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