OBSTRUCTIVE

UROPATHY
Dr. Bassem W. Yani ,MD
Diploma, FEBU, FCS urology
CONSULTANT UROLOGIST
UTH LUSAKA ZAMBIA
Definitions
• Hydronephrosis- Dilation of the renal
pelvis or calyces
• Obstructive uropathy- functional or
anatomic obstruction of urine flow at
any level of the urinary tract
• Obstructive nephropathy- when
obstruction causes function or
anatomic renal damage
Prevalence
• 3.1% in autopsy series
• 2-2.5% of children at autopsy
• No gender differences until THE AGE
OF 20 years
– Females are more common 20-60 years
– Males are more common older than 60
years
ssifications
1/onset :acute or chronic
2/ site: unilateral or bilateral
3/degree : partial or complete
4/aetiology :
mechanical or functional
congenital or acquired
 Causes of Obstructive Nephropathy
• Renal:
– Congenital, Polycystic
kidney, ureteropelvic junction
obstruction
– Neoplastic- Wilms' tumor,
Renal cell carcinoma,
Transitional cell carcinoma of
the renal pelvis, Multiple
myeloma
– Inflammatory-
Tuberculosis,
– Metabolic- Calculi
– Miscellaneous- Sloughed
papillae, Trauma, Renal artery
aneurysm
 Causes of Obstructive Nephropathy
• Ureter:
Congenital- Stricture,
Ureterocele, Ureterovesical
reflux, , Retrocaval ureter
Neoplastic- Primary
carcinoma of ureter,
Metastatic carcinoma
Inflammatory-
Tuberculosis ,post radiation
Metabolic stone ureter
Traumatic mostly iatrogenic
External compression
Retroperitoneal fibrosis,
Aortic aneurysm, Pregnancy
 Causes of Obstructive Nephropathy
• Bladder and Urethra
Congenital- Posterior
urethral valve,
Neoplastic- Bladder
carcinoma, Prostate
carcinoma, Carcinoma of
urethra, Carcinoma of
penis
Inflammatory- Para
urethral abscess, phimosis
Miscellaneous-Benign
prostatic hypertrophy
Functional Neurogenic
bladder
Metabolic stone bladder or
urethra
Traumatic stricture urethra
 Global Renal Functional Changes
• Obstruction can affect hemodynamic variables and GFR
– Degree of affect depends on extent and severity of
obstruction, whether UUO or BUO, and whether it has
been relieved or not
• GFR= Kf(PGC-PT-PGC)
– Need to understand in order to comprehend the
relationships between changes in renal hemodynamics and
alterations in GFR during and after obstruction
– Kf glomerular ultrafiltration coeffecient related to the surface
area and permeability of the capillary membrane
– PGC glomerular capillary pressure. Influenced by renal plasma
flow and the resistance of the afferent and efferent arterioles
– PT Hydraulic pressure of fluid in the tubule
-P the oncotic pressure of the proteins in the glomerular capillary
and efferent arteriolar blood
Global Renal Functional Changes

• RPF= (aortic pressure-renal venous

pressure)
renal vascular resistance
– Influences PGC
– Constriction of the afferent arteriole
will result in a decrease of PGC and
GFR
– An increase in efferent arteriolar
resistance will increase PGC
Hemodynamic Changes with Unilateral
Ureteral Occlusion
Triphasic pattern of renal blood flow and
ureteral pressure changes
1.RBF increases during the first 1-2 hours and
is accompanied by a high PT and collecting
system pressure
2. For another 3-4 hours, the pres. remains
elevated but the RBF begins to decline.
3. 5 hours after obstruction, further decline in
RBF occurs. A decrease in PT and collecting
system pressure also occurs
Triphasic pattern of UUO
Hemodynamic Changes with Unilateral
Ureteral Occlusion
Alterations in flow dynamics within the
kidney occur due to biochemical and
hormonal changes regulating renal
resistance
Phase I: increased PT is counterbalanced
by an increase in renal blood flow via
net renal vasodilation, which limits the
fall of GFR.
PGE2, NO. Contribute to net renal
vasodilatation early in UUO
Hemodynamic Changes with Unilateral
Ureteral Occlusion
Phase II and III- An increase in afferent
arteriolar resistance occurs causing a
decrease RPF. A shift in RBF from the
outer cortex to the inner cortex also
occurs all reducing GFR
Angiotensin II, TXA2, Endothelin - mediators of
the pre-glomerular vasoconstriction during
the 2nd and 3rd phase of UUO
Hemodynamic Changes with Bilateral
Ureteral Occlusion
Only a modest increase in RBF lasting 90 min.
followed by prolonged and profound decrease
in RBF that is even more than with UUO
• The intrarenal distribution of blood flow
changes from the inner to the outer cortex
(opposite from UUO)
• Accumulation of vasoactive substances (ANP)
in BUO, contributes to pre-glomerular
vasodilatation and post-glomerular
vasoconstriction
 Hemodynamic Changes with Bilateral
Ureteral Occlusion
With UUO, these substances would be excreted
by the normal kidney.
• When obstruction is released, GFR and RBF
remain depressed due to persistent
vasoconstriction of the afferent arteriole
The post-obstructive diuresis is much greater
than with UUO
Partial Ureteral Occlusion: Changes in renal
hemodynamics and tubular function are similar
to complete models of obstruction, but it
Develops more slowly
Effects of Obstruction on Tubular
Function
• Dys-regulation of aquaporin water channels
in the proximal tubule, thin descending
loop, and collecting tubule. Lead to polyuria
and impaired concentrating capacity
• Sodium Transport
• Potassium and phosphate excretions follow
changes in sodium
• Deficit in urinary acidification
• Magnesium excretion is increased after
release of UUO or BUO
• Changes in pepetide excretion mark renal
damage
Cellular and Molecular Changes lead to
Fiborosis and Tubular Cell Death
• Obstruction leads to biochemical, immunologic,
hemodynamic, and functional Kediny’s changes
• These changes lead to release of angiotensin II,
cytokines, and growth factors (TGF-B, TNF-a,
NFkB): Some mediators are produced directly
from the renal tubular and interstitial cells. Others
are generated by way of fibroblasts and
macrophages
• Progressive and permanent changes to the kidney
occur:
Tubulointerstitial fibrosis, Tubular atrophy and
apoptosis, Interstitial inflammation
Pathologic Changes of Obstruction
Gross Changes
42 hours- Dilation of the pelvis and ureter and
blunting of the papillary tips. Kidney is also
heavier
7days- Increased pelvi-ureteric dilation and the
Parenchyma is edematous
21-28 days- External dimensions of kidneys are
similar but the cortex and medullary tissue is
diffusely thinned
6 weeks- Enlarged, cystic appearing, weighs less
than non-obstructed kidney
Did not see such differences in partially obstruct. kidneys
 Pathologic Changes of Obstruction
• Microscopic Pathologic Findings
– 42 hours- Lymphatic dilation, interstitial edema,
tubular and glomerular preservation
– 7 days- Collecting duct and tubular dilation,
widening of Bowman’s space, tubular basement
membrane thickening, cell flattening
– 12 days- Papillary tip necrosis, regional tubular
destruction, inflammatory cell response
– 5-6 weeks- widespread glomeular collapse and
tubular atrophy, interstitial fibrosis, proliferation
of connective tissue in the collecting system
Compensatory Renal Growth
• Enlargement of the contra lateral
kidney with unilateral advanced
hydronephrosis or renal agenesis
• A reduction in compensatory growth
occurs with age
• An increase in the number of
nephrons or glomeruli does not occur,
despite enlargement
 Diagnosis
• History:
– Pain, renal colic
– Inability to void effectively
– Alteration in pattern of micturition (anuria,
polyuria, nocturia)
– Abdominal swelling
– Recurrent UTI
– New-onset or poorly controlled hypertension
– History of pelvic radiation
– Recent gynecologic or abdominal surgery
 Diagnosis
• Physical Examination
– Signs of uremia or acidosis
– Peripheral edema, hypertension, signs
of congestive heart failure
– Palpable kidney or bladder
– Enlargement of pelvic organs (eg.
Prostate, uterus)
– Examination of external urethra for
phimosis, meatal stenosis
Diagnosis
Laboratory investigations
1/urine analysis
2/kidney function tests
3/ full blood count
4/arterial blood gas …
 Diagnosis: Radiological
• Renal US
– Safe in pregnant and pediatric patients
– Good initial screening test
– No need for IV contrast
– May have false negative in acute obstruction (35%)
– Hydronephrosis= anatomic diagnosis
• Can have caliectasis or pelviectasis in an
unobstructed system
– Doppler- measures renal resistive index (RI), an
assessment of obstruction : RI= (PSV-EDV)/PSV
– RI > 0.7 is suggestive elevated resistance to
blood flow suggesting obstructive uropathy
 Diagnosis: Radiological
• Excretory
Urography
– Applies anatomic and
functional information
– disadvantages
1- Limited use in
patients with renal
insufficiency
2- Increased risk of
contrast-induced
nephropathy
3-Cannot use in patients
 Diagnosis: Radiological
• CT • MRI
– Can identify
– Most accurate hydronephrosis but unable
study to diagnose to identify calculi and
ureteral calculi ureteral anatomy of
unobstructed systems
– More sensitive to – Diuretic MRU can
identify cause of demonstrate obstruction
obstruction – advantages
• Especially accurate with
strictures or congenital
abnormalities
• No contrast
• More safe
Diagnosis: Radiological
• voiding urethro cystogram
helpful in diagnosis of stricture urethra

• uroflow meter
Helpful in diagnosis of infra vesicle
obstruction
 Diagnosis: Radiological
• Nuclear Renography
– Provides functional assessment without contrast
• Obstruction is measured by the clearance
curves
– Tc 99m DTPA- glomerular agent
– Tc 99m MAG3 – tubular agent

– Diuretic renogram- maximizes flow and

distinguishes true obstruction from dilated and
unobstructed
Normal = T ½ < 10 min Indeterminate = T ½ 10-20 min Obstructed T ½ > 20 min
Diagnostic Imaging
• Retrograde • Antegrade Pyelography
Pyelography – Can do if RGP is not
– Gives accurate details of possible and other
ureteral and collecting imaging doesn’t offer
system anatomy enough details
– Good if renal
insufficiency or other
risks for contrast
Diagnostic Imaging

• Whitaker Test
– “True pressure” within the pelvis =
Collecting system pressure – intravesicle presure
• Saline or contrast though a percutaneous
needle or nephrostomy tube at a rate of 10mL/
min
• Catheter in bladder to monitor intravesicle
pressure
Normal < 15 cm H2O Indeterminate = 15-22 cm H2O Obstruction > 22 cm H2O

– Invasiveness and discordant results limit clinical usefulness

Management

• Relief of obstruction first followed by

Treatment of the cause of the
obstruction
• Or treatment of the obstruction and
the cause at the same time
• Treatment of the associated conditions
Management
• Depend on the following
• 1 /general condition of the patient
• 2 /facilities
• 3 /surgical experience
 Management
1 relief of the obstruction
Infra vesicle obstruction
immediate Relief of the obstruction (urine
retention ) using urethral Foleys catheter or
supra pubic catheter in cases of
1/ acute urine retention
2/chronic urine retention with:
• impaired kid function
• urine incontinence
• unresolved infection
 Management
1 relief of the obstruction
Vesicle or supra vesicle obstruction
– End urologic ureteric stents or percutaneous
nephrostomy procedures allow prompt
temporary and occasionally permanent
drainage .it Is mostly indicated in acute BUO
with anurea at the vesicle and supra vesicle
level.
Management
2/ Treatment of the cause of obstructive
uropathy ,
We can start to treat the cause of
obstruction together with relief of the
obstruction it self in cases of
1/ partial or complete UUO.
2 / partial BUO .
3/ management of associated
condition
• Pain
• Hypertension
• Urinary tract infection
• Post obstructive duresis
Renal Recovery after Obstruction
• Degree of obstruction, age of patient, and
baseline renal function affect chance of
recovery
– Two phases of recovery may occur
• Tubular function recovery
• GFR recovery
• Duration has a significant influence
– Full recovery of GFR seen with relief of acute
complete obstruction
– Longer periods of complete obstruction are
associated with diminished return of GFR

• DMSA scan is predicative of renal recovery