Obstructive uropathy can be caused by various congenital and acquired conditions that obstruct the urinary tract. This obstruction can occur at any level and lead to hydronephrosis or kidney damage if not relieved. Kidney stones, also known as urolithiasis, are a common cause of obstruction and can form from substances like calcium, uric acid, cystine, or struvite bacteria. The formation of stones is due to an imbalance between constituents in urine that cause supersaturation and crystallization. Long-term obstruction can result in hydronephrosis, or dilation of the renal pelvis and calyces, due to continued kidney filtration against resistance. This causes compression of the medullary blood

1. OBSTRUCTIVE UROPATHY
Dr. Arvind MD

2. OBJECTIVES
Define obstructive uropathy
List the etiology of obstructive uropathy
Discuss the pathogenesis of urolithiasis and hydronephrosis
List the types of renal stones and discuss the etiopathogenesis
Describe the morphology of renal stone
Define hydronephrosis and describe its pathogenesis

3. DEFINITION
Obstructive lesions of the urinary tract increase susceptibility
to infection and stone formation.
 Unrelieved obstruction almost always leads to permanent
renal atrophy - Hydronephrosis or obstructive uropathy.

4. OBSTRUCTIVE UROPATHY / URINARY TRACT OBSTRUCTION

5. OBSTRUCTION
• Sudden/ Insidious
• Partial/ complete
• Unilateral/ Bilateral
• At any level of the urinary
tract

6. ETIOLOGY - OBSTRUCTIVE LESIONS

7. URETER/ PELVIS
CONGENITAL ACQUIRED INTRINSIC ACQUIRED EXTRINSIC
PUJ narrowing/obstruction Calculi Pregnant uterus
UVJ narrowing/obstruction Inflammation Retroperitoneal fibrosis
Ureterocele Infection Aortic aneurysm
Retrocaval ureter Trauma Uterine leiomyoma
Sloughed papillae Carcinoma uterus, prostate,
bladder, rectum
Tumour Lymphoma
PID
Accidental surgical ligation

8. BLADDER OUTLET
CONGENITAL ACQUIRED INTRINSIC ACQUIRED EXTRINSIC
Bladder neck obstruction Benign prostatic hyperplasia Carcinoma cervix
Ureterocele Cancer of prostate, bladder Carcinoma colon
Calculi Trauma
Diabetic neuropathy
Spinal cord disease
Anticholinergic drugs and
Alpha adrenergic
antagonists

9. URETHRA
CONGENITAL ACQUIRED INTRINSIC ACQUIRED EXTRINSIC
Posterior urethral valve Stricture Trauma
Stricture Tumour
Meatal stenosis Calculi
Phimosis Trauma
Phimosis

10. UROLITHIASIS
Formed anywhere in the urinary tract, mostly in kidney
M>F
Age: Peak between 20 and 30 years
 Familial and hereditary predisposition; Many inborn errors of
metabolism (like cystinuria & primary hyperoxaluria)

11. UROLITHIASIS - PATHOGENESIS
• Increased urinary supersaturation – Stone constituents exceeds
solubility (Hyperoxaluria, hypercalciuria, decreased urine volume,
increased urine pH)
Crystal nucleation
Crystal growth
Crystal aggregation
Crystal-cell interaction
Crystal retention within the kidney or renal collecting duct
Stone formation

12. UROLITHIASIS - PATHOGENESIS
• Stone formation - enhanced by deficiency of inhibitors of crystal
formation in urine.
• These inhibitors for crystal formation are pyrophosphate,
diphosphonate, citrate, glycosaminoglycans, osteopontin and
glycoprotein called nephrocalcin.

13. UROLITHIASIS
TYPES:
1) Calcium oxalate stones
• Incidence: 70%
• Composition: calcium oxalate (OR)
calcium oxalate + calcium phosphate

14. UROLITHIASIS -Calcium oxalate stones
• Etiopathogenesis:
Hypercalciuria without hypercalcemia
(55%)
Hypercalciuria and hypercalcemia (5%)
Hyperuricosuria
Hyperoxaluria: primary, enteric

15. UROLITHIASIS
2) Struvite stones or Triple stones
• Incidence: 15%
• Composition: Magnesium, Ammonium, Phosphate stones
• Etiopathogenesis:
• Urea splitting bacteria (protease, staphylococci) –
convert urea  ammonia  resultant alkaline urine causes precipitation of
magnesium ammonium phosphate salts  Staghorn calculi

16. UROLITHIASIS
Staghorn calculi Struvite stones

17. UROLITHIASIS
3) Uric acid stones
• Incidence: 5-10 %
• Etiopathogenesis:
 common with hyperuricemia (gout)
and diseases involving rapid cell
turnover (leukemias)

18. UROLITHIASIS
3) Uric acid stones
 However, more than 50% have neither
hyperuricemia nor increased urinary uric acid
• Predisposing factors: Acidic urine (pH <5.5)
• RADIOLUCENT

19. UROLITHIASIS
4) Cystine stones
• Incidence: 1-2%
• Etiopathogenesis: genetic defects
in renal reabsorption of
aminoacids (cystine) 
cystinuria
• Form at low urinary pH

20. UROLITHIASIS – Clinical features
• Asymptomatic (OR) severe renal colic and abdominal pain (OR)
significant renal damage
• Small stones: may pass through (OR) ureteral obstruction
“loin to groin” pain
• Larger stones: often Haematuria

21. UROLITHIASIS – Complications
• Hematuria
• Hydronephrosis
• Pyelonephritis and pyonephrosis

22. HYDRONEPHROSIS
• Dilatation of renal pelvis and
calyces associated with progressive
atrophy of kidney due to obstruction
to the outflow of urine

23. HYDRONEPHROSIS

24. HYDRONEPHROSIS
• OBSTRUCTION
-sudden/insidious
- partial/complete
-unilateral/bilateral
This obstruction can occur at any level of the urinary tract.

25. HYDRONEPHROSIS - Pathogenesis
Obstruction in urinary tract + continued GF(Glomerular filtration)
Dilatation of pelvis and calyces
High pressure in the pelvis that transmits back through collecting duct
Initially: renal vasculature of medulla Later: Cortical atrophy & decreased GFR
is compressed
Diminished inner medullary blood flow
Deranged tubular function in the medulla
(medullary vascular defects initially reversible)
Manifested as: impaired concentrating ability
Dilatation of pelvis and calyces and parenchymal atrophy
HYDRONEPHROSIS

26. HYDRONEPHROSIS – Clinical features
• Asymptomatic
• Compensated by other kidney
U/L -partial/complete hydronephrosis
• Polyuria & Nocturia
• Due to inability to concentrate the urine (tubular dysfunction)
B/L partial obstruction
• Oliguria or Anuria
B/L complete obstruction

27. THANK YOU