Pathophysiology of Urinary
Tract Obstruction
chapter 40
Dr.Mariam Malallah
Dr.Abdullatif Al-Terki
Obstruction of the urinary tract
• Obstruction of the urinary tract can occur
during fetal development, childhood, or
adulthood.
• The point of obstruction:
Proximal -> calyces
Distal -> urethral meatus.
• lead to  permanent renal damage 
limiting the excretion of metabolic wastes 
altering water and electrolyte balance.
• Hydronephrosis:
- Is the dilation of the renal pelvis or calyces.
- Associated with obstruction.
- may be present in the absence of obstruction.
• Obstructive uropathy:
- The functional or anatomic obstruction of
urinary flow at any level of the urinary tract.
- The obstruction causes:
functional or anatomic renal damage.
GLOBAL RENAL FUNCTIONAL CHANGES
Glomerular Filtration, Renal Blood Flow, Collecting System Pressure
• Functional changes associated with
obstructive nephropathy.
- Renal hemodynamic variables
- Glomerular filtration.
• influenced by:
- The extent and severity of obstruction
- Unilateral or bilateral
- Persists or has been relieved.
• Factors influencing GFR are expressed in the following
equation:
GFR = Kf (PGC −PT −πGC)
• Kf: glomerular ultrafiltration coefficient
• PGC: glomerular capillary pressure
Influenced by:
- Renal plasma flow (RPF)
- The resistances of the afferent and efferent arterioles.
• The hydraulic pressure of fluid in the tubule (PT)
• oncotic pressure (π) of the proteins
• RPF depends upon:
- The renal perfusion pressure
- Intrarenal resistance to flow is mediated by the
resistances in the afferent and efferent arterioles.
RPF = aortic pressure − renal venous pressure
renal vascular resistance
• Obstruction can transiently or permanently alter GFR
and some or all of the determinants of GFR.
• Unilateral and bilateral ureteral obstructions
differ in
- the patterns of hemodynamic
- ureteral pressure changes
- distribution of renal blood flow.
Hemodynamic Changes with
Unilateral Ureteral Occlusion
• Animal experiments have demonstrated a triphasic
pattern of RBF and ureteral pressure changes in UUO
• first 1 to 2 hours
-RBF increases
-high PT and collecting system pressure
• second phase lasting 3 to 4 hours
-pressure parameters remain elevated
-RBF begins to decline.
• third phase beginning about 5 hours after obstruction
-a further decline in RBF
-decrease in PT and collecting system pressure.
• Triphasic relationship between ipsilateral renal blood flow and left ureteral
pressure during 18 hours of left-sided occlusion.
• The three phases are designated by roman numerals and separated by vertical
dashed lines.
• In phase I, renal blood flow and ureteral pressure rise together.
• In phase II, the left renal blood flow begins to decline and ureteral pressure
remains elevated and, in fact, continues to rise.
• In phase III, the left renal blood flow and ureteral pressure decline together.
• It is likely that both PGE2 and NO contribute
to the net renal vasodilation that occurs early
following UUO.
• Thus reduced whole kidney GFR at this stage
of obstruction is due
not only to reduced perfusion of individual
glomeruli, related to afferent
vasoconstriction and reduced PGC,
but also to global reduction in filtration
related to no perfusion or underperfusion of
many glomeruli.
Hemodynamic Changes with
Bilateral Ureteral Occlusion
• A modest increase in RBF with BUO that lasts
approximately 90 minutes
followed by a prolonged and profound decrease
in RBF that is greater than found with UUO.
• The intrarenal distribution of blood flow is quite
different with BUO than with models of UUO.
• Thus the shift seen with UUO of blood flow from
outer to inner cortex is the opposite of that with
BUO.
• Ureteral pressure is higher with BUO than
with UUO.
• In both cases ureteral and tubular pressures
are increased for the first 4 to 5 hours.
-The ureteral pressure remains elevated for at
least 24 hours with BUO
-The ureteral pressure begins to decline and
approaches preocclusion pressures by 24
hours with UUO.
• This difference between the two pathophysiologic
conditions has been hypothesized to be
-due to an accumulation of vasoactive substances in
BUO that
could contribute to preglomerular vasodilation and
postglomerular vasoconstriction.
-Such substances would not accumulate in UUO because
they would be excreted by the contralateral kidney.
E.g. Atrial natriuretic peptide (ANP)
In summary,
• both UUO and BUO involve increases in renal vascular resistances
and increases in ureteral pressures.
the timing and regulation of these changes differ
• With UUO, early renal vasodilation primarily mediated by
prostaglandins and NO is followed by prolonged vasoconstriction
and normalization of intratubular-ureteral pressure as the
contralateral kidney contributes to fluid balance.
• With BUO, little early vasodilation is seen, and vasoconstriction is
more profound.
When the obstruction is released, the postobstructive diuresis is
much greater with BUO because volume expansion, urea and
other osmolytes, and secreted ANP contribute to a profound
diuresis and natriuresis.
Partial Ureteral Occlusion
• Formation of glomeruli and tubules may be
compromised so that irreversible changes occur
without total loss of kidney function.
• Partial neonatal obstruction can impair
nephrogenesis independently of renal functional
decline
• these changes may depend upon :
-species
-stage of renal development
-degree of occlusion.
Egress of Urine from the Kidney
• urine may still egress from the kidney.
• extravasation at the calyceal fornix
(pyelosinus) that occurs with acute
obstruction, typically ureteral stones.
• Extravasation of urine into the venous
(pyelovenous) and lymphatic system
(pyelolymphatic)
• In chronic obstruction, fluid is thought to exit
into the renal venous system.
Effects of Obstruction on Tubular
Function
• Postobstructive diuresis:
- Commonly after reversal of BUO
- uncommonly after release of UUO
probably as a consequence of the
contralateral renal unit’s functional capacities
that are enhanced by an upregulation of ion
transporters
Urinary Concentrating Ability
• Normal urine concentrating ability requires:
- Hypertonic medullary interstitial gradient
because of active salt reabsorption from the thick
ascending limb of Henle.
- Urea back flux from the inner medullary collecting
duct
- Water permeability of the collecting duct mediated
by vasopressin and aquaporin water channels.
• Obstructive nephropathy can disrupt some or all of
these mechanisms.
• Thus dysregulation of aquaporin water
channels contribute to the long-term polyuria
and impaired concentrating capacity
• These defects are enduring and correct slowly
with time.
Sodium Transport
• Although ANP appears to play a role in
sodium diuresis after release of BUO, it is
unlikely to affect sodium transport defects
associated with UUO.
• Sodium excretion is greater after relief of BUO
because extracellular volume is expanded and
ANP directly affects transport and glomerular
filtration.
• The sodium transport defects associated with UUO is most likely
due to selective cell membrane changes in the nephron that reduce
the number and effectiveness of sodium transporters. Such changes
may also occur with BUO.
• Ischemia can also be a mediator of reduced transporter expression.
• changes in renal interstitial pressure and local generation of
natriuretic substances.
• Thus substrate delivery may be a regulatory step in the expression
of sodium and possibly other transporters.
• Intrarenal and extrarenal substances and hormones can also
modulate sodium transport. E.g. PGE2 in the renal medulla
• The FENa following relief of BUO is typically greater than that
after UUO because BUO causes retention of Na, water, urea
nitrogen, and other osmolar substances and increased production
of ANP, all of which stimulate a profound natriuresis.
Potassium Transport
• Potassium and phosphate excretions follow changes in sodium;
they are decreased with UUO because of altered transporters and
postobstructive retention
and increased transiently with BUO in parallel with the massive
natriuresis.
• there is a decrease in K+ excretion, with the relief of UUO.
-due to reduced delivery of Na+ to the distal nephron
-low volume flow rate that would minimize the transmembrane gradient
for K+ secretion.
-an intrinsic defect in K+ secretion
• K+ excretion increases , with the relief of BUO.
-due to the massive increases in Na+ and water delivery to the collecting
duct acting as stimuli to secretion
- also to the presence of high levels of ANP that can stimulate K+
secretion in the distal nephron
Hydrogen Ion Transport and Urinary
Acidification
• Obstruction causes a deficit in urinary
acidification that has been demonstrated in
human subjects as well as animal models.
• A number of causes for the lack of acidification,
including:
- defects in H+-ATPase or H+
- K+-ATPase
- Cl−/HCO3− exchange
- Back leak of protons into the renal interstitium
- Failure to generate a satisfactory transluminal
electrical gradient.
Effects of Obstruction on Anion and
Other Cation Transport
• The effects on phosphate reabsorption after the
release of obstruction vary depending upon whether it
was bilateral or unilateral.
• When BUO is released, accumulated phosphate is
rapidly excreted in proportion to sodium
• Conversely, a decrease in phosphate excretion and a
net retention occur with release of UUO.
• Magnesium excretion is markedly increased after the
release of either UUO or BUO.
• calcium excretion may be increased or decreased,
depending to a degree on the type of obstruction and
the species.
Effect of Obstruction on the Excretion
of Peptides and Proteins
• Changes in peptide excretion reflect mediators and markers of renal
damage.
• Monocyte chemoattractant protein 1
- Its excretion in the urine after UUO increases
- an index of tubular damage.
• - Epidermal growth factor (EGF) excretion
- The renal cortical and outer medullary concentration of pre-pro-EGF
- The excretion of Tamm-Horsfall protein
All decrease with obstruction.
•
Urinary enzymes derived from the proximal tubule,
e.g. alkaline phosphatase, γ-glutamyltransferase, N-acetyl-β-Dglucosaminidase, and leucine aminopeptidase
- elevated in patients with obstructed kidneys
Metabolic Determinants of Ion
Transport
• Renal obstruction provokes a number of changes
in the metabolic cascade.
• There is a shift from oxidative metabolism to
anaerobic respiration.
• This shift results in a reduction of renal ATP
levels, an increase in amounts of adenosine
diphosphate (ADP) and adenosine monophosphate (AMP), and an increase in the renal
lactate- to-pyruvate ratio
Cellular and Molecular Mechanisms
Leading to Tubular Cell Death through
Apoptosis
• Renal obstruction  tubular atrophy and cell
death.
• Apoptosis  triggered by both intrinsic and
extrinsic factors  degradation and condensation
of the nucleus  cells further degrades into
apoptotic bodies  phagocytized by healthy cells
• Glomerular cells appear to be resistant to
obstruction-induced apoptosis.
• Caspases  mediate apoptotic cell death in
obstructed kidneys
• Two distinct pathways of caspase
1- activation of membrane death receptors by extrinsic
binding of tumor necrosis factor alpha (TNF-α) to its
receptor.
2- involves intrinsic stress signals that result in
mitochondrial release of proapoptotic proteins such as
cytochrome c.
• The two pathways  activate effector caspases 
cleave nuclear and cytoplasmic components 
condensation of nuclear material  cell death.
• Angiotensin blockade or ACE inhibition has
been shown by some investigators to reduce
apoptosis in the early phases of renal
obstruction
• TNF-α can be a directly cytotoxic cytokine
that can induce apoptosis in addition to its
role in renal inflammation.
Cellular and Molecular Changes
Leading to Fibrosis
• Urinary tract obstruction leads to progressive
and, eventually, permanent changes in the
structure of the kidney, including:
-tubulointerstitial fibrosis
-tubular atrophy and apoptosis
-interstitial inflammation.
• In other words:
Ureteral obstruction leads to renal inflammation,
increased extracellular matrix formation,
tubulointerstitial fibrosis, and apoptosis of renal
tubule cells.
• Although the events leading to fibrosis are
thought to be initiated by increased angiotensin
II, other profibrotic factors appear to play a
significant role because inhibition of angiotensin
synthesis by ACE inhibitors or antagonism of the
AT1 receptors blunts but does not completely
abolish the fibrotic process
Experimental Treatment Approaches
to Attenuate Renal Fibrosis and
Functional Impairment
• These studies suggest an important role of
angiotensin-mediated profibrotic and
apoptotic events occurring with renal
obstruction that can be reduced with
currently available inhibitors of angiotensin
synthesis or receptor blockade.
Compensatory Renal Growth
• An increase in contralateral renal volume has been detected
ultrasonographically when contralateral hydronephrosis or
unilateral renal agenesis is present.
• influenced by several factors including:
-age
-degree of obstruction
-duration of obstruction.
• Both hyperplastic and hypertrophic CRG
• Studies of humans subjected to nephrectomy, a functional
surrogate for obstruction, have demonstrated that a reduction in
CRG occurs with increasing age
• less prominent with partial than with total UUO
• While the kidney enlarges -an increase in the number of nephrons
or glomeruli does not occur.
• Insulin-like growth factor I (IGF- I) may play a role.
• Other growth factors, cytokines, and enzymes
may be involved in regulating CRG, including IGF
binding protein–3 (IGFBP-3), vascular endothelial
growth factor (VEGF), matrix metalloproteinase–9
(MMP-9), interleukin-10 (IL-10), and TGF-β
• CRG may be influenced by mitochondrial
respiration
Renal Recovery after Obstruction
• When acute, complete ureteral obstruction is
promptly relieved, full recovery of global GFR
can occur.
• Longer periods of complete ureteral
obstruction are associated with diminished
return of GFR.
• Histopathological findings may predict recovery of renal function.
• Renal parenchymal thickness based on computed tomography (CT)
Further studies are needed to corroborate these results before
this approach is used in clinical practice.
• Other factors influence functional return
Factors that have a positive influence on functional recovery include:
- a smaller degree of obstruction
- greater compliance of the collecting system
- presence of pyelolymphatic backflow
Predictors of diminished recovery of renal function
-older age
-decreased renal cortical thickness
• Nuclear renography - is the best predictor.
• For example:
dimercaptosuccinic acid (DMSA), a cortical
agent, has been shown to be superior to
tubular selective agents, such as
diethylenetriaminepentaacetic acid (DTPA) or
mercaptoacetyltriglycine (MAG3), for the
prediction of renal recovery
PATHOLOGIC CHANGES OF
OBSTRUCTION
• These may be affected by:
-the presence of infection
-duration of obstruction
-intra versus extrarenal localization of the renal
pelvis.
Gross Pathologic Findings
•
•
•
•
•
at 42 hours after obstruction :
Dilation of the pelvis and ureter
blunting of the papillary tips
the weight of this renal unit heavier.
at 7 days.
Pelviureteric dilation
weight further increased
parenchyma became edematous
at 12 days
The cortex remained slightly enlarged
increased calyceal dilatation
at 21 and 28 days
the external renal dimensions of both kidneys were similar.
the cortex and medullary tissue diffusely thinned.
At 6 weeks
The totally obstructed kidneys  enlarged, had a cystic appearance, and weighed
less than the contralateral renal unit
The partially obstructed kidneys  no gross differences in appearance
Microscopic Pathologic Findings
• Widespread glomerular collapse and tubular
atrophy, interstitial fibrosis, and proliferation of
connective tissue in the collecting system were
reported at 5 to 6 weeks after obstruction
• This is believed to be a result of interplay of
several cellular and molecular mechanisms that
collectively lead to the subtle development of
tubular atrophy, macrophage
infiltration/proliferation in the renal interstitial
tissue, interstitial fibrosis and progressive loss of
nephrons
Electron Microscopic Pathologic
Findings
• Including:
-tubular atrophy
-glomerular collapse
-renal pelvic smooth muscle atrophy
at 5 to 6 weeks after obstruction
• other changes including:
-a cell-poor stroma composed of elastic and
collagen fibers in the renal interstitium
-obstructed portions of the collecting system.
GENERAL ISSUES IN MANAGEMENT
OF PATIENTS
•
-
Diagnostic Imaging
Ultrasonography
excretory urography (EXU)
retrograde pyelography
antegrade pyelography
isotopic renograph
computed tomography (helical)
magnetic resonance imaging
pressure flow study (Whitaker test).
Ultrasonography
• Although it is primarily an anatomic study,
Doppler modifications may add a functional
component.
- A prospective study of ultrasonography in
obstruction revealed a 35% false-negative
rate in acute obstruction, underscoring the
need to correlate the clinical picture carefully
with the radiologic findings.
• Doppler ultrasonography
allows measurement of the renal resistive index (RI),
which has been used to assess for obstruction.
The RI is defined as peak systolic velocity (PSV) minus
the end-diastolic velocity (EDV) divided by the PSV.
• values greater than 0.7 reflecting elevated resistance to
blood flow and thus suggesting obstructive uropathy.
• Although the presence of hydronephrosis associated
with an abnormally elevated RI may be indicative of
the severity of obstruction
Excretory Urography
• the “gold standard” for the evaluation of the upper urinary
tract
• Advantages:
it provides both anatomic and functional information:
• Disadvantages:
- the utility of EXU is limited in those with renal
insufficiency.
- risk of contrast nephropathy increases with increasing
serum creatinine.
- Radiation exposure limits its utility in pregnancy
Retrograde Pyelography
• Defines ureteral and collecting system anatomy
• considered in:
- renal insufficiency
- risks for receiving intravenous iodinated
contrast material
- anatomy is not sufficiently defined with other
imaging studies.
• Loopogram:
- another form of retrograde pyelography
- evaluating patients with cutaneous urinary
diversion when obstruction is suspected.
Antegrade Pyelography
• Helpful
- when other imaging studies do not
adequately define collecting system or
ureteral anatomy
- when retrograde pyelography is not
technically feasible.
Whitaker Test (pressure flow study)
• First described by Whitaker in 1973
• Measurement of renal pelvic pressure during infusion of either
saline or contrast material into the collecting system through a
percutaneous needle or nephrostomy at a fixed rate of 10
mL/min.
• A catheter is placed in the bladder to monitor intravesical pressure
• subtracted from the measured collecting system pressures to
calculate the “true pressure” within the pelvis.
• -A true intrapelvic pressure of less than 15 cm H2O is considered
normal
- greater than 22 cm H2O indicative of obstruction
- between 15 and 22 cm H2O indeterminate.
• The noted discordant results and the invasiveness of the study
limited its applicability in clinical practice.
Nuclear Renography
• noninvasive test
• It provides a functional assessment
• without exposure to iodinated contrast
material.
• The glomerular agent technetium (Tc) 99m
DTPA and The tubular agent 99mTc-MAG3
are most commonly used in the evaluation of
obstruction.
• Obstruction can be assessed by measuring the
clearance curves,
either:
from a visual assessment of the pattern
or from calculation of the half-time (time at
which 50% of the radiopharmaceutical is
eliminated from the collecting system).
-a half-time less than 10 minutes is considered
normal
-greater than 20 minutes is considered
obstructed
-between 10 and 20 minutes is equivocal
• The diuretic renogram is a modification, distinguish
truly obstructed collecting systems from those that are
dilated but unobstructed.
• In diuretic renography, the diuretic, typically
furosemide (F)
• although an F+20 study is reliable when obstruction is
demonstrated, both the F−15 and F+0 sequences can
induce obstructed patterns in previously equivocal
cases
• With the emergence of such techniques in isotopic
renography, the differential renal function and
drainage can be estimated with greater precision
Computed Tomography and Magnetic
Resonance Imaging
• Both CT and MRU provide superior imaging of the obstructed
upper urinary tract as compared to EXU
• Other advantages include its speed, reproducibility, and ability to
detect other pathologic entities
• Noncontrast CT directly demonstrates calculi classically
considered radiolucent when evaluated by plain radiography,
including uric acid, xanthine, dihydroxyadenine, and many druginduced stones. Exceptions, however, are calculi composed of
protease inhibitors, which are not visualized by noncontrast CT.
• both MRU and CT have critical roles in evaluating select patients
with urinary tract obstruction.
• Although these studies can estimate renal function nuclear
renography remains the current gold standard.
Hypertension
• A well-recognized sequela of BUO or obstruction
of a solitary kidney.
• Hypertension is significantly less common,
however, with UUO
• UUO the contralateral, unobstructed kidney
compensates and eliminates excess volume and
solutes.
• In summary, there is a good chance of reversal
of new-onset hypertension with relief of BUO,
but this is less likely with UUO.
Renal Drainage
• immediate drainage of the affected renal unit(s) in case of Ureteral
obstruction that is
- symptomatic
- accompanied by fever
- complicated by an undrained infection
- high grade
- bilateral
- inducing renal failure
• may allow temporary drainage until a definitive procedure is
performed
• may be a permanent form of management.
• urinalysis and culture
• Antibiotic therapy
• The choice of drainage ultimately depends on the clinical setting.
indwelling ureteral stents and percutaneous nephrostomy tubes
• Ureteral stenting may not be as effective for
treating patients with extrinsic ureteral
obstruction.
• A diagnosis of cancer, metastatic disease
requiring chemotherapy or radiation, and renal
insufficiency were predictors of stent failure in
this series.
• Closer monitoring for stent failure should thus
be considered in patients with extrinsic ureteral
obstruction
• risk factors for stent failure:
- higher serum creatinine value
-The presence of extrinsic ureteral obstruction due to
bladder or prostatic pathology, especially advanced
malignancies
-Encrustation:
pregnant patients, due to increased calcium excretion
during pregnancy
urinary tract infection (UTI)
stasis
dehydration
renal insufficiency
prolonged dwell time
history of nephrolithiasis
Choice of Surgical Intervention
• Definitive management is based upon:
- cause of the obstruction
-functional recovery of the affected kidney
-condition of its counterpart
-patient’s age
-medical status.
• Endoscopic, open, or laparoscopic ablative and
reconstructive procedures may all be used.
• The decision to remove a kidney should be made only
after the affected kidney has been adequately drained
for a sufficient period of time, 6 to 8 weeks
Pain Management
• Five classes of drugs are used to treat pain associated
with acute renal colic:
- nonsteroidal anti-inflammatory drugs (NSAIDs)
- narcotic analgesics
- calcium channel blockers
- corticosteroids
- α1 blockers
• The present level of evidence supports the role of
NSAIDs as first-line drugs for the management of
renal colic presenting to the emergency department,
with narcotics being reserved as second-line drugs.
• The choice of pain management should be based on the
patient’s clinical profile.
• NSAIDs should not be used in patients with renal
insufficiency, because this could be exacerbated by the
induced reduction in RBF.
• COX-1 inhibitors should not be administered to patients at
risk for gastrointestinal bleeding or when optimal platelet
function is needed.
• the market withdrawal of some COX-2 inhibitors, related to
increased risk of cardiac morbidity, underscores the need
for prospective trials to assess their long-term safety in
managing patients with renal colic.
• Patients may be fluid depleted as a result of
anorexia and emesis, and therefore should
receive intravenous hydration.
• there is no evidence that intravenous
hydration facilitates stone passage
Post obstructive Diuresis
• Mechanisms
• Following the relief of urinary tract obstruction, postobstructive diuresis—a period of significant polyuria—
may ensue.
• Urine outputs of 200 mL/hr or greater may be
encountered.
• Postobstructive diuresis occurs primarily with BUO and is
usually self-limiting.
• mainly after relief of BUO or obstruction of a solitary kidney
• rarely occur when there is a normal, contralateral kidney
• a “pathologic” postobstructive diuresis may
ensue, characterized by:
inappropriate renal handling of water or solutes,
or both.
• It is due to a number of mechanisms, including:
- a derangement of the medullary solute gradient
- a number of altered signaling and transport
pathways.
• Downregulation of sodium transporters
• The increased ANP induce a saline diuresis
• other natriuretic peptides, such as the
Dendroaspis natriuretic peptide, may play a role.
• poor responsiveness of the collecting duct to
antidiuretic hormone (ADH).
due to a downregulation of aquaporin water
channels in this segment of the nephron and
perhaps in the proximal tubule
Clinical Management of
Postobstructive Diuresis
• The majority of patients do not demonstrate a
clinically significant postobstructive diuresis
following relief of urinary tract obstruction.
• Those who are susceptible to this phenomenon
typically have signs of fluid overload:
-edema
-congestive heart failure
-hypertension
• A catheter should be placed to drain the bladder
rapidly in those with urinary retention.
• should be monitored for a postobstructive diuresis.
-Serum electrolytes
-magnesium
-blood urea nitrogen (BUN)
-creatinine
• monitoring depends on:
-presence of risk factors for postobstructive diuresis
-mental status
-renal function
-electrolyte status.
• Those with normal renal function and electrolytes, no
evidence of fluid overload, and who are mentally alert
- should have their vital signs and urine output
monitored.
- They are allowed free access to oral fluids,
- and if they do not manifest signs of a postobstructive
diuresis they can be discharged and return later for
further urologic evaluation and care.
• If they show signs of a postobstructive diuresis but are
alert, able to consume fluids, and have normal vital
signs.
- observation is continued and the patients may
consume fluids as desired.
• If patients have signs of fluid overload,
azotemia, or poor cognitive function, or if
hypotension or other indicators of hypovolemia
develop
-more intense monitoring should be instituted.
-Vital signs
- urine output are checked more frequently.
- Electrolytes, BUN, magnesium, and creatinine
are assessed every 12 hours, and more frequently
if necessary.
- Urinary osmolarity should be checked in this
setting.
• The clinically stable patient with good
cognitive function
-free access to oral fluids.
-Intravenous fluids should probably not be
administered, because this may prolong the
period of diuresis.
However, there may be a theoretical role for
maintenance of volume expansion in this
setting
• Those with poor cognitive function
• should receive intravenous hydration, but below the
normal maintenance amounts.
• The majority have a self-limiting physiologic diuresis.
On rare occasions, a pathologic diuresis develops
and the patients can become hypovolemic because of
excess water loss.
• These patients warrant the most intense monitoring and
require careful electrolyte and fluid replacement, initially
by an intravenous route.
• The urine is usually isosthenuric initially and intravenous
fluid replacement with 0.45% saline administration at a rate
lower than the urine output is recommended
SELECTED EXTRINSIC CAUSES OF
URETERAL OBSTRUCTION
Retroperitoneal Fibrosis
• uncommon
• a fibrotic and inflammatory mass envelops
and potentially obstructs retroperitoneal
structures including either or both ureters.
• Grossly, retroperitoneal fibrosis appears as:
a fibrous, whitish plaque that encases
-the aorta,
-inferior vena cava,
-their major branches,
-the ureters,
-other retroperitoneal structures
-intra- peritoneal structures including the
gastrointestinal tract.
• Its longitudinal axis
extends from the renal hilum to the pelvic brim
may extend into the pelvis, mediastinum, and even the
optic orbit.
• The etiology - not well characterized.
• A number of mechanisms have been proposed.
- the development of vasculitis in the adventitial
vessels of the aorta and perioaortic small vessels.
- Other immunologic events may play a role.
- The presence of clonal and oligoclonal B cells
suggest that an errant B-cell disorder may play a
role.
- Environmental toxins may play a role
• Epidemiology:
• It is more common in males, with a 2 to 3 : 1
male-to-female ratio.
• The mean age at onset is typically 50 to 60 years,
• it may manifest in children as well as the elderly
• Genetic influence is not thought to play a major
role
• Retroperitoneal fibrosis is associated with HLADRB1*03, an allele linked to a number of
autoimmune diseases.
• Numerous medications have been associated with the
development of retroperitoneal fibrosis
• An underlying malignancy should always be
considered, because one is reported to be present in
8% to 10% of such cases
• Unique infections such as tuberculosis, histoplasmosis,
and actinomycosis.
- It can occur after abdominal or pelvic surgery as well
as abdominal trauma.
• Radiation and systemic chemotherapy .
• systemic diseases including autoimmune and
inflammatory processes.
• Symptoms:
back, abdominal, or flank pain, weight loss, anorexia, and
malaise.
• Signs:
hypertension (in 50%), fever, and lower extremity edema.
signs or symptoms attributable to ureteral or vascular
obstruction
• laboratory abnormalities:
- elevations in acute phase reactants e.g. ESR and CRP
- elevated serum creatinine
- hypergammaglobulinemia
- normochromic, normocytic anemia.
- Tests for autoimmune diseases may also be positive
• The classic radiologic findings:
-medial deviation of extrinsically compressed ureters
-hydronephrosis.
- smooth, well- demarcated, hypoechoic or isoechoic mass anterior
to the lumbar or sacral spine
• Retrograde pyelography demonstrates hydronephrosis, with
medially deviated and segmentally narrowed ureters without filling
defects
• CT or MRI
- CT typically reveals a well- demarcated retroperitoneal mass,
isodense with muscle on unenhanced studies
- MRI allows superior soft tissue discrimination and can more
accurately distinguish the plaque from the great vessels than
unenhanced CT.
• If there is evidence of obstructive uropathy at
presentation, therapy should be first directed
at its correction.
-internalized ureteral stents
-percutaneous nephrostomy
• Biopsy to exclude malignancy should be
performed next.
This can be attempted percutaneously with
CT, MRI, or ultrasound guidance.
• The potential morbidity of ureterolysis, accurate imageguided biopsy techniques, and more sensitive crosssectional imaging studies for diagnosis and follow-up have
made medical therapy the preferred approach in this
setting.
• no randomized prospective studies addressing the merits
of initial medical therapy versus a surgical approach.
• Medical therapy has been directed to address the
presumed autoimmune and inflammatory components of
retroperitoneal fibrosis.
• corticosteroids
• Tamoxifen, a nonsteroidal antiestrogen
• Ureterolysis is undertaken if medical therapy
fails or if the patient is not a candidate for
medical therapy.
• Bilateral ureterolysis is recommended progresses to involve the contralateral side.
• The ureteral dissection
- care to avoid devascularization of the ureter.
• A biopsy should be repeated - sampling error
associated with percutaneous biopsy.
• Several strategies have been employed to prevent
recurrent ureteral involvement in the fibrotic process:
- The ureter may be displaced to a lateral position
- brought to an intraperitoneal location by closing the
peritoneum behind it, or wrapped within a sleeve of
omentum.
• No single method has been definitively demonstrated to
generate superior results
• alternatives include:
ileal ureter replacement
autotransplantation
chronic ureteral stenting
nephrostomy tube drainage.
• Ureteral stents can generally be removed 6 to
8 weeks after ureterolysis
• Long-term follow-up in those subjected to
medical or surgical therapy is warranted.
• Serial cross-sectional imaging to assess
recurrence, progression, malignancy.
• Renal function monitored.
Pelvic Lipomatosis
• Rare
benign condition
marked by exuberant pelvic overgrowth of
nonmalignant but infiltrative adipose tissue,
usually in the abdominal and pelvic cavities.
• Occur in perivesical and perirectal spaces
• The etiology and incidence are unknown.
• Obesity play a role
• radiographic improvement and worsening in
response to weight loss and gain, respectively.
• Possible genetic etiology :
- An abnormality in the chromatin-regulating
high-mobility group A (HMGA) proteins has
been implicated
- genetic mutations have been traced to the
HMGA2 gene located on the hypermobile
cluster on chromosome 12
• chronic inflammatory response triggered by
urinary tract infection.
• Presentation:
- one half of patients present with lower urinary tract symptoms
- one quarter with bowel symptoms, typically constipation.
- Suprapubic, back, flank, or perineal discomfort
• Physical findings:
- a suprapubic mass
- a high-riding prostate
- indistinct pelvic mass.
- Hypertension
• Radiologic signs:
- On plain film, increased pelvic lucency
- On excretory urography, the bladder characteristically assumes a
pear or gourd shape, extrinsically compressed and elongated, and
the bladder base is frequently elevated
• leads to severe bilateral hydronephrosis.
• causes significant displacement of the distal
ureters medially
• Hydroureteronephrosis
• CT demonstrates
-pelvic fat
-Extrinsic compression of the rectum
-differentiating pelvic lipomatosis from other
• MRI - permits characterization of fat deposits
• Evaluation should include cystoscopy
- because some form of proliferative cystitis has been found in
75% of patients, including cystitis glandularis in up to 40%
However, the majority of patients with cystitis glandularis do not
have pelvic lipomatosis.
• cystitis glandularis
due to accumulation of perivesical fat
causing compression of the bladder
that leads to venous stasis,
and the development of an edematous urothelium
that subsequently sloughs off.
As the urothelium regenerates
undergo a metaplastic change
leading to development of cystitis glandularis.
• Continued cystoscopic surveillance is
recommended - risk of bladder
adenocarcinoma
Elongation of the prostatic urethra, elevation
of the bladder neck, and pelvic fixation may
impair cystoscopic access to the bladder.
• flexible cystoscopy may be required if
anatomic distortion precludes rigid
cystoscopy.
• The clinical signs and symptoms:
lower urinary tract symptoms
hematuria
passage of debris in the urine
problems with defecation.
• there is agreement that in light of the
potential for progressive ureteral obstruction,
long-term follow-up is mandated.
• steroids, chemotherapy, radiotherapy, and chronic
antibiotic therapy
have not been reported to be successful.
• Surgical options include:
ureteral stenting
percutaneous nephrostomy
ureteral reimplantation
urinary diversion with or without cystoprostatectomy.
• Pelvic exploration – cautiously due to obliteration of
normal anatomic planes and increased vascularity
within the fatty mass.
Obstetric and Gynecologic
Pregnancy
• Hydronephrosis develops commonly during
pregnancy
• occurrence varying between 43% and 100%.
• Approximately one third of patients may
have persistent hydronephrosis during the
first postpartum week, but it resolves in the
majority within 6 weeks
• Two etiologies for hydronephrosis of pregnancy:
- hormonal
- mechanical.
• nonmechanical mechanism.
Progesterone promote ureteral dilatation and
subsequent development of hydronephrosis
• mechanical etiology
after the 20th week of gestation, a time when the
uterus is large enough to compress the ureters
extrinsically
• Ultrasonographic finding: hydroureteronephrosis
extending to the pelvic brim.
• Magnetic resonance urography has been advocated
by some as a noninvasive, nonradiating method of
assessing those with hydronephrosis of pregnancy.
The presence of hydroureter below the pelvic brim is
readily apparent on high-resolution T2 sequences,
and filling defects representing stones or soft tissue
may be seen
• Mx:
• conservative measures:
- intravenous hydration
- analgesics
- antibiotic therapy
• placement of ureteral stents may be necessary
- Rapid stent encrustation may be problematic,
as urinary calcium excretion increases during
pregnancy
- necessitate more frequent stent changes.
• Percutaneous nephrostomy is an alternative
Benign Pelvic Abnormalities
Tubo-ovarian Abscess.
• Tubo-ovarian abscess, occurring in approximately 15% of those afflicted with PID,
may cause extrinsic ureteral obstruction, lead to anuria
• Ureteral obstruction may resolve with:
- antibiotic therapy
- transvaginal drainage of the abscess.
- open surgical or laparoscopic intervention
- Placement of an internalized ureteral stent or percutaneous nephrostomy
Endometriosis.
• Defined as the presence of functional endometrial tissue
in an ectopic site.
• potential for malignant transformation
• 10% to 20% of women of reproductive age
• peak incidence in the mid-20s
• Genitourinary endometriosis is a rare condition
• involvement of the urinary tract in 1% to 5% of
those afflicted with this disorder.
• - found in the bladder, accounting for 70% to
80%.
- The ureter may be involved in 15% to 20%
- Rarely, renal and urethral involvement
• may be either intrinsic or extrinsic.
• -Eighty percent of ureteral endometriosis is
extrinsic
• One theory for ureteral involvement:
is the occurrence of retrograde menstruation
and implantation of endometrial cells.
• Vesical endometriosis
- solitary
- involves the dome of the bladder.
• Notably, a significant portion of patients with
ureteral endometriosis do not have
genitourinary symptoms.
• Because a large percentage of patients with
ureteral endometriosis can have asymptomatic
obstruction of the kidney with a loss of renal
function, it has been recommended to image
the upper urinary tract in all patients with pelvic
endometriosis.
• Treatment goals:
(1) preservation of renal function, with long-term
relief of urinary obstruction,
(2) management of the ongoing disease process
by completely excising or ablating the
endometriotic tissue with its reactive fibrotic
component,
(3) maintenance of the patient’s fertility
(4) relief of the patient’s symptoms with the least
invasive methods available.
• If renal function is normal
and there is minimal to mild hydronephrosis
with no functional obstruction as determined by
radionuclide renal scanning,
hormone therapy may be prescribed.
• Ovarian hormonal ablation with gonadotropin-releasing
hormone agonists
• Postmenopausal patients controlled with
luteinizing hormone–releasing hormone (LHRH) analogues.
• Surgical intervention:
• total abdominal hysterectomy and bilateral salpingo-oophorectomy.
- If not desire future pregnancy
• lesser extirpative procedures, such as unilateral oophorectomy.
- If pregnancy is desired
• Ureterolysis – ureteral obstruction with extrinsic disease.
If laparoscopic ureterolysis - Success rates of 85%
• ureteroscopic resection or ablation- If intraluminal ureteral
• distal ureterectomy with reimplantation. by an open surgical, laparoscopic
or robotic-assisted approach.
- if unsuccessful or extensive disease
• Surveillance with sonography is advisable to detect recurrent ureteral
obstruction in patients with ureteral endometriosis treated by
hormones, endourological ablation, or surgical extirpation
Ovarian Remnants
• from residual, viable ovarian tissue after bilateral
salpingo-oophorectomy.
• complication of a technically difficult oophorectomy
• Mass effect or a localized fibrosis may cause extrinsic
ureteral obstruction.
• Treatment:
surgical excision of the mass and ureterolysis.
• Preoperative ureteral stenting
• Medical management
leuprolide acetate therapy - chronic medical therapy to
prevent recurrence
Mass Lesions of the Uterus and Ovaries.
• include uterine fibroids, ovarian cysts, and
ovarian fibromas.
• Uterine fibroids, the most common tumor of the
upper female genital tract, are also the most
common, benign gynecologic neoplasm causing
ureteral obstruction
• The most common site of extrinsic ureteral
obstruction at the level of the pelvic brim.
• Surgical resection or ablation of the leiomyomas
Vascular Causes of Ureteral
Obstruction
Arterial Causes of Obstruction
Abdominal Aortic Aneurysm.
• Clinical signs and symptoms of ureteral obstruction may be the initial
manifestation of an abdominal aortic aneurysm (AAA)
• due to a mass effect or localized inflammation
• CT scanning
• Ureteral findings vary.
- pushed laterally on both sides
- one side may deviate laterally while the opposite side is drawn medially within
the perianeurysmal inflammation
- both may be medially deviated.
• lateral deviation of the ureter with AAA - not associated with obstruction
• The medial deviation of the ureter associated with the desmoplastic reaction of
inflammatory aneurysms (IAAA), however, carries a more significant risk of
ureteral obstruction. Placement of internalized ureteral stents
• open surgery or an endovascular approach warrant close monitoring for recurrent
or de novo ureteral obstruction
Arterial Causes of Obstruction
Iliac Artery Aneurysms.
• can cause ureteral obstruction, which may even lead to renal failure
• 35% of those with common iliac artery aneurysms
• 19% of those involving the internal iliac artery.
• if a pulsatile mass is palpated on rectal examination.
• ultrasonography, MRI, and CT.
• extrinsic compression or localized inflammation
• Treatment options for obstructing common iliac artery aneurysm include:
-ureterolysis
-aneurysm resection and graft placement
-endovascular graft placement.
• Options for obstructing internal iliac artery aneurysms include:
-open surgical ligation
-ureterolysis
-initial endovascular occlusion and subsequent retrograde placement of an iliac
artery endovascular graft.
Arterial Causes of Obstruction
• Internalized ureteral stents are typically
placed before these procedures and are
removed 6 to 8 weeks later.
• observed closely - ureteral obstruction
resolves or recurs.
• If it recurs, management options include:
-chronic internalized ureteral stenting
-ureterolysis,
-ureteral reconstruction
Arterial Causes of Obstruction
• An additional cause is the retroiliac ureter
• Treatment :
- transection of the ureter and transposition to the normal, anterior
position.
• Other genitourinary abnormalities are associated with this condition,
including
renal hypoplasia
vesicoureteral reflux
ureteral ectopia,
ectopic vas deferens
hypospadias
bifid scrotum
hypoplastic or duplex uterus
hydrometrocolpos.
• Therefore a search for other genitourinary abnormalities should be
undertaken in patients with retroiliac ureter.
Arterial Causes of Obstruction
Ureteral Obstruction after Vascular Graft Placement.
• Hydronephrosis occur 10% to 20% after aortic bypass graft surgery.
• several possible causes
- Mechanical obstruction of the ureter due to graft placement anterior to
the ureter
- ureteral entrapment in perigraft fibrosis
- ureteral devascularization
- unidentified ureteral ligation
- ureteral compression from a postoperative pseudoaneurysm .
• Symptoms and signs :
- arise in the first postoperative year
- flank pain
- anorexia
- hypertension
- anuria
- renal failure or insufficiency.
- asymptomatic
Arterial Causes of Obstruction
•
•
•
•
•
•
•
Management of this problem varies.
If hydronephrosis early in the postoperative and renal function is not
compromised:
- close observation
- Temporary internalized ureteral stent or percutaneous nephrostomy drainage
If not resolve spontaneously and the graft is placed anteriorly
- transposition of the ureter
- vascular graft
To reduce the risk of graft infection
- vascular graft transected and repositioned
if persistent ureteral obstruction to perigraft fibrosis.
- steroid or tamoxifen therapy
- careful follow-up is mandatory - because delayed treatment failure.
if the former is not feasible or if medical therapy is not successful.
- Ureterolysis, and ileal ureter substitution
Chronic ureteral stenting - not candidates
Arterial Causes of Obstruction
Uterine Artery Aneurysms/Pseudoaneurysms
(UAA).
• associated with pregnancy.
• Symptomatic ureteral obstruction leading to
hydronephrosis
• Managed:
-radiographic embolization
-surgical ligation.
Venous Causes of Obstruction
Puerperal Ovarian Vein Thrombophlebitis
•
a mechanical effect from a dilated ovarian vein
• “ovarian vein syndrome.”
• Puerperal ovarian vein thrombophlebitis
• postpartum condition - cause ureteral obstruction -due to perivenous phlegmon formation and
resultant periureteritis
• more common on the right
•
may occur in either or both ovarian veins.
• signs and symptoms:
-nonspecificu sually beginning 2 to 3 days after birth.
-abdominal or flank pain and fever
• On physical examination:
- abdominal tenderness and guarding
- A tender indurated adnexal mass may be discerned in 50% of patients
• - The majority of patients respond to conservative measures, including antibiotic therapy
- Internalized ureteral stent placement
- Laparoscopic or open surgical ureterolysis
- ovarian vein resection
Venous Causes of Obstruction
Testicular Vein Thrombophlebitis.
• Thrombophlebitis of the left testicular vein
• causing extrinsic obstruction of the left ureter
• surgical exploration revealed
a dilated and thrombosed left testicular vein
impinging upon the proximal ureter.
• Ureterolysis and excision of the thrombosed vein
eradicated the obstruction.
• Also occur on the right side
Venous Causes of Obstruction
Circumcaval Ureter.
• an anomalous course posterior, medial, anterior, and finally lateral to the
inferior vena cava (IVC) may lead to extrinsic obstruction of the ureter.
• incidence of circumcaval ureter is approximately 1 in 1100.
• 2.8-fold male predominance
• Symptomatic patients - in the third or fourth decade of life
• This vascular anomaly is not always associated with ureteral obstruction
• The majority involve the right ureter
• although left-sided circumcaval ureter has been reported in association
with a duplicated IVC and in association with situs inversus
• Other genitourinary anomalies may be present.
• Circumcaval right ureter with a retrocaval horse-shoe isthmus
Venous Causes of Obstruction
• Circumcaval ureter classified using different parameters
based on intravenous urography or retrograde pyelographic
findings.
• Bateson and Atkinson (1969) classified a ureter with an
S-shaped
fish hook
shepherd’s crook appearance
as type I
• A less-angulated “sickle-shaped” ureteral deformity
is classified as type II
• The point of maximal obstruction in type I is lateral to the lateral
margin of the IVC
and is associated with a greater degree of hydronephrosis than
type II, in which the point of obstruction is at the lateral border of
the IVC
Venous Causes of Obstruction
• Another classification scheme is based on the
level of obstruction:
- type I crosses at the level of the third lumbar
vertebra
- type II crosses at the level of the ureteropelvic
junction.
• The diagnosis:
pyelographic findings
confirmed with CT and MRI
Diuretic renography
Venous Causes of Obstruction
• Treatment is undertaken only in the presence of
obstruction.
- The ureter is divided proximally and at the distal
point, from which it emerges lateral to the IVC.
- A spatulated ureteroureterostomy is performed.
by open, laparoscopic, and retroperitoneoscopic
approaches and is best dictated by the surgeon’s
experience.
- pure robotic repair of retrocaval ureter
• The most common complication:
ureteral stricture 13%