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Pathophysiology of Urinary Tract Obstruction


Pathophysiology of Urinary Tract Obstruction Jamie Bartley D.O. PGY 3..almost 4 5/27/09 MSU-COM Metro Detroit Urology Outline I. Background II. Pathophysiology and ... – PowerPoint PPT presentation

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Title: Pathophysiology of Urinary Tract Obstruction

Pathophysiology of Urinary Tract Obstruction
  • Jamie Bartley D.O.
  • PGY 3..almost 4
  • 5/27/09
  • MSU-COM Metro Detroit Urology

  • I. Background
  • II. Pathophysiology and pathological changes with
    urinary tract obstruction
  • III. Patient work-up and management
  • IV. Causes of urinary tract obstruction

  • Hydronephrosis- Dilation of the renal pelvis or
  • 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

  • 3.1 in autopsy series
  • No gender differences until 20 years
  • Females more common 20-60
  • Males more common older than 60
  • 2-2.5 of children at autopsy

Causes of Obstructive Nephropathy
  • Table 37-1   -- Possible Causes of Obstructive
  • Renal-
  • Congenital, Polycystic kidney, Renal cyst,
    Fibrous obstruction at ureteropelvic junction,
    Peripelvic cyst, Aberrant vessel at ureteropelvic
  • Neoplastic- Wilms' tumor, Renal cell carcinoma,
    Transitional cell carcinoma of the renal pelvis,
    Multiple myeloma
  • Inflammatory- Tuberculosis, Echinococcus
  • Metabolic- Calculi
  • Miscellaneous- Sloughed papillae, Trauma, Renal
    artery aneurysm
  • Ureter
  • Congenital- Stricture, Ureterocele,
    Ureterovesical reflux, Ureteral valve, Ectopic
    kidney, Retrocaval ureter, Prune-belly syndrome
  • Neoplastic- Primary carcinoma of ureter,
    Metastatic carcinoma
  • Inflammatory- Tuberculosis, Schistosomiasis,
    Abscess, Ureteritis cystica, Endometriosis
  • Miscellaneous- Retroperitoneal fibrosis, Pelvic
    lipomatosis, Aortic aneurysm, Radiation therapy,
    Lymphocele, Trauma, Urinoma, Pregnancy
  • Bladder and Urethra
  • Congenital- Posterior urethral valve, Phimosis,
    Urethral stricture, Hypospadias and epispadias,
  • Neoplastic- Bladder carcinoma, Prostate
    carcinoma, Carcinoma of urethra, Carcinoma of
  • Inflammatory- Prostatitis, Paraurethral abscess
  • Miscellaneous-Benign prostatic hypertrophy,
    Neurogenic bladder

Global Renal Functional Changes
  • Obstruction can affect hemodynamic variables and
  • Degree of affect depends on extent and severity
    of obstruction, whether UUO or BUO, and whether
    it has been relieved or not
  • Need to understand in order to comprehend the
    relationships between changes in renal
    hemodynamics and alterations in GFR during and
    after obstruction
  • 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

Kf- flomerular 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
Hemodynamic Changes with Unilateral Ureteral
  • 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
  • 2. For another 3-4 hours, the pressures 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
  • Alterations in flow dynamics within the kidney
    occur dye to changes in the biochemical and
    hormonal milieu regulating renal resistance
  • Phase I- The 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 vasodilation
    early in UUO
  • 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 preglomerular vasoconstriction during the 2nd
    and 3rd phase of UUO

Hemodynamic Changes with Bilateral Ureteral
  • Only a modest increase in RBF lasting 90 minutes
    followed by a 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
  • Accumulation of vasoactive substances (ANP) in
    BUO that contributes to preglomerular
    vasodilation and postglomerular vasoconstriction
  • With UUO, these substances would be excreted by
    the normal kidney
  • When obstruction is released, GFR and RBF remain
    depressed due to persisent vasoconstriction of
    the afferent arteriole
  • The post-obstructive diuresis is much greater
    than with UUO

Summary of UUO and BUO
Partial Ureteral Occlusion
  • Changes in renal hemodynamics and tubular
    function are similar to complete models of
  • Develop more slowly
  • Animal Studies- Difficult to imitate partial
  • 14 days- normal functional recovery
  • 28 days- recover 31 of function
  • 60 days- recovery 8 of function

Effects of Obstruction on Tubular Function
  • Dysregulation of aquaporin water channels in the
    proximal tubule, thin descending loop, and
    collecting tubule
  • Lead to polyuria and impaired concentrating
  • Sodium Transport
  • Decreased which leads to a role in the
    postobstructed kidneys impaired ability to
    concentrate and dilute urine
  • Much greater sodium and water excretion after
    release of BUO than UUO
  • Thought to be due to the retention of Na, water,
    urea nitrogen and increased ANP, all which
    stimulate a profound naturesis
  • Potassium and phosphate excretions follow changes
    in sodium
  • Decreased with UUO
  • Increased transiently with BUO in parallel with
    the massive diuresis
  • 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 changes of the kidney
  • A cascade of events occur which 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
  • Progressive and permanent changes to the kidney
  • Tubulointerstitial fibrosis
  • Tubular atrophy and apoptosis
  • Interstitial inflammation

Pathologic Changes of Obstruction(porcine model)
  • Gross Pathologic Changes
  • 42 hours- Dilation of the pelvis and ureter and
    blunting of the papillary tips. Kidney also
  • 7days- Increased pelviureteric dilation and
    weight. 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
    obstructed kidneys

Pathologic Changes of Obstruction (porcine model)
  • Microscopic Pathologic Findings
  • 42 hours- Lymphatic dilation, interstitial edema,
    tubular and glomerular preservation
  • 7 days- Collecting duct and tubular dilation,
    widening of Bowmans 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 contralateral kidney with
    unilateral hydronephrosis or renal agenesis
  • A reduction in compensatory growth occurs with
  • An increase in the number of nephrons or
    glomeruli does not occur, despite enlargement

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

Now on to the Clinical Stuff
Management of Patients with ObstructionDiagnostic
  • Renal US
  • Safe in pregnant and pediatric patients
  • Good initial screening test
  • No need for IV contrast
  • May have false negative in acute obstruction
  • Hydronephrosis anatomic diagnosis
  • Can have caliectasis or pelviectasis in an
    unobstructed system
  • Doppler- measures renal resistive index (RI), an
    assessment of obstruction
  • RI gt 0.7 is suggestive elevated resistance to
    blood flow suggesting obstructive uropathy

Diagnostic Imaging
  • Excretory Urography
  • Applies anatomic and functional information
  • Limited use in patients with renal insufficiency
  • Increased risk of contrast-induced nephropathy
  • Cannot use in patients with contrast allergy

Diagnostic Imaging
  • Retrograde Pyelography
  • Gives accurate details of ureteral and collecting
    system anatomy
  • Good if renal insufficiency or other risks for
  • Loopogram- use for evaluation of patients with
    cutaneous diversions
  • Antegrade Pyelography
  • Can do if RGP is not possible and other imaging
    doesnt offer enough details

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
  • Invasiveness and discordant results limit
    clinical usefulness

Normal lt 15 cm H2O Indeterminate 15-22 cm
H2O Obstruction gt 22 cm H2O
Diagnostic Imaging
  • 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

Normal T ½ lt 10 min Indeterminate T ½ 10-20
min Obstructed T ½ gt 20 min
Diagnostic Imaging
  • MRI
  • Can identify hydro but unable to identify calculi
    and ureteral anatomy of unobstructed systems
  • Diuretic MRU can demonstrate obstruction
  • Especially accurate with strictures or congential
  • IV gadopentetate-DTPA allows functional
    assessment of collecting system while providing
    anatomic detail
  • GFR assessment
  • Renal clearance
  • Still several limitations in its use
  • CT
  • Most accurate study to diagnose ureteral calculi
  • More sensitive to identify cause of obstruction
  • Helpul in surgical planning
  • Preferred initial imaging study in those with
    suspected ureteral obstruction

Issues in Patient Management
  • Hypertension
  • Can be caused by ureteral obstruction
  • Especially BUO or obstruction of a solitary
  • Less common with UUO
  • Volume-mediated
  • Increased ANP with obstruction which normalizes
    after drainage
  • Decreased plasma renin activity

Issues in Patient Management
  • Renal Drainage
  • Endourologic or IR procedures allow prompt
    temporary and occasionally permanent drainage
  • No statistically significant difference in HRQL
    between the two techniques
  • Patients with extrinsic compression causing
    obstruction have a high risk of ureteral stent
  • 42-56.4 failure rate at 3 months
  • 43 failed within 6 days of placement in one
  • High failure rate at even getting placement(27)
  • Stent diameter did not predict risk of failure
  • Ultrasound guided percutaneous drainage should be
    initial consideration in pregnant patients
  • Percutaneous placement with suspected
  • Large diameter ureteral stents

Issues in Patient ManagementConsiderations in
Surgical Intervention
  • Reconstruction
  • Endoscopic, open and laparoscopic techniques
    should be considered
  • Need for nephrectomy?
  • Allow 6-8 weeks for adequate drainage before
  • Nuclear imaging provides accurate functional
  • lt 10 contribution to global renal function is
    considered threshold for nephrectomy

Issues in Patient ManagementPain
  • Increases in collecting system pressure and
    ureteral wall tension contribute to renal colic
  • Results in spinothalamic C-fiber excitation
  • Treating Pain
  • Narcotics
  • Rapid onset, nausea, sedation, abuse
  • Targets the inflammatory basis of pain by
    inhibiting prostaglandin synthesis
  • Reduces collecting system pressure by decreasing
    renal blood flow
  • Avoid in patients with renal insufficiency, GI

Issues in Patient ManagementPostobstructive
  • Usually with BUO or solitary kidney
  • Urine output gt 200ml/hour
  • A normal physiologic response to volume expansion
    and solute accumulation
  • Elimination of sodium, urea, and free water
  • Diuresis ends when homeostasis returns
  • Pathologic postobstructive diuresis
  • Impaired concentating abilility or sodium
  • Downregulation of sodium transporters and sodium
    reabsorption in the thick ascending loop of Henle
  • Increased production and altered regulation of
  • Poor response of collecting system to ADH

Issues in Patient ManagementPostobstructive
  • Management
  • Monitor those with BUO or UUO in solitary kidney
    for POD
  • Electrolytes, Mg, BUN, Cr
  • Intensity of monitoring depends on clinical
  • If no signs of POD? If alert, no fluid overload,
    normal renal function, normal lytes, ? discharge
    and follow up
  • If signs of POD ? If alert, able to consume
    fluids, normal VS? continue in-patient
    observation, free access to oral fluids, and
    daily labs until diuresis resolves (No IV
  • If signs of POD and signs of fluid overload, poor
    renal function, hypovolemia, or MS changes?
    Frequent VS and u.o records, labs q 12 hrs (or
    more), urinary osmolarity, restrict oral
    hydration (Minimal IV fluid hydration)
  • Most have self-limiting physiologic diuresis
  • If pathologic diuresis occurs- very intense
    monitoring is indicated

Selected Causes of Extrinsic Ureteral Obstruction
Retroperitonal Fibrosis
  • Condition in which an inflammatory mass, a
    fibrous whitish plaque, envelops and potentially
    obstructs retroperitoneal structures
  • Usually extends from the renal hilum to pelvic
  • May involve the mediastinum and the pelvis
  • 2 phases lead to its development
  • 1. Autoimmune reaction thought to occur due to
    leakage of ceroid from the atheromatous plaques
    in the aorta
  • Local inflammatory reaction characterized by
    plasma cells, lymphocytes, macrophages,
  • 2. Fibrotic maturation with development of
    homogeneous fibrous tissue with limited

Retroperitoneal Fibrosis
  • 1 200,000, 31 Male Female, Age 50
  • 2/3s of Cases are Idiopathic
  • 8-10 of cases have underlying malignancy
  • Other causes Medications (methysergide,
    hydralazine, Haldol, B-Blockers, LSD, Phenacetin,
    Amphetamines), RP hemorrhage, urinary
    extravasation, trauma, radiation, IBD, Gonorrhea,
    collagen disease, peri-aneurysmal inflammation
  • Symptoms- Dull, non-colicky pain in a girdle
    distribution, ureteral or vascular obstruction

Retroperitoneal Fibrosis
  • Diagnosis
  • IVP- Medial deviation of the ureters
  • Can be seen in 18 of normal subjects
  • CT well demarcated mass that is isodense with
    muscle (non-contrast study)
  • MRI- Allows superior soft tissue discrimination
    and can more accurately distinguish the plaque
    from the great vessels

Diagnosis of Retroperiteoneal Fibrosis
Retroperitoneal Fibrosis
  • Treatment
  • 1. Correct obstructive uropathy
  • 2. Biopsy to exclude malignancy
  • 3. If biopsy is negative, medical therapy is
  • Discontinue any offending medications
  • Corticosteroids- prednisolone 60mg qod x 2 mos,
    tapered to 5mg daily over the next 2 months, then
    continue 5mg daily for 2 years
  • Tamoxifen
  • Immunotherapy
  • 4. Ureterolysis- if patient not a candidate for
    medical therapy or if it fails
  • - May do open or laparoscopic
  • - Bilateral treatment is recommended even if
  • disease
  • - To prevent recurrent ureteral involvement?
    bring ureter
  • intraperitoneal, or wrap in omentum
  • - Stents can usually be removed 6-8 wks after

Pelvic Lipomatosis
  • Rare benign proliferative disease involving the
    mature fatty tissues of the pelvic
  • 181 Male to female
  • More common in African American men
  • Unknown etiology
  • Obesity?
  • Genetic?

Pelvic Lipomatosis
  • Patient Presentation and Diagnosis
  • LUTS, Constipation, non-specific pain, HTN
  • Physical Exam- suprapubic mass, high riding
    prostate, indistinct pelvic mass
  • Younger patients are thought to have a more
    progressive course than older patients who have a
    more indolent course

Pelvic Lipomatosis
  • Imaging
  • KUB- Pelvic lucency
  • IVP- Bladder is pear-shaped and elevated,
    hydronephrosis may be evident
  • CT- pelvic fat is readily demonstrated

Pelvic Lipomatosis
  • Other evaluation
  • Cystoscopy- cystitis cystica, cystitis glandular
    (40), adenocarcinoma, chronic UTI
  • High bladder neck, pelvic fixation, and elongated
    prostatic urethra may impair rigid cystoscopy
  • Treatment
  • Exploration is not recommended due to the
    obliteration of normal planes and increased
    vascularity of the mass
  • In patients with obstructive uropathy? stents,
    PCNs, ureteral reimplanation, urinary diversion

  • Reported to occur in 43-100
  • Right gt Left
  • Etiology
  • Hormonal- progesterone thought to promote
    ureteral dilation
  • Mechanical increased degree of dilation after
    20 weeks when the uterus reaches the pelvic brim

  • Diagnosis
  • Usually asymptomatic
  • If symptoms, may have flank pain or
  • US will show dilation to the pelvic brim
  • If it extends below this, consider other
    etiologies (stone)
  • Limited IVU or MRI to diagnose
  • Treatment
  • Most respond to conservative treatment
  • IVF, analgesics, antibiotics
  • If signs of sepsis or compromised renal function
    may need ureteral stents or nephrostomy tubes

  • GU involvement
  • Bladder 70-80
  • Ureter 15-20
  • May be intrinsic or extrinsic (80)
  • Cyclical flank pain, dysuria, urgency, UTI,
    hematuria, or no GU symptoms (silent loss of
    renal function may occur)
  • Recommended to image the Upper tracts in all
    patients with pelvic endometriosis (RUS or EXU)

  • Treatment
  • Hormone therapy- if normal renal function with
    mild hydro and no functional obstruction seen on
  • GnRH agonists
  • Surgery- treatment of choice for patients with
    significant disease
  • TAH with BSO
  • Unilateral oopherectomy
  • Ureterolysis if extrinsic disease
  • Distal ureterectomy with reimplantation

Vascular Causes of Ureteral Obstruction
  • Abdominal Aortic Aneurysm
  • Ureteral obstruction may be the first sign
  • Medial deviation of the ureters associated with
    the desmoplastic reaction of inflammatory AAA
    (IAAA) more likely to cause obstruction than
    lateral deviation
  • Stent placement usually recommended prior to
    aneurysmal repair
  • Ureterolysis usually not needed and obstruction
    resolves with correction of the aneurysm

Circumcaval Ureter
  • Anomalous course of the ureter to the IVC leading
    to extrinsic obstruction
  • Thought to be due to the persistence of the
    subcardinal vein as the infrarenal IVC, causing
    medial migration and compression of the right
  • Other theories involve persistence of the
    posterior cardinal vein as the infrarenal cava
  • Both, theories note failure of the supracardinal
    vein to develop into the infrarenal IVC

Circumcaval Ureter
Circumcaval Ureter
  • Treatment is performed only in presence of
  • Divide ureter proximally and at the distal point
    it emerges lateral to the IVC
  • Spatulated ureterostomy performed

Other causes of vascular obstruction
  • Iliac Artery Aneurysm
  • Typically place internal ureteral stents prior to
    aneurysmal repair
  • Obstruction after Vascular Graft placement
  • Usually resolves spontaneously
  • Graft transection and repositioning
  • Chronic stenting
  • Puerperal Ovarian Vein Thrombophlebitis
  • Antiobiotic therapy usually resolves
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