DESCRIPES THE CAUSES OF UTI

1. Outline
• Urinary Tract Infection (UTI)
• Obstructive uropathy
• Nephrolithiasis (renal calculi)
• Hypertensive Vascular Disease

2. UTI
• Lower: cystitis,
urethritis, prostatitis
• Upper: pyelonephritis
• Acute cystitis:
hyperemia of the
mucosa

3. Pyelonephritis & UTI
 Acute/chronic; suppurative infection of
tubules, interstitium, & renal pelvis
 Routes: ascending (common) &
hematogenous
 Cause:>85% gram -ve bacteria (fecal flora)
 F>M

4. UTI
 Risk factors: obstruction (congenital, BPH,
calculi & tumors), catheterization, DM,
vesicoureteral reflux, pregnancy,
immunosuppression, instrumentation

5. Steps in ascending infection
 1st colonization of distal urethra and introitus (in the
female) by bacteria
 From urethra to the bladder (by catheterization or
instrumentation) or in females due to short urethra,
no anti-bacterial prostatic fluid, hormonal changes
affecting adherence of bacteria to the mucosa, sex-
related urethral trauma
 Multiplication of bacteria in the bladder (favored by
outflow obstructon)
 Vesicoureteric reflux through incompetent
vesicoureteral orifice
 Intrarenal reflux through open papillae to kidney

6. Acute
Pyelonephritis
• Causes:
– ascending infection -
vesicoureteral reflux into the
renal pelvis and papillae; E.
coli, Proteus, Enterobacter.
– hematogenous seeding -
due to septicemia or
endocarditis; Staphlococcus
and E. coli.
• Patchy process, pinpoint
microabscesses on cortical
surface.

7. Acute pyelonephritis

8. Acute pyelonephritis

9. Acute pyelonephritis

10. Acute pyelonephritis
• Numerous neutrophils are seen filling renal tubules

11. Complications of acute pyelonephritis
• Papillary necrosis: coagulative necrosis of
tubules; common in DM & urinary tract
obstruction, usually bilateral
• Perinephric abscess: extension of pus into
adjacent tissue
• Pyonephrosis (pelvis filled with pus): total or
almost complete obstruction prevents
drainage of pus
• Chronic pyelonephritis

12. Renal papillary necrosis

13. Chronic Pyelonephritis
• Chronic tubulointerstitial inflammation with renal scarring with deformed calyces
• Important cause of end-stage renal disease in 10%-20%
• Two forms:
– reflux-associated: common, congenital vesicourtehral reflux or intrarenal
reflux
– obstructive: posterior urethral valves, ureteral calculi, etc

14. Vesicoureteric reflux (VUR)
demonstrated by a voiding cystourethrogram

15. Chronic pyelonephritis
thyroidization

16. Chronic pyelonephritis
• Irregular scarred
cortical surface

17. Chronic
Pyelonephritis
• Microscopic:
– tubules and interstitium.
– tubules show atrophy in
some areas and hypertrophy
in others.
– thyroidization: dilated tubules
may be filled with colloid
casts.
– varying degrees of chronic
inflammation and fibrosis.
– a variety of glomerular
changes may be present.
• Clinical: recurrent infections,
tubular dysfunction,
hypertension, chronic renal
failure.

18. Xanthogranulomatous
pyelonephritis
• Special type of Chronic pyelonephritis

19. Obstructive uropathy
o Unilateral or bilateral
o From urethra to renal pelvis
o ↑ susceptibility to infection & stone
formation
o Chronic obstruction causes hydronephrosis:
cystic pelvis & calyceal dilation with
progressive cortical atrophy

20. Common sites of obstruction

21. • Causes of obstructive
uropathy

22. Hydronephrosis
• Normal Hydronephrosis

23. Nephrolithiasis (renal calculi)
• 80% unilateral, grow in renal papilla or pelvis
• M>F, peak 20-30yrs
• Supersaturation of stone forming substances,
changes in urinary pH, ↓urine volume, bacteria,
deficiency of crystal inhibitors (citrate,
pyrophosphate, etc)
 Presentation:
 Pain
 Hematuria
 Recurrent & intractable UTI

24. Types of renal calculi
• 75%
• Alkaline urine
• Radio-opaque
• Calcium oxalate
• Calcium phosphate

25. Staghorn calculi
• 15%
• Triple struvite
• Magnesium ammonia
phosphate
• Urea-splitting bacteria
such as Proteus
converts the urea to
ammonia

26. • Uric acid stone
• 6%, acidic urine,
radiolucent
• Cysteine Stone
• 2%

27. Passage of a stone through the
urinary tract

28. • Bilateral renal stones Ureteral stone
•

29. Urinary Bladder Stone

30. Tubulo-interstitial disorders
Acute tubular necrosis
• Acute renal failure associated with dysfunction & necrosis of tubular
epithelial cells
• Classification:
– ischemic: shock, sepsis, burns, transfusion, other
– toxic: drugs, metals, poisons, solvents, other
• focal to extensive epithelial necrosis
• Pathogenesis:
– vasoconstriction, obstruction, tubular leakage of filtrate.
 Oliguric phase (risk of hyperkalemia) => diuretic phase (risk of
hypokalemia)
 Prognosis depends in part on the cause

31. Acute Tubular Necrosis
• Pathogenesis: sloughing and necrosis of epithelial cells results in cast formation. The
presence of casts leads to obstruction and increased intraluminal pressure, which reduces
glomerular filtration. Afferent arteriolar vasoconstriction, caused in part by tubuloglomerular
feedback, results in decreased glomerular capillary filtration pressure. Tubular injury and
increased intraluminal pressure cause fluid backleak from the lumen into the interstitium.

32. Acute Tubular
Necrosis
• Patterns of damage:
– Ischemic:
• necrosis is patchy
• relatively short lengths of
tubules are affected
• straight segments of the
proximal tubules and
ascending limbs of Henle’s
loop are most vulnerable
– Toxic:
• necrosis of proximal tubule
segments with many
toxins.
• necrosis of distal tubule
may also occur.
• In both types, the lumens of the
distal convoluted tubules and
collecting ducts contain casts.

33. Ischemic ATN: characterized by
swollen kidneys with a pale cortex &
congested medulla
Acute tubular necrosis

34. Acute Tubular
Necrosis
• Microscopic: some tubular cells
are necrotic whereas others are
flattened, stretched out and
regenerating.
• Distal convoluted tubules and
collecting ducts contain hyaline
casts.

35. Tubulointerstitial nephrititis
• 10
or 20,
acute or chronic
• 10
lacks significant glomerular or vascular injury,
causes 20-40% of cases of end stage renal disease
• 20
is due to glomerular disease, systemic or vascular
disorders
• Causes: infections, toxins, metabolic disease,
tumors, vascular diseases
• Tubular defects: inability to concentrate urine
(polyuria, nocturia), salt wasting, diminished ability
to excrete acids (metabolic acidosis)

36. Tubulointerstitial nephrititis

37. ANALGESIC NEPHROPATHY

38. Tubulointerstitial nephrititis cont.
• scattered eosinophils, along with neutrophils &
mononuclear cells in the inflamed interstitium

39. Hypertensive Vascular Disease
• Benign hypertension (diastolic > 90 mm Hg)
• Benign nephrosclerosis: granular surface of the kidney
results from small cortical scars
• Malignant hypertension (diastolic > 130 mm Hg):
vascular necrosis & hemorrhage with acute cardiac &
renal failure

40. Benign “nephrosclerosis”
• Hyalin arteriolosclerosis: small
arteriole at the lower right is
markedly thickened in this
case of a diabetic (note the
nodular glomerulosclerosis)
with hypertension

41. Benign nephrosclerosis

42. kidneys of malignant hypertension
• Diastolic pressure may exceed 130mmHg => 300/150 mm Hg
• small petechiae throughout the kidney due to the necrosis of
vessels so-called “flea-bitten kidney”

43. kidney of malignant hypertension
• The pink material
resembling fibrin seen
in the wall of this
arteriole is indicative of
the process of fibrinoid
necrosis as a
consequence of
malignant hypertension

44. kidney of malignant hypertension
• The concentric thickening of
this renal arteriole, giving it
an "onion skin" appearance,
is indicative of hyperplastic
arteriolosclerosis with
malignant hypertension

45. kidney in malignant hypertension

46. Malignant Nephrosclerosis
• Malignant hypertension (diastolic >
130 mm Hg).
• Rapidly progressive, accelerated
nephrosclerosis.
• Affects the heart, brain, kidneys:
– papilledema.
– encephalopathy.
– cardiovascular. abnormalities
– renal failure.
• Microvascular changes:
– fibrinoid necrosis.
– smooth muscle proliferation.

47. Intravenous pyelogram (IVP)

48. IV pyelogram (IVP) showing bilateral
hydronephrosis