Dr. Khalil Al_Najjar provides an in-depth overview of obstructive uropathy (O.U). He discusses the prevalence and causes of O.U, including stones, strictures, BPH, cancers, and congenital abnormalities. The degree of renal damage depends on factors like duration and severity of obstruction. Histopathological changes include inflammatory cell infiltration, tubular dilation, and interstitial fibrosis. Clinical presentation varies based on acuteness and location of obstruction. Diagnostic tests include urine analysis, blood tests of kidney function, ultrasound, CT, and measurement of GFR. Treatment involves relieving obstruction through drainage or stenting. Renal recovery depends on how long the obstruction was present,

1. Dr: Khalil Al_Najjar
Doctorate Of Urology
Post-Doctorate Graduate
Of Endourology

2. OBSTRUCTIVE UROPATHY
( O.U )

3. Prevalence & Etiology
• Obstructive Uropathy accounts for 10 % of all cases of renal failure
• O.U is a major clinical problem that can result in permanent renal
damage
• The cause of urinary tract obstruction can be congenital or acquired
and benign or malignant

4. O.U generally caused by :-
• Stone-trauma-stricture-BPH-prostate cancer-bladder cancer-
metastatic carcinoma-RCC - UPJO (ureteropelvic junction
obstruction)- PCKD-peripelvic cyst- NB- -wilms tumor-TB-
Schistosomiasis-echinococcus infection-pregnancy-PUV-uretrocele-
RP fibrosis

5. • Hydronephrosis(HN) in children is because of congenital abnormality
• HN in women more 20-60 y/o due to pregnancy and gynecologic
malignancy
• HN >60 Y/O more in male due to prostatic dx

6. The degree of renal damage depends on severity&duration of
obstruction:-
• Acute or chronic obstruction
• Partial or complete obstruction
• Unilateral or bilateral obstruction
• The baseline condition of the kidneys
• Presence of other mitigating factors UTI

7. Histopathologic Changes

8. Microscopic Changes
Primarily localized to tubulointerstitial part
including :-
• Inflammatory cell infiltration start after 4 hr
• Massive tubular dilation
• Progressive tubulointerstitial fibrosis
• Loss of renal mass due to apoptosis cell death

9. Apoptosis
• Apoptosis of tubular cell start after 4 days and peaking after 15 days
of obstruction
• Interstitial cell apoptosis increase over the duration of obstruction
• Glomerular cell apoptosis not seen even after 90 days of obstruction
• Apoptosis may not stop even after relife of obstruction

10. Progressive tubulointerstitial fibrosis is the final
common pathway for all kidney disease that lead to
chronic renal failure (CRF)

11. Macroscopic Changes
After 42 hr of obstruction :-
• HN or dilation of renal pelvis or calyces
( collecting system dilation)
• Blunting of the papillary tipsa
• Increase weight of kidney

12. • After 1 wk  dilation and renal weight increase and parenchyma is
edematous
• After 2 wk further dilation developed
• After 3 – 4 wk  diffuse thining of cortex and medulla
• After 6 wk kidney is enlarged with cystic appearance but lower
weight compared to contralateral NL kidney

13. Clinical Presentation

14. • Quite variable depending on site,degree and chronicity of the
obstruction
Chronic O.U
• Chronic obstructive uropathy relatively painless or asymptomatic

15. Acute Obstruction
Flank pain:-
• The most common symptom in acute O.U
• Due to stretching of collecting system
• Colic-sever –unrelenting-excruciating pain
• Radiation to lower abdomen,testicles or labia
• Associated with nausea and vomitting

16. Bldder Outlet Obstruction
BOO often with voiding symptoms:-
• Frequency- urgency-hesitancy
• Nocturia-poor urinary stream
• Incomplete emptying sensation
• AUR
• Anuria

17. O.U always should be considered in :-
• Patient with new onset of HTN
• Patient with renal failure without hx of renal diseases, D.M or HTN
• Recurrent UTI

18. Laboratory Studies

19. U/A :-
• Estmation of osmolality
• UTI
• Crystalindicate stone formation
• Protein or cellur castmedical renal diseases

20. Blood tests:-
• CBC Anemia or Infection
• Cr, ureakidney function
• Electrolytes NA, K and CL

21. FEna
• FE na fractional excretion of sodium
• FEna = (Pcr×Una) / (Pna×Ucr)
In Renal Failure :-
• FEna<1%Prerenal ARF(CHD-hypovolemia-sepsis-renal artery
stenosis)
• FEna>1%intrinsic ARF(GN-ATN-AIN)
• FEna>4%post renal ARF(BUO-BPH Bladder.stone)

22. • Cr is the best single test to evaluate kedney function
• Cr is variable normal range with age-gender-race-and relationship
with muscle mass, so GFR formulas are helpful
• GFR is the gold standard measurement in renal insufficiency or renal
failure

23. GFR
(140-age) × wt(kg) × 0.85 if female
• GFR=------------------------------------------------
72×Serum Cr (milligrams per deciliter)

24. • GFR > 90  NL
• GFR=60-90 mild decline in Renal function
• GFR=30-60moderate decline renal function
• GFR =15-30sever decline in Renal function
• GFR < 15  considered Renal failure

25. Diagnostic Imaging

26. Ultrasound
• The first line imaging in O.U
• Available-low cost-safe-no contrast
• Provides anatomic information includind :- renal size-cortical
thickness-corticomedullary differentiation-grade of hydronephrosis
• Parenchymal thinning or small size kidney may due to chronic renal
obstruction
• Bladder distention with HN BOO

27. Ultrasound
• HN can be absence in obstructed kidney (rare)
• HN can be present without obstruction due to another diseases
• NL in 50 % of acute urinary obstruction especially when obstructing
agent is not seen
• Bowel gas&fat make stone diagnosis difficult
• US overestimate renal stone size < 5 mm

28. Ultrasound
Ureteral Jets :-
• Seen in bladder by color doppler US
• In O.U  Decreased ureteral jet frequency ,duration and peak
velocity when compared with NL contralateral ureteral jet
Frequency = 1.5 jets/min
• Differences of:- Duration = 2.5 seconds
Peak velocity = 19.5 cm/sec

29. CT SCAN
• Provides anatomic definition more than US
• Non contrast helical CT(NHCT) is the choice for suspected ureteral
stone or obstruction
• CTs can detect all radiolucent stone except:-
*Proteuse inhibitor stone ( indinavir stone)
*mucoid matrix stone

30. Unilateral Ureteral Obstruction
(UUO)

31. UUO
• Differences exist in hemodynamic change that occur in UUO as
compared to BUO
• In UUO there is triphasic pattern of RBF (Renal blood flow) and
ureteral pressure changes
• Acute phase lasts 1 – 2 hr
• Mid phase lasts 3 – 4 hr
• Late phase lasts 24 hr

32. Acute Phase
• Ureteral pressure and RBF rise togather
• Increase in renal tubules pressure secondary to obstruction 
subsequent decrease in GFR
• Renal vasculature attempts to compensate decreased GFR within
increase of RBF by release of vasodilators  nitric oxide(NO) and
prostaglandin E2 (PGE2)

33. Mid Phase
In this second phase :-
• Ureteral pressure remains elevated
• RBF begins to decline

34. Late Phase
• Increase in afferent arteriolar resistance decrease in effective
glomerular capillary pressure decrease in tubular pressure
• Shift in RBF from the outer cortex to the juxtamedullary region  so
large portions of cortex become underperfused or unperfused
• So reduction of GFR in this phase is result of decreased glomerular
capillary pressure and global lack of perfusion on many glomeruli

35. Late Phase
So the result is
• Both ureteral pressure and RBF progressively
decline
• Subsequent gradual loss in renal function

36. Bilateral Ureteral Obstruction
(BUO)

37. BUO
• BUO or obstructed single kidney
• Characterized by only modest initial increase in RBF lasting about 90
minutes fallowed by decrease in bilateral RBF
• Shift of blood flow from juxtamedullary to the outer cortex

38. • Unlike UUO that ureteral pressure is initially elevated then quickly
decreases to preocclusion pressure by 24 hr , in BUO uereteral
pressure remains elevated for 24 hr
• This prolonged elevation in tubular pressure contributes to the
decrease of GFR in BUO

39. Partial Ureteral Obstruction
(PUO)

40. PUO
• Depending on the severity (degree) and duration of obstruction
• Shift of blood flow from outer to inner cortex
• PUO result in decreased RBF and GFR
• Chronic PUO can decrease RBF to 25% of NL
• When ureter was reduced by 70-75%GFR was reduced by 80%
after 4 wk of PUO

41. Egress Of Urine
• Urine may still egress from the kidney
• Rupture of calyceal fornix and extravasation can occur such as
ureteral stone during acute obstruction or PUV in chronic obstruction
• Urinary extravasation into the venous or lymphatic system may occur
• During chronic obstruction fluid is thought to exit primarily into the
renal venous system

42. Clinical Impact Of O.U

43. Hypertension
• HTN can developed in response to urinary tract obstruction
• More common in BUO than UUO
• HTN in BUO is due to volume overload and usually is reversible by
relief of obstruction
• HTN in UUO is not because of volume overload due to kidney
compensation

44. • HTN less common in UUO, usually occur due to renin angiotensin
system upregulation
• ARI(angiotensin receptor inhibitor) type 2 receptor such as losartan
can control HTN in chronic HTN associated with UUO
• HTN treated by relief of obstruction observed more in BUO compared
with UUO

45. Compensatory Renal Growth
• It’s a response to UUO in contralteral kidney influenced by age-
degree-duration of O.U
• Renal growth decreased by increasing age
• GFR also increases
• Number of nephrons and glomeruli dose not increase 
• Renal growth is due to cellular hypertrophy rather than hyperplasia

46. Treatment Of Renal Obstruction

47. • Renal colic arise from increase collecting system pressure and acute
distention
• The first line in renal colic is analgesic
• Obioid have rapid onset but may cause nausea and vomitting and
emesis with risk to be abused

48. NSAID
• NSAIDs target the inflammatory basis of pain
• NSAIDs reduce collecting system pressure by reduction in RBF
• NSAIDs are superior to obioids due to less emesis and greater
reduction in pain
• NSAIDs are contraindicated in renal insufficiency

49. • COX-2 ihibitors are from NSAIDs that block prostaglandin synthesis
resulting decrease in hydrostatic pressure within tubules and reduce
intrapelvic pressure
• COX-2 inhibitors have risk for MI and CVA
• COX-1 inhibitors are contraindicated in risk of gastrointestinal
bleeding

50. Renal Drainage
• Even by nephrostomy tube or Double J stent
• Some times immediate drainage or emergency relieving of
obstruction is Important to relieve pain and prevent functional
decline
• If infection is suspected, urine culture from obstructed side in
needed and AB therapy started

51. Nephrostomy for :-
• Ill patient or no risk of bleeding
• More purulent fluid
Double J for:-
• Well patient or risk of bleeding(coaglopathy)
• No more purulent fluid
• Pregnancy or patient refuse external tube

52. Renal Recovery After
Obstruction

53. • Renal Recovery depends on duration and severity of obstruction
• Acute complete ureteral abstruction relief of obstruction in
approperiat time  full recovery of global GFR can occur
• Long time obstruction  relief of O.U  associated with diminished
return of GFR
• Persistent decrease in GFR and RBF after relief of O.U is due to
persistent vasoconstruction of afferent arteriole

54. Recovery After UUO
• After 1 wk of UUO  full recovery of GFR
• After 2 wk of UUO  70 % recovery of GFR
• After 4 wk of UUO  30 % recovery of GFR
• After 6 wk of UUO  no recovery of GFR

55. Recovery After UUO
UUO in previously obstructed kidney:-
• After 3 days GFR &RBF return to the paseline level within 2 wk ,
But interstitial fibrosis and tubular apoptosis continued to increase
after relief of obstruction
• After 1 wkNL renal function is not restored even after 30 days of
recovery and GFR&RBF reduced by 40%

56. GENERALLY
In humans ,delayed relief of
obstruction > 2 wk has been
demonstrated to decrease renal
function and increase risk of HTN

57. Good factors influencing return of renal function afetr relief of O.U
including:-
• Lesser degree of obstruction
• Greater compliance of collecting system
• Presense of pyelolymphatic back flow
• Non decreased cortical thickness
• First time obstructed kidney
• Younger age
• Good overall medical status