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.
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.
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
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
Obstruction in urinary tract and important because it increases the susceptibility to infection……chronic obstruction
Any age
Urinary tract obstruction leads to impairment in normal flow of urine-urinary stasis & increased pressure in part proximal to obstruction- increased pressure impairs renal and UT functions- increased susceptibility to hypertension, infection, and stone formation – chronic obstruction-cortical thinning -permentant loss of renal mass(renal atrophy) and excretory capacity lead to end stage disease
Obstruction can be
Complete bilateral obs.. Result in irreversible renal failure
Long standing / partial – functional abnormalities & anatomical changes
Level urinary tract – renal pelvis, ureters, urinary bladder, urethra
Intrinsic inside
Extrinsic – outside
Pelvic uretric junction narrowing – portion of collecting system that connects the renal pelvis to ureter
Ureterovesical junction- blockage area where ureter meets bladder
Ureterocele – swelling of ureter at bottom near bladder- birth defect – prevents flow of urine into urethra
Urinary calculi
Prostatitis, ureteritis, urethritis,
Renal calculi /stones
Hyperoxaluria provide examples of heridary disease – characterized by excessive production and excretion of stone forming substance
There are many causes for initation and propagation of stone
Most important determinant is increase urinary concentration of stone constituents such that it exceeds their solubility- supersaturation
Nucleation of calcium oxalate by uric acid crystals in collecting ducts
Hy[percalciuria- too much of calcium in urine
1- hyperabsorption of calcium from intestine (absortive hypercalcuria)- intrinsic impairement of renal tubular reabsorption of calcium
2-hyperparathyroidism – diffuse bone disease-sarcoidosis
3-20% stone ass with increased uric acid secretion
4- hereditary (primary)- acquired by interstinal overabsorption with enteric disease
Formed after largely after infections by urea spitting bacteria (proteus and staphylococci) that converts urea to ammonia
Result alkaline urine causes precipitation of magnesium ammonium phosphate salts. – large stone
Uric acid stone will be radiolucent
Calcium stone will be radioopaque
Hematuria – blood in urine
Hydronephrosis – dilation of renal pelvis and calyces
Pyelonephritis-inflammation of kidney due to infection
Pyonephrosis – collection of pus in renal pelvis - obstruction
Hydronephrosis of kidney – marked dilation of the pelvis and calyces and thinning of renal parenchyma
Affects pelvis and calyces – dilated
High….. Collecting ducts into the cortex causing renal atrophy