MEDI7111 Lecture Notes - Lecture 4: Necrosis, Thrombus, Urinary Retention
Renal 4
Pathology
Urolithiasis
Urolithiasis or urinary/renal calculi are a common condition of the urinary tract. The peak age of
incidence is 20-30 years, with males more commonly affected than females. Typically there is a
familial predisposition to stone formation such as gout, cystinuria or hyperoxaluria.
There are four main types of calculi:
Calcium oxalate/calcium phosphate stones (70%)
Struvite stones (calcium, magnesium and ammonium) (15%)
Uric acid stones (5-10%)
Cysteine stones (~1%)
Stones typically precipitate due to super-saturation of urine with particular solute. This is usually due
to a genetic defect in PCT transporters that allow a greater amount of solute to remain in the filtrate
but occasionally can occur from reduced GFR.
Calculi Type Causes Treatment
Calcium
Oxalate/Calcium
Phosphate
Idiopathic hypercalciuria
Hypercalcemia
Crohn’s disease (due to increased
resorption of oxalate)
Hydrochlorothiazide (HCT)
- Is a calcium sparing diuretic
(removes calcium from the
filtrate therefore harder for
stones to precipitate
Ammonium
Magnesium
Phosphate (AMP
or struvite or
triple stones)
Infection with urease positive
organisms
- Proteus vulgans
- Klebsiella
Alkalinisation of urine
Produces staghorn calculi, can only
be removed surgically
Urease inhibitors can help reducing
stone formation until bacterial
infection is eradicated
Uric Acid Caused by increased uric acid in the
urine
Risk factors include:
Gout
High protein diet
Acidic urine
Low urine volume
Leukaemia
Myeloproliferative disorder
Bicarbonate supplementation
(increased pH)
Rehydration
Allopurinol (gout medication)
Cysteine Genetic defect in tubule transporters
leading to decreased cysteine
resorption
Produces staghorn calculi, can only
be removed surgically
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Staghorn Calculi
Staghorn calculi are large calculi that involve the renal pelvis and at least two major calyxes.
Clinical Presentation
The signs and symptoms of the patient are dependent upon the location and extent of the blockage
caused by the stone. Occasionally there may be haematuria and
Stone Location Site of Pain
Uretopelvic junction Mild to severe deep flank pain
No radiation
Irritative voiding symptoms (e.g. frequency, dysuria etc.)
Suprapubic pain
Ureters Abrupt severe colicky pain
Intense nausea (+/- vomiting)
Upper ureteral stone Purely flank/loin pain
Middle ureteral stone Radiates anteriorly and superiorly
Distal ureteral stone Radiates to groin (vulva or testes)
Bladder stones Mostly asymptomatic
Positional urinary retention (from stone moving around and blocking
urethral opening)
Management
Typically management is conservative, providing fluids and pain relief to allow the stone to pass on
its own. Depending on the size of the stone, alpha blockers and calcium channel blockers can be
used to relax the smooth muscle in the internal urethral sphincter and ureters (respectively) to dilate
the lumen.
If the stone does not pass on its own or if it is >10mm, surgery is required to remove the stone.
Typically non-invasive methods are used to fragment the stone and allow it to be passed, such as
shockwave lithotripsy, in immovable stones <10mm. Larger stones require surgical intervention such
as percutaneous nephrostolithomy or open stone removal.
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Benign Neoplasms of the Urinary Tract
Epithelial:
Oncocytoma
Papillary adenoma
o>20% of population have these
o<5mm
oNo nuclear atypia
Cystic nephroma
Metanephric adenoma
Papillary Adenoma
Finger-like projections at the periphery of the
tumour
Oncocytoma
Large circumscribed tumours with a central scar
Very eosinophilic on H&E staining
Stromal:
Angiomyolipoma
Angioma
Leiomyoma
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Document Summary
Urolithiasis or urinary/renal calculi are a common condition of the urinary tract. The peak age of incidence is 20-30 years, with males more commonly affected than females. Typically there is a familial predisposition to stone formation such as gout, cystinuria or hyperoxaluria. Stones typically precipitate due to super-saturation of urine with particular solute. This is usually due to a genetic defect in pct transporters that allow a greater amount of solute to remain in the filtrate but occasionally can occur from reduced gfr. Crohn"s disease (due to increased resorption of oxalate) Caused by increased uric acid in the urine. Genetic defect in tubule transporters leading to decreased cysteine resorption. Is a calcium sparing diuretic (removes calcium from the filtrate therefore harder for stones to precipitate. Urease inhibitors can help reducing stone formation until bacterial infection is eradicated. Produces staghorn calculi, can only be removed surgically.
