This document provides an overview of obstructive uropathy. It begins by defining obstructive uropathy as the functional or anatomic obstruction of urine flow at any level of the urinary tract. It then discusses the prevalence of obstructive uropathy and how it can be classified based on factors like duration and site of obstruction. Potential causes of obstructive uropathy are then reviewed for different parts of the urinary tract. The pathophysiology and hemodynamic changes that occur with obstruction are explained. Cellular and molecular changes that can lead to fibrosis and tubular cell death are described. Management of patients is discussed including diagnostic imaging, issues in patient care like hypertension and pain management, and considerations for surgical intervention.

1. Dr. Khaing Zay Aung
25/2/2016
Obstructive Uropathy
1

2. • Functional or anatomic obstruction of urine flow at any
level of the urinary tract.
• Obstructive nephropathy – when obstruction causes
functional or anatomic renal damage.
• Hydronephrosis – aseptic dilatation of the renal pelvis or
calyces.
What is obstructive uropathy?
2

3. • 3.1% of autopsy cases
• Until 20 yrs – no gender difference
• 20- 60 yrs – females more common
• >6o yrs – males more common
Prevalence
3

4. • Acute or chronic – duration
• Congenital or acquired
• Unilateral or bilateral
• Upper tract obstruction and lower tract obstruction – site of
obstruction
• Mechanical or functional
• Intraluminal
• Intramural or agent of obstruction (mechanical)
• Extra luminal
Can be clssified:
4

5. Possible Causes of Obstructive Nephropathy
•Renal
• Congenital, Polycystic kidney, Renal cyst, Fibrous obstruction at ureteropelvic
junction, Peripelvic cyst, Aberrant vessel at ureteropelvic junction
• Neoplastic- Wilms' tumor, Renal cell carcinoma, Transitional cell carcinoma of
the renal pelvis, Multiple myeloma
• Inflammatory- Tuberculosis, Echinococcus Infection
• Metabolic- Calculi
• Miscellaneous- Sloughed papillae, Trauma, Renal artery aneurysm
Causes
5

6. 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, Hydrocolpos
•Neoplastic- Bladder carcinoma, Prostate carcinoma, Carcinoma of
urethra, Carcinoma of penis
•Inflammatory- Prostatitis, Paraurethral abscess
•Miscellaneous-Benign prostatic hypertrophy, Neurogenic bladder
6

7. 7

8. • Unilateral ureteral occlusion
• Triphasic pattern of renal blood flow and ureteral pressure
changes
• during first 1-2 hrs - Renal blood flow increases and is
accompanied by a high pressure in tubule and collecting system
pressure
• Another 3-4 hours – the pressures remains elevated but renal
blood flow begins to decline
• 6 hrs – further decline in RBF and decrease in PT and also the
collecting system pressure.
Pathophysiology of obstructive uropathy
8

9. 9

10. • Alterations in flow dynamics within the kidney occur due 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
10

11. Hemodynamic Changes with Bilateral Ureteral
Occlusion
• 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 UUO)
• 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
11

12. Summary of UUO and BUO
12

13. Partial Ureteral Occlusion
• Changes in renal hemodynamics and tubular function are
similar to complete models of obstruction
• Develop more slowly
• Animal Studies- Difficult to imitate partial obstruction
• 14 days- normal functional recovery
• 28 days- recover 31% of function
• 60 days- recovery 8% of function
13

14. 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 capacity
• Sodium Transport
• Decreased which leads to a role in the post-obstructed kidney’s 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 natriuresis
14

15. • 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
15

16. 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-Β, TNF-α, NFκΒ)
• 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 16

17. 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 heavier
• 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
17

18. 18

19. 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
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
19

20. Compensatory Renal Growth
• Enlargement of the contralateral kidney with unilateral
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
20

21. 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
21

22. Management of Patients with Obstruction
Diagnostic Imaging
• 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
22

23. Grading of Hydronephrosis by ultrasound
23

24. 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
24

25. Diagnostic Imaging
• Retrograde Pyelography
• Gives accurate details of ureteral
and collecting system anatomy
• Good if renal insufficiency or
other risks for contrast
• Loopogram- use for evaluation of
patients with cutaneous
diversions
• Antegrade Pyelography
• Can do if RGP is not possible
and other imaging doesn’t
offer enough details
25

26. 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
• Invasiveness and discordant results limit clinical usefulness
Normal < 15 cm H2O Indeterminate = 15-22 cm H2O Obstruction > 22 cm H2O
26

27. 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 unobstructed
Normal = T ½ < 10 min Indeterminate = T ½ 10-20 min Obstructed T ½ > 20 min
27

28. Diagnostic Imaging
• 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
• 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
abnormalities
• IV gadopentetate-DTPA
allows functional assessment
of collecting system while
providing anatomic detail
• GFR assessment
• Renal clearance
• Still several limitations in its use
28

29. Issues in Patient Management
• Hypertension
• Can be caused by ureteral obstruction
• Especially BUO or obstruction of a solitary kidney
• Less common with UUO
• Volume-mediated
• Increased ANP with obstruction which normalizes after drainage
• Decreased plasma renin activity
29

30. • Renal Drainage
• Endourologic or IR procedures allow prompt temporary and
occasionally permanent drainage
• Patients with extrinsic compression causing obstruction
have a high risk of ureteral stent failure
• 42-56.4 % failure rate at 3 months
• 43% failed within 6 days of placement in one study
• 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 pyonephrosis
• Large diameter ureteral stents
30

31. Issues in Patient Management
Considerations in Surgical Intervention
• Reconstruction
• Endoscopic, open and laparoscopic
techniques should be considered
• Need for nephrectomy?
• Allow 6-8 weeks for adequate drainage
before proceeding
• Nuclear imaging provides accurate functional
information
• < 10% contribution to global renal function is
considered threshold for nephrectomy
31

32. Issues in Patient Management
Pain
• 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
• NSAIDS
• 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 bleeds
32

33. Issues in Patient Management
Post-obstructive Diuresis
• Usually with BUO or solitary kidney
• Urine output > 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 absorption
• Downregulation of sodium transporters and sodium reabsorption in the
thick ascending loop of Henle
• Increased production and altered regulation of ANP
• Poor response of collecting system to ADH 33

34. Issues in Patient Management
Post-obstructive Diuresis
• Management
• Monitor those with BUO or UUO in solitary kidney for POD
• Electrolytes, Mg, BUN, Cr
• Intensity of monitoring depends on clinical factors
• 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 Fluids)
• 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
34

35. • Obstruction of the bladder outflow and the condition is
collectively known as BOO.
• Symptoms can be categorised into – obstructive
symptoms and irritative symptoms.
• Among the causes of BOO – BPH and urethral strictures.
Lower urinary tract obstruction
35

36. 36

37. • Obstructive symptoms
• Weak stream
• Hesitancy
• Internittentency
• Dribbling
• Straining to void
• Irritative symptoms
• Frequency
• Urgency
• Nocturia
• Dysuria
• Urge incontinence
37

38. • 50% of men over age 60
• Hyperplasia of both stromal and glandular portions
• Static theory and dynamic theory
• Prostatism
• Investigations
• Urinalysis
• Ultrasound – to estimate the prostatic volume and also impact
on baldder
• KUB / IVU
• Urea, electrolyte, creatinine, CBC
Benign prostatic hyperplasia
38

39. • Treatment
• Medical
• Alfa antagonists
• 5ARI
• Other supportive medications
• Surgical
• TURP
• Minimally invasive surgical treatment
• Transurethral microwave therapy
• Transurethral needle ablation
• PUL
• Open prostatectomy
• Transvesical prostatectomy
• Retropubic
• preineal
39

40. • Recurrent UTI, BXO
• Trauma
• Iatrogenic
Obstructive symptoms
Irritative symptoms if infection (+)
May be associated with stone formation
Urethral strictures
40

41. • Diagnostic work-up
• In addition to
• Ascending and descending urethrogram
• Treatment
• Optical urethrotomy
• Open urethrotomy
41

42. • May result in renal impairment
• Kidneys respond to partial or complete obstruction by
reduce in ipsilateral renal blood flow and by increase in
contralateral renal blood flow
• Unrelieved obstruction – due to ischaemic and pressure
atrophy
Upper urinary tract obstruction
42

43. • Intraluminal obstruction
• Due to calculus commonly
• Presents with ureteric colic
• Pain X ray KUB will confirm 90% of stones
• IVU will confirm the site of obstruction and also the functional
status
• Clots from bleeding in renal pelvis
• Renal papillary necrosis is uncommon
Unilateral obstruction
43

44. Intramural obstruction
•Congenital obstruction of the pelviureteric junction
• Congenital PUJ obstruction is common caused by failure of
tranission of peristalsis from the pelvis to ureter
• May be asymptomatic or may present with loin pain esply after
the fluid load (Dietl’s crisis)
• The ureter wouldn’t be seen in IVU
• Treatment is surgical
44

45. • Obstruction of the ureterovesical junction
• Obstructed megaureter
• Pain, haematuria and infection
• Reinplantation of the the ureter after excision of the diseased
distal portion
• Ureteric strictures
• May occur after ureteroscopy and stone manipulation
• Pelvic surgery, irridiation or chronic inflammatory conditions
• Ureteric tumours
• Accounts for appx 1% of all urothelial tumours
• Haematuria and colic
• Cytology of urine and IVU
• Nephroureterectomy and regular followup cystoscopy
• Recurrences in bladder are common
45

46. Extramural obstruction
•Rare
•Especially due to tumours
46

47. • Causes of unilateral upper tract obstruction
47

48. Bilateral upper tract obstruction
• Tumours of the pelvis and retroperitoneum
• Most tumours of the retroperitoneum are malignant
• Cervix, prostate, bladder, breast, colon, ovary and uterus
• Other primary retroperitoneal tumours
• Ureters may be reinplanted or consider urinary diversion
48

49. • Retroperitoneal fibrosis
• Usually idiopathic
• Due to the process of fibrosis – ureters – usu pulled towards the
midline and gradually obstructed
• May be silent and present with renal failure
• IVU will show deviation of ureters to midline and hydronephrosis
• Relieve of ureteric obstruction, ureterolysis, and wrapping of
ureters with omental tubes to prevent recurrent
49

50. • Causes of bilateral urinary tract obstruction
(Both upper and lower)
50

51. 51