This document discusses urinary obstruction, including its pathophysiology, causes, effects on renal physiology and function, histological changes, clinical impact, and renal recovery after relief of obstruction. It provides an overview of how urinary obstruction can lead to permanent kidney damage depending on the severity, chronicity, and baseline kidney condition. Both unilateral and bilateral obstruction are examined, along with the triphasic response and changes in renal blood flow, filtration, and tubular transport that occur.

1. Urinary Obstruction
Pathophysiology
Dept of Urology
Govt Royapettah Hospital and Kilpauk Medical College
Chennai

2. Moderators:
Professors:
• Prof. Dr. G. Sivasankar, M.S., M.Ch.,
• Prof. Dr. A. Senthilvel, M.S., M.Ch.,
Asst Professors:
• Dr. J. Sivabalan, M.S., M.Ch.,
• Dr. R. Bhargavi, M.S., M.Ch.,
• Dr. S. Raju, M.S., M.Ch.,
• Dr. K. Muthurathinam, M.S., M.Ch.,
• Dr. D. Tamilselvan, M.S., M.Ch.,
• Dr. K. Senthilkumar, M.S., M.Ch.
Dept of Urology, GRH and KMC, Chennai. 2

3. Urinary Obstruction
Urinary tract obstruction can result in permanent renal
damage.
The degree of injury depends on:
• Severity of the obstruction. (Partial or complete,
unilateral or bilateral),
• Chronicity of the obstruction (acute vs chronic),
• Baseline condition of the kidneys and
• Other mitigating factors such as UTI.
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Dept of Urology, GRH and KMC, Chennai.

4. Causes
of
Urinary Obstruction
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Dept of Urology, GRH and KMC, Chennai.

5. Congenital
Renal
• Polycystic kidney
• Renal cyst
• Peripelvic cyst
• Ureteropelvic junction
obstruction
Ureter
• Stricture
• Ureterocele
• Obstructing megaureter
• Retrocaval ureter
• Prune belly syndrome
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Dept of Urology, GRH and KMC, Chennai.

6. Neoplastic
Renal
• Wilms tumor
• Renal cell carcinoma
• Transitional cell
carcinoma of the
collecting system
• Multiple myeloma
Ureter
• Primary carcinoma of
ureter
• Metastatic carcinoma
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Dept of Urology, GRH and KMC, Chennai.

7. Infective and Inflammatory
Renal
• Tuberculosis
• Echinococcus infection
Ureter
• Tuberculosis
• Amyloidosis
• Schistosomiasis
• Abscess
• Ureteritis cystica
• Endometriosis
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Dept of Urology, GRH and KMC, Chennai.

8. Renal and Ureteric Causes
Metabolic
• Calculi
Miscellaneous
• Sloughed papillae
• Trauma
• Renal artery aneurysm
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Dept of Urology, GRH and KMC, Chennai.

9. Lower Genitourinary Causes
Congenital
• Posterior urethral valve
• Phimosis
• Hydrocolpos
Neoplastic
• Bladder carcinoma
• Prostate carcinoma
• Carcinoma of urethra
• Carcinoma of penis
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Dept of Urology, GRH and KMC, Chennai.

10. Lower Genitourinary Causes
Inflammatory
• Prostatitis
• Paraurethral abscess
Miscellaneous
• Benign prostatic
hypertrophy
• Neurogenic bladder
• Urethral stricture
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Dept of Urology, GRH and KMC, Chennai.

11. Other Miscellaneous
• Retroperitoneal fibrosis
• Pelvic lipomatosis
• Aortic aneurysm
• Radiation therapy
• Lymphocele
• Trauma
• Urinoma
• Pregnancy
• Radiofrequency
ablation
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Dept of Urology, GRH and KMC, Chennai.

12. Physiology
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13. 13
Dept of Urology, GRH and KMC, Chennai.

14. Glomerular Filtration Rate
The GFR is determined by
1. The sum of the hydrostatic and colloid osmotic forces
across the glomerular membrane, which gives the
net filtration pressure, and
2. The glomerular capillary filtration coefficient, Kf
GFR = Kf x Net filtration pressure
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Dept of Urology, GRH and KMC, Chennai.

15. Pressures In Filtration
1. Glomerular hydrostatic pressure,
2. Bowman’s capsule hydrostatic pressure,
3. Glomerular oncotic pressure,
4. Bowman’s capsule oncotic pressure.
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Dept of Urology, GRH and KMC, Chennai.

16. Net filtration pressure
Net filtration pressure represents:
• The sum of the hydrostatic and colloid osmotic forces
• That either favor or oppose filtration
• Across the glomerular capillaries.
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Dept of Urology, GRH and KMC, Chennai.

17. Net Filtration Pressure
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Dept of Urology, GRH and KMC, Chennai.

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Dept of Urology, GRH and KMC, Chennai.

20. Renal Plasma Flow
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Dept of Urology, GRH and KMC, Chennai.

21. Unilateral Urinary Obstruction
• More commonly encountered.
• Triphasic changes in RBF and ureteral pressure changes
have been noted.
• Phase 1 – one to two hours
• Phase 2 – Three to four hours
• Phase 3- Late phase
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Dept of Urology, GRH and KMC, Chennai.

22. Triphasic
Pattern
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23. Key Chemical Mediators
Increase RBF
RAS
NO
PGE2
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Dept of Urology, GRH and KMC, Chennai.

24. Renin Angiotensin System
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25. Unilateral Urinary Obstruction
Decrease
GFR
Increase
RBF
Increase
Filtration
pressure
More
urine in
Ureter
Increased
Ureteric
Pressure
UUO
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Dept of Urology, GRH and KMC, Chennai.

26. Unilateral Urinary Obstruction
Decrease
GFR
Increase
RBF
Increase
Filtration
pressure
More
urine in
Ureter
Increased
Ureteric
Pressure
UUO
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Dept of Urology, GRH and KMC, Chennai.

27. Triphasic Response
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28. NOS expression
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29. iNOS in Late Phase
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30. Late Phase
• NO production declines with depletion of L-arginine
substrate or
• Decreased NOS activity or
• Vascular endothelium becomes less responsive to the
action of NO following UO.
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Dept of Urology, GRH and KMC, Chennai.

31. Unilateral Ureteric Obstruction
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32. Bilateral Ureteric Obstruction
Afferent Dilataion,
Efferent Constriction
ANP
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Dept of Urology, GRH and KMC, Chennai.

33. Bilateral Ureteric Obstruction
P Ureter ↑
GFR ↓
Hypervolemia
Atrial Natriuretic Peptide Production
Afferent Arteriolar Dilatation,
Efferent Arteriolar Constriction,
↑ P Glomerular Capillaries.
P Ureter ↑
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Dept of Urology, GRH and KMC, Chennai.

34. Bilateral Ureteric Obstruction
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35. Cortical Vs Juxtamedullary Nephrons
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36. Cortical Vs Juxtaglomerular Nephrons
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37. Cortical Blood Flow Redistribution
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38. Partial Ureteral Obstruction
• Proper animal models not available.
• Behaves mostly like UUO.
• Generally there is decreased RBF and GFR.
• Shift in blood flow from outer cortex to inner cortex is
noted.
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Dept of Urology, GRH and KMC, Chennai.

39. Effects
on
Tubular Function
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Dept of Urology, GRH and KMC, Chennai.

40. Urinary Concentrating Ability
• AQP 2 expressed exclusively in Principal cells of collecting
tubule and collecting duct.
• It is vasopressin regulated.
• Downregulated in BUO.
• AQP 1, 3, 4 also decreased.
• Downregulation causes polyuria after obstruction relief.
• AQP 1 downregulation can cause polyuria upto 30 days.
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41. AQP 2 Expression
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42. AQP 2 Downregulation
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43. Sodium Transport
• Down regulation of important Na transporters noted in
both UUO and BUO.
• Leads to salt wasting after relief of obstruction.
• Natriuresis is greater in BUO than UUO.
• PGE2 inhibits NaCl reabsorption acting on Na
transporters in loop of henle and through AQP 2.
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Dept of Urology, GRH and KMC, Chennai.

44. Hydrogen ion transport
• Obstruction causes urinary acidification.
• Associated with decreased H+ secretion and defective
HCO3- absorption.
• Multiple acid-base transporters are downregulated.
• Mediated by iNOS.
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Dept of Urology, GRH and KMC, Chennai.

45. Other Cation Transport
• In UUO, K+ secretion is decreased.
• K+ excretion increases with increase in GFR in BUO after
relief, due to ANP.
• Magnesium excretion is also increased after the release
of UUO and BUO.
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Dept of Urology, GRH and KMC, Chennai.

46. 46
Dept of Urology, GRH and KMC, Chennai.

47. Gross Pathologic Changes
42 Hrs
• Dilatation of collecting system
• Blunting of papillary tips with increase in kidney weight
7 Days
• Further collecting system dilatation
• Further increase in renal weight
• Edema of renal parenchyma
21-28
• Cortex and medulla diffusely thinned
6 Wks
• Enlarged cystic appearance, lower weight compared to normal kidney.
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Dept of Urology, GRH and KMC, Chennai.

48. Microscopic Changes
Early Changes:
• Massive tubular dilatation
• Progressive tubulointerstitial fibrosis
• Inflammatory cell infiltration
• Apoptic renal tubular cell death
Late Changes:
• Glomerulosclerosis
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Dept of Urology, GRH and KMC, Chennai.

49. Early obstruction
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Dept of Urology, GRH and KMC, Chennai.

50. Chronic Obstruction
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51. Chronic Obstruction
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Dept of Urology, GRH and KMC, Chennai.

52. Tubulointerstitial fibrosis
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Dept of Urology, GRH and KMC, Chennai.

53. Clinical Impact
of
Urinary Obstruction
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Dept of Urology, GRH and KMC, Chennai.

54. Hypertension
• Common with BUO than UUO
• Mostly reversible after relief of obstruction
• Due to volume mediated mechanism due to increased
ANP and intravascular volume.
• RAS is implicated for UUO associated hypertension.
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Dept of Urology, GRH and KMC, Chennai.

55. Compensatory Renal Growth
• Seen in UUO, in contralateral kidney.
• Influenced by age and degree and duration of
obstruction.
• Less prominent in partial UUO.
• Increase in volume is due to hypertrophy not due to
hyperplasia.
• IGF 1 is involvedin renal hypertrophy.
• Sex hormones may also have a role.
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Dept of Urology, GRH and KMC, Chennai.

56. Renal Recovery after Obstruction
• Duration and severity of obstruction has significant
influence.
• Longer periods are associated with diminished GFR
return.
• It is due to persistent vasoconstriction of afferent
arteriole.
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Dept of Urology, GRH and KMC, Chennai.

57. Vaughan et al, Canine model
Duration Recovery
7 days 100%
14 days 70%
4 weeks 30%
6 weeks 0%
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Dept of Urology, GRH and KMC, Chennai.

58. 58
Dept of Urology, GRH and KMC, Chennai.