edge relating to animal and human studies
after unilateral and bilateral ureteric
obstruction.
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Table 1. A classification of obstructive nephropathy
Obstructive nephropathy
Complete or partial
Acute or chronic
Unilateral Bilateral ureteric obstruction
Infra-vesical Supra-vesical
Causes of Obstructive Nephropathy
The incidence of human obstructive uropa-
thy has a bimodal distribution peaking in child-
hood and at 60 years of age [1, 2]. It is the com-
monest cause of end-stage renal failure in chil-
dren.
The reasons for obstruction vary with the
age and sex of the patient. In early life devel-
opmental abnormalities predominate, while in
the young adult and in middle age calculus
obstruction, which may be transient, is fre-
quently encountered. Gynaecological malig-
nancy and iatrogenic obstruction affect the
middle-aged female. In the older male prostat-
ic enlargement, both benign and malignant, is
the major offender.
A working classification of obstructive
uropathy is shown in table 1.
The common causes of obstructive uropa-
thy are listed in table 2.
It is appropriate to consider the changes
which have been demonstrated in studies of
kidney function following obstruction of the
ureter. There are differences which are impor-
tant for renal preservation. Essentially unilat-
eral obstruction results in a shutting down of
the affected kidney in an attempt to preserve
renal function. In bilateral obstruction and
obstruction of the solitary kidney, the renal
mass does not have the option of beneficial
compensatory changes in the unobstructed
unit and thus the ability to recover in the long
term is impaired.
2 nephritis exhibits a cellular infiltrate with col-
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Table 2. Some causes of obstructive nephropathy
A Infravesical
Urethral stricture, posterior urethral valves
Prostatic benign hypertrophy, carcinoma
B Supravesical
1 Extrinsic obstruction
– Vascular lesions
Retroperitoneal great vessel aneurysms: conditions
associated with graft repairs
Arterial and venous anomalies, including retrocaval
ureter
– Obstetric and gynaecological lesions
Benign and malignant, including pregnancy,
uterine prolapse, endometriosis, and
intraoperative injury
– Gastrointestinal lesions
Crohn's disease, diverticulitis, and appendiceal
pathology
Pancreatitis
– Retroperitoneal conditions
Retroperitoneal fibrosis, following DXT,
haemorrhage, infection, retroperitoneal
tumours, lymphocele
2 Intraluminal/mural obstruction
Stone disease
Haematoma
Transitional cell carcinoma
Sloughed renal papilla
Fungus ball
Pelviureteric junction obstruction
TB
Anatomical and Physiological
Changes in Obstructive Nephropathy
The anatomical and physiological changes
in obstructive nephropathy have been exten-
sively studied predominantly in animal models
[4–6]. When obstructed the kidney becomes
acutely oedematous with an initial increase in
bulk and weight mainly due to accumulation
of tissue fluid. If unrelieved, atrophic changes
become more marked over the ensuing weeks
with a corresponding decrease in parenchymal
mass. The ureter proximal to the obstruction
dilates, increases in length, and develops asso-
ciated smooth muscle hypertrophy.
Microscopically the findings of long-stand-
ing obstruction are of a non-specific interstitial
nephritis with tubular changes of collapse in
unilateral obstruction, as opposed to dilatation
in bilateral obstruction. Histologically the
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Table 3. Molecular changes leading to interstitial fibrosis
qAngiotensin II levels
Q
qTGF-b1 mRNA
Q Klahr [2].
qTGF-b1
Q
QMMPs qTIMPs
qmRNA for ECM
components (collagens) Q Q
Q els [8, 9]. The presence of apoptosis signals the
qCollagen deposition QDegradation of
ECM components
Q
Accumulation of ECM components
MMP = Matrix metalloproteinase; TIMP = tissue inhibitor
of MMP; TGF-b1 = transforming growth factor b1; ECM =
extracellular matrix. Adapted from Klahr [2].
lagen deposition and fibrosis. This is particular-
ly marked around the Bowman's capsule
where the changes may be irreversible and are
first seen with light microscopy around the
glomerulus at 28 days. With electron mi-
croscopy, however, changes are apparent in the
glomerular basement membrane after only
30 h [1]. The pathogenesis appears to involve
disordered extracellular matrix metabolism
[6a]. In animal models the interstitial space is
expanded with a mononuclear cell infiltrate
which consists primarily of macrophages, but
also includes cytotoxic and suppressor T lym-
phocytes. These seem to be recruited in
response to the release of chemoattractant mol-
ecules by the renal tubular cells and intersti-
tium as a response to obstruction. The mole-
cules include transforming growth factor (TGF-
b), intercellular adhesion molecule-1, osteo-
pontin, and monocyte chemoattractant pep-
tide-1 [2]. Thromboxane A2 (TxA2) contributes
to the vascular changes and specifically to vaso-
constriction.
Fibroblast and interstitial cell proliferation
together with deposition of collagen I, III and
IV plus fibronectin lead to tubular basement
membrane thickening after 2 weeks of unilat-
eral obstruction [7]. The interactions between
chemoactive molecules is complex. Enalapril
has been shown to block the increased expres-
sion of TGF-b1 suggesting a primary role for
Obstructive Nephropathy: Causes and Management
angiotensin II in obstruction. A suggested path-
way for the development of interstitial fibrosis
in obstructive nephropathy is in table 3. For an
indepth discourse the reader is referred to
Prolonged ureteric ligation results in hy-
dronephrosis and tissue loss with tubular cell
apoptosis reaching a peak at 30 days in rat mod-
irreversibility of renal damage [2, 9]. This is
associated in the rat with upregulation of P53
expression [2].
Physiological Changes
The variables which have been measured
following experimentally induced ureteric
obstruction include: (1) ureteric pressure; (2)
renal blood flow (RBF); (3) glomerular-filtra-
tion rate (GFR), and (4) tubular function.
Ureteric Pressure
In the aftermath of acute complete ureteric
obstruction a triphasic series of changes occurs
over a period of 18 h [4]. These changes tend
to be protective to the kidney with parallel and
often inverse effects on the contralateral, unob-
structed kidney (table 4). The physiological
changes are reflected in an initial intense effort
to overcome the loss of contractility at the lev-
el of the obstruction. This is apparent in the first
3 h as waves of increased frequency and ampli-
tude. Dissipation of the initially increased intra-
luminal pressure occurs via pyelovenous,
pyelolymphatic and pyelotubular backflow,
and in some cases more dramatically by rup-
ture and extravasation from the renal pelvis
[10].
After 24 h of complete obstruction the
ureteric pressure falls to 50% of peak levels,
that is to pre-obstructive ‘normal’ levels or
below. It continues to decrease over 6–8 weeks
of continued obstruction. Microscopically col-
lapsed tubules and glomeruli are seen suggest-
ing a pre-glomerular arteriolar constriction.
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Table 4. Response to acute obstruction
Ureteric pressure
Phase 1 (0–90 min) Increase to
50–70 mm Hg
Phase 2 (90 min to 5 h) Plateau
Phase 3 (5–18 h) Gradual decrease in
parallel with reduced
renal blood flow
Renal Blood Flow
The kidney responds to obstruction initially
by an increase in RBF due to vasodilatation of
the afferent arteriole presumably in an attempt
to maintain the GFR. The mediators for the
phases of change in RBF appear to be
eicosanoidal since the initial increase in blood
flow and related increase in ureteric pressure
can be prevented by administration of non-
steroidal anti-inflammatory drugs acting to
inhibit prostaglandin formation. A relative
increase in PGE2 is also seen in the non-
obstructed moiety.
Angiotensin II and TxA2 have a vasocon-
strictor role in the obstructed kidney resulting
in effective shutdown of that side with transfer
of function to the remaining normal renal
mass. Suppression of these pathways by ACE
inhibitors or prostaglandin synthetase inhib-
itors may accelerate injury [11].
The blood flow to the affected kidney con-
tinues to fall to around 12% of control levels at
8 weeks, though this is not of uniform distrib-
ution in the renal substance. A relative
decrease in the proportion of blood flow to the
outer cortex is noted with a redistribution of
flow to the inner cortex and to the medulla
[12]. The balance between the effects of the
renin-angiotensin and prostaglandin-throm-
boxane systems on RBF are not fully under-
stood. Initial studies in canine models using
indomethacin and thromboxane synthetase
4 inhibitors confirm the enhanced levels of PGE2
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GFR Renal blood flow
Initial sharp fall Initial increase
due to pre-glomerular
vasodilatation
Reduced to Reduced with
52% at 4 h post-glomerular rise
in resistance
Reduced to Progressive reduction
23% at 12 h with pre-glomerular
2% at 48 h vasoconstriction
and TxA2 following obstruction [13]. The renin
secretion effects can be reversed by cyclo-oxy-
genase pathway inhibition. Histamine via H1
receptors and atrial natriuretic peptide are also
likely to be involved in the RBF changes which
are unaffected by adrenergic blockage. The
renin-angiotensin system is important in both
renal perfusion and in renal development [14].
Inhibition of ACE and angiotensin II receptor
blockade attenuate the increased expression of
TGF-b1 in tubular cells and may slow the
fibrotic process in obstructed kidneys via
increased bradykinin levels and nitric oxide
generation [2]. The balance of effect of ACE
inhibitors in the acute obstructive phase lies
between the protection against the fibrosing
processes and the vascular effects on the
glomerular arteriole which may compromise
GFR.
Glomerular Filtration Rate
Following ureteric obstruction the GFR falls
mainly due to decreased afferent arteriolar
pressure which reduces blood flow and conse-
quently the glomerular capillary pressure. The
increase in intratubular pressure resulting from
obstruction exacerbates the situation within
the glomerulus. The selective diversion of RBF
to the cortical areas may also play a part in
reducing the ultrafiltration coefficient of the
glomerular capillary wall and consequently
GFR. The difference in hydrostatic pressure
between the glomerular capillary lumen and
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Bowman's space, together with the mean
oncotic pressure gradient across the capillary
wall is critical to the maintenance of GFR fol-
lowing obstruction.
Renal Tubular Function
The urinary concentrating ability is affected
relatively early by obstruction with the pro-
duction of large volumes of hypotonic urine.
The tubular effects of antidiuretic hormone
may be blocked by PGE2 which is significantly
increased in the obstructed state.
Acidification is likewise impaired with the
development of renal tubular acidosis and the
inability to acidify the urine in response to
ammonium chloride provocation. Ammonia
excretion, titratable acidity, bicarbonate
absorption and distal tubule hydrogen ion
excretion are all adversely affected.
The fractional excretion of potassium is
decreased after 24 h of obstruction in both ani-
mal and human systems resulting in hyper-
kalaemia [12]. Finally, following the increase
in tubular intraluminal pressure both proximal
and distal tubules exhibit increased permeabil-
ity to creatinine, mannitol and sucrose [1]:
(1) urinary concentrating ability impaired;
(2) defective acidification; (3) development of
hyperkalaemia, and (4) increased tubular per-
meability.
Features of Chronic Obstruction
Metabolic Pathways
Following ureteric obstruction a transfer
from aerobic to anaerobic renal metabolism is
seen. This is clearly important in terms of
decreased RBF, but also has implications in
terms of the redistribution of intra-renal blood.
A resultant deterioration in fatty acid and
a-keto-glutarate utilisation occurs with an
eventual loss of renal gluconeogenesis. This
may be irreversible after 6 weeks of obstruc-
tion.
Obstructive Nephropathy: Causes and Management
Effects on Renal Development
In the neonatal rat unilateral ureteral
obstruction (UUO) may result in delayed mat-
uration and impairment of renal growth [8].
This may be a result of TGF-b1 activation by the
renin-angiotensin system. Increased apoptosis
relating to decreased bcl-2 expression has been
implicated. In the adult rat protection may be
conveyed by expression of a glycoprotein clus-
tering.
Other Features of Obstruction
Polycythaemia may occur probably in
response to erythropoietin. Chronically, how-
ever, uraemia may result in anaemia. The
serum urea is increased disproportionately as a
result of distal tubular reabsorption. Plasma
calcium and phosphate levels decrease. Hyper-
tension appears to be volume related as a con-
sequence of salt and water retention. Hyper-
tension as a result of chronic unilateral obstruc-
tion appears to be a relatively uncommon
event.
Differences between Unilateral and
Bilateral Ureteric Obstruction
The changes described for bilateral ureteric
obstruction are mirrored in obstruction of the
solitary kidney. However:
(1) The overall RBF and ureteric pressure
changes in bilateral ureteric obstruction (BUO)
are not apparent as the characteristic triphasic
pattern.
(2) Following a similar intial increase in RBF
over the first 1–2 h intra-renal resistance
increases markedly and RBF falls to a much
lower level than in UUO over the following
24 h.
(3) The bilaterally obstructed system does
not have the benefit of compensatory changes
in an unobstructed kidney and thus cannot
close down to protect function as seems to be
the aim in UUO. Ureteric pressure rises and
remains high. In an attempt to maintain GFR
the preglomerular (afferent) arteriole remains
maximally dilated, whereas in UUO this is a rel-
atively short-lasting state.
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(4) RBF is decreased in BUO although the
medullo-cortical redistribution of flow noted in
unilateral obstruction does not occur [4]. The
decreased filtration in juxtamedullary neph-
rons so marked in UUO is not therefore appar-
ent in bilateral obstruction.
(5) GFR is reduced in both circumstances,
but for different reasons. In UUO there is vaso-
constriction in the afferent glomerular arteriole
with tubular collapse microscopically evident.
In BUO the GFR is reduced as a result of
increased proximal tubular pressure and
despite efferent arteriolar constriction.
(6) Following relief of obstruction natriure-
sis and diuresis occur in BUO but not UUO.
Serum atrial natriuretic peptide (ANP) is ele-
vated in BUO as a result of fluid overload via
stimulation of atrial receptors [1]. Whether this
is the primary cause for the inability to con-
centrate urine following relief of obstruction is
not clear.
The expression of aquaporin-2, one of a
group of transmembrane water channels sen-
sitive to antidiuretic hormone, is decreased in
BUO and persists following release of obstruc-
tion providing further evidence that the direct
effect of obstruction on the kidney may impair
the return of function [2].
Investigation of Obstructive
Nephropathy
In the majority of cases diagnosis of the
cause of the obstruction can be made by eval-
uation of clinical symptoms and signs (table 5).
A well-taken clinical history augmented by
careful examination will direct attention to the
site of the blockage. An acute onset with con-
comitant pyrexia, loin tenderness, vomiting
and electrolyte disturbance will require speedy
diagnosis and intervention. This is one of the
few genuine emergencies in urology practice.
It is vital to know the state of function of both
kidneys, particularly in supravesical obstruc-
tion.
Ultrasonography provides an immediate
rapid non-invasive assessment of both kidney
F and bladder anatomy. This combined with a
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Table 5. Investigation of obstructive nephropathy
1 Medical history, symptoms, signs and careful clinical
examination
2 Plain abdominal film
3 Ultrasound of upper and lower urinary tracts
4 Intravenous urogram
5 CT or MRI scanning
6 Retrograde pyelography and screening
7 Isotope renography
plain abdominal X-ray will confirm the clinical
diagnosis in most cases. It must be emphasised,
however, that dilatation does not necessarily
mean obstruction.
The ‘casualty officer intravenous urogram’
(IVU), a single shot of contrast given at the time
of the initial plain abdominal film, and followed
20 min later by a further film, may still be a
valuable acute investigation in departments
with limited radiology facilities. It will provide
immediate confirmation of an effectively func-
tioning contralateral kidney in unilateral
obstruction, and will give an indication of the
severity and level of obstruction on the affect-
ed side.
Infinitely preferable is a properly conducted
urogram by an experienced radiologist. Atten-
tion to the nephrogram phases and repeated
later films may confirm residual function in an
obstructed unit up to 24 h after contrast injec-
tion.
The development of interventional radiolo-
gy as a specialty has meant that an immediate
decision can be taken to proceed to percuta-
neous nephrostomy for the relief of intralumi-
nal pressure, to obtain samples for microbio-
logical analysis, and to conduct further evalu-
ation by gentle antegrade pyelography.
The ‘gold standard’ in urological obstruction
at present is spiral CT or other cross-sectional
imaging techniques used to provide an imme-
diate definitive diagnosis and opportunity for
interventional radiology.
When the acute situation has been effec-
tively treated, a more leisurely approach to
investigation by isotope renography, retro-
grade catheterisation and screening, CT scan-
ning and MRI studies can be undertaken.
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Ability to Recover on Relief of
Obstruction
The ability to recover depends on the sever-
ity and duration of the renal injury and the
presence of infection. The latter accelerates the
insult to the kidney. The extent of recovery is
also determined by the completeness of the
obstruction and whether this is unilateral or
bilateral. Most studies have concentrated on
animal models. In the dog kidney with unilat-
eral complete obstruction no return of function
in terms of measured GFR was seen if the dura-
tion of occlusion exceeded 6 weeks [5]. There
seems to be a gradual decrease in recoverable
function. After 2 weeks of obstruction, 50% of
baseline renal function was achieved following
relief of obstruction.
Studies of tubular function suggest that
after 4 weeks of complete obstruction there is
a permanent deficit in the concentrating abili-
ty of the kidney. However, after 1 week of
obstruction complete recovery may occur. The
limited human experience suggests that in the
absence of infection and nephrotoxic medica-
tion full recovery may be achieved even after
20 weeks, particularly in UUO [5, 15]. The
prognosis for recovery is important, but uncer-
tain. Some indication of the ability to recover
can be obtained by inspection of the nephro-
gram phase of the IVU. Classically a dense
nephrogram seen in acute obstruction and
partly due to increased sodium reabsorption is
a more favourable prognostic indicator than
the dilute pyelogram of chronic obstruction.
When chronic obstruction becomes more
severe the typical ‘shell nephrogram’ is seen
with areas of dense opacification surrounding
dilated calyces. This indicates that the tubular
concentrating function is retained and may be
alleviated by release of obstruction.
The use of 99Tc-dimercaptosuccinic acid
which accumulates in the proximal tubule cells
is of limited value as a predictor of recovery of
function, though commonly used to monitor
the progress of the obstructed state. The diure-
sis renogram is particularly useful in this situa-
tion and eliminates the heavy dose of radiation
required by serial IVU follow-up. The basic
Obstructive Nephropathy: Causes and Management
principles of measuring urine osmolality, crea-
tinine clearance, water balance, serial elec-
trolyte estimations and in particular sodium
excretion (together with acidifying ability)
remain the most useful clinical investigations
which may indicate the potential for recovery.
Management of Obstructive
Nephropathy
The deterioration in renal function can be
reversed or reduced by early relief of urinary
tract obstruction. Details of the surgical reme-
dy in specific situations are beyond the scope of
this article, particularly since open surgical
intervention is now rarely required for early
relief of obstruction.
This situation has resulted from develop-
ments in three main areas of urology: (1) inter-
ventional radiology; (2) development of intra-
luminal prostheses, and (3) evolution of tech-
nology in surgery. Radiological expertise has
simplified the accurate non-invasive diagnosis
of urinary tract obstruction. In complete
obstruction, whether unilateral or bilateral,
careful monitoring is essentially if lasting renal
impairment is to be avoided. Obstruction com-
plicated by infection is a genuine surgical emer-
gency. Each hour that passes will result in pro-
gressive nephron damage and threaten the
development of sepsis. Percutaneous nephros-
tomy will contain the emergency and is safer
than attempted retrograde catheterisation
which may introduce infection into the closed
drainage system, a recipe for disaster. Elective
surgery may then be undertaken after ade-
quate definition of the causality and evaluation
of renal function. If surgery is to be deferred,
initial drainage by a JJ stent is preferable to
pigtail nephrostomy. The perils of the dry
unstented ureter are well known. A further
advantage of a JJ stent is to permit passive
dilatation of the ureter which may allow the
intraluminal obstruction to pass spontaneous-
ly, and will subsequently make ureteroscopy
almost invariably successful and atraumatic.
Attempted endoscopic relief of obstruction,
whether by simple stent insertion or manipu-
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Table 6. Surgical management of obstructive uropathy

Percutaneous nephrostomy
JJ stent insertion antegrade or retrograde
Endoscopic manipulation under radiological control
Ureteroscopic and pyeloscopic intervention
Dormia basket extraction
Lithoclast or laser fragmentation
Diathermy or laser coagulation and vapourisation
Open surgery
Exicision and anastomosis
Psoas hitch
Boari flap

lation by an intraluminal extraction or ablative

device, should invariably be conducted under
radiological control or image intensification.
The key to success is the accurate positioning
and establishment of a suitable guidewire at the
beginning of the technique. This should be
maintained in position throughout the proce-
dure and will ensure accurate placement of a
JJ stent in the event of failure or extravasation.
The evolution of the intraluminal prosthesis or
stent has facilitated bypass of the obstruction
either temporarily or for definitive treatment.
The third significant advance is the devel-
opment of sophisticated small calibre uretero-
renoscopes, either rigid or flexible, which used
in conjunction with stone fragmentation
devices and laser fibres permit endoscopic
access to the entire upper urinary tract. The
combination of direct vision ureterorenoscopy
and simultaneous radiological screening will
allow most upper tract occlusions to be dealt
with safely and efficiently.
There are nevertheless situations in which
only open surgical reconstruction will suffice.
Localised ureteric tumours, the dreadful stric-
tures which can follow iatrogenic injury or lig-
ation, and chronic inflammatory disease, par-
ticularly tuberculosis, will not respond to sim-
ple stenting or an intraluminal prosthesis (table
6). These are best dealt with by excision and
reanastomosis of the ureter using an adjuvant
psoas hitch following mobilisation of the blad-
der. For higher strictures a well-constructed
boari flap will allow a suprising length of
ureteric loss to be replaced without tension on
the anastomosis. A judicious combination of
intraluminal stenting and reconstruction will
8 minimise post-operative morbidity.
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Appendix

Illustrative Cases

Case 1. a–d Dynamic renogram of a 56-year-

old female with acute right loin pain demon-
strating incomplete pelvoureteric junction
obstruction on the right side with good preser-
vation of renal substance and effective
c response to diuretic challenge.
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a b

Case 2. a–d Dynamic renogram of a 38-year-

old female with chronic left loin pain demon-
strating complete pelvoureteric junction ob- d
struction with poor function, loss of renal sub-
stance and no response to diuretic challenge.

Case 3. CT demonstrating gross

J hydronephrosis.
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a b
Case 4. A 68-year-old male with left loin pain
and haematuria presenting with fluctuant
swelling over the left loin and upper abdomen.
CT scan had shown urinoma in the left
retroperitoneum following spontaneous rup-
ture of the left renal pelvis due to an obstruct-
ing colonic carcinoma invading the ureter.
a Pigtail stent draining the urinoma. Sponta-
neous extravasation from the pelvicalyceal sys-
tem. b Pigtail stent decompressing the left kid-
ney and below the stent in the urinoma. Stric-
ture in the lower left ureter. c Pigtail stent in the
renal pelvis and another in the urinoma. JJ
stent in position in the left ureter. d JJ stent in
the left ureter and pigtail stent in the left renal
pelvis.
References
11 Gulmi FA, Felsen D, Vaughan ED Jr: Pathophysiology of
urinary tract obstruction; in Walsh PC, Retik AB, Vaugh-
an ED Jr, Wein A (eds): Campbell's Urology, ed 7. Philadel-
phia, Saunders, 1997, pp 342–385.
12 Klahr S: Obstructive nephropathy. Kidney Int 1998;
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