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Urinary Stone Disease

Spectrum of the Disease
 Upper tract tends to be idiopathic, infective, metabolic or staghorn (large calculus with multiple projections)
 Males are more likely than females to have the disease
 In the lower tract, it is usually caused by obstruction or a foreign body
 0.5%-1.0% oh Hospital admissions are for Renal Colic
In situ
 Note the white stone in the ureter, between the kidney and
bladder
 Also note the dilation of vessels around the kidney as a result
of backflow due to obstruction
Symptoms
 Sudden, severe onset of pain
 Movement usually okay
 Spasmodic pain
 Loin to groin
 Nausea if stone is close to kidney as this organ has cross over supply with the stomach via coeliac plexus
 Frequency if near the bladder, flank pain if mid ureter
Signs
 Tenderness of the stone and flank
 Haematuria
 Fever
 Asymptomatic
Investigation
 Take a history
 Examine the patient
 Cat Scan + KUB (abdo xray- kidney, ureter, bladder)
 Renal function, urine check
 Other possibilities (DDx)
o Gastroenteritis, appendicitis, colitis, sapingitis and vascular diseases
Who to admit:
 Severe pain
 Septic people
 When stone size is too large to excrete (>6-7mm)
 When stone is in a position that may contraindicate
its excretion
 When the person has a single kidney
Stone types
 Calcium Oxalate 65%
 Uric Acid 10-15%
 Infection (struvite) 10-15%
 Cystine 1%
 Rare (Xanthine, Indiniver)

Why stones form
 Supersaturation (depends on the type of crystal and the pH)
 Inhibitor deficiency (citrate?)
 Metabolic
 Uncertainty about cause
Calcium stones
 Ca Ox + Phosphate
 M:F = 3:1
 Recurrence
o 10% at 1 year
o 50% at 10 year
 Incidence 0.16%
Causes
 Idiopathic
 Hypercalciuria
o Excess GIT absorption
o Renal leak
o Secondary due to excess PTH  more calcium in blood , sarcoid granuloma, bone METs
 Hyperoxaluria
 Hypocitraturia
Hypercalciuria
GIT issue
 Hyperabsorption in the small bowel
 Renal loss of CA compensates by low PTH level
 Normocalcaemic
 30% of calcium stones
Renal leak
 Impained tubular reabsorption
 Increased PTH compensates
 Leads to increased GIT absorption
 Normocalcemia
 30% of calcium stones


Hyperparathyroid
 Large increase in PTH secretion
 Increased bone loss
 Increased GIT calcium absorption
 Hypercalcemia
 10% of calcium stones
Other risk factors
 Hot Climate
 Diet high in protein (acid) or high in salt
 Reduced fluid intake
 High Oxalate intake
 Low calcium intake  more liberation into blood stream
 IBD
Lifestyle management
 High fluid intake ‘flush out’ kidneys, decrease chance of crystallising
 Moderate protein intake
 Reduce salt
 Reduce oxalate rich foods like chocolate, green vegetables, coke and black tea.
Treatment of colic
 Pain relief
o Anti inflammatory drug NSAID
o Alpha blocker like Tamsulosin
o Reduce fluid intake as it puts less pressure on
the system and increase fluids when pain settles
 Antispasmodic like Buscopan
Uric acid stones
 Male rate = Female rate
 10% of all stnes
 Not visible on plain film
 Poorly soluble in urine

Causes of Uric acid stones
 Gout
 Idiopathic
 High protein diet
 Inflammatory bowel disease (acidosis)
 Genetic
 Myelopolfierative disorders
Therapy for Uric acid stones
 Identify and treat primary cause
 Raise urine pH >6
 High fluid intake
 Allopurinol – product xanthine is more soluble
Infection stones
 Magnesium ammonium phosphate (struvite)
 Uease producing bacteria produce high urine pH
o Proteus is most common
 Tendency for staghorn stones
o Image to the right
 15-20% are upper tract stones
 More common in females
 Complications
o Obstruction
o Pyonephrosis
o Renal abscess/ sepsis
o Renal loss
 Treatment
o Complete stone eradiaction
o Long term antibiotics
o Treat contributing factors