URINARY

LITHIASIS

Etiology, Epidemiology and

Pathogenesis
Urology Division, Surgery Department
Medical Faculty,
University of Sumatera Utara

References

Epidemiology
Prevalence of kidney stone 1 15 %, and in
hot area such as the mountains, desert & tropical
areas
: = 2 to 3 : 1, peak age onset 40 - 60 yrs
The third most common affliction of the urinary
tract, after UTI and pathologic conditions of the
prostate
Race : Whites > Asian > African
Individual occupations eg. manager and

Epidemiology
25% stone formers have a family history
Risk of stone correlates with weight and
body mass index
Uric acid and Ca stones more frequent in,
infectious stones more common in
The most common kinds of stones are
calcium oxalate, uric acid, struvite and
cysteine

Etiology
1. Definitive causes :

Metabolic
Infection
Anatomic
Functional
2. Idiopathic

Definitive causes
Defects in purine metabolism (uric acid
related disorders)
Hyperoxaluric states
- Primary hyperoxaluria
- Enteric hyperoxaluria
Hypercalcemic states
- Primary hyperparathyroidism
- Hyperthyroidism
- Vitamin D abuse

Hypercalcemic states (cont.)

- Immobilization
- Disseminated malignancies
- Sarcoidosis
- Renal tubular acidosis
Chronic diarrheal states
Cystinuria
Urinary infection with urease producing
microorganisms
Anatomical and functional abnormalities

Risk factors
Genetics :
Cystinuria : autosomal recessive
RTA (renal tubular acidosis) type I
Medullary sponge kidney

Geography : temperature & humidity

Diet : calcium / oxalate intake >>
Profession : sedentary

Classification
Defenition

Non Calcium Stones

Calcium Stones

Infection stones:
Magnesium
ammonium
phosphate
Carbonate apatite
Ammonium uratea
Uric acid
Ammonium uratea
Sodium urate
Cystine

Stone Composition and

Relative Occurrence
Stone Composition

Occurrence (%)

Calcium-Containing Stones
Calcium oxalate

60

Hydroxyapatite

20

Brushite

NonCalcium-Containing Stones
Uric acid

Struvite

Cystine

13

Triamterene

<1

Silica

<1

2,8-Dihyroxyadenine

<1

Stone formation

Stone formation
Crystallization
Stone salts that precipitate out of urine
The point of saturation of a salt in solution is
called the
solubility product (Ksp)
When the product of the components of a salt
(e.g.
calcium and oxalate) exceeds Ksp, salt crystals
will
precipitate out of solution
Crystallization is based on Ksp, pH, and the
presence of

Nucleation

- Is the process by which stones form

around a
core, or nucleus
- Homogeneous stone nuclei form in
solution
- Heterogeneous stone nuclei form
around
existing structures, such as cellular
debris

Inhibitors and Promoters of

Crystal Formation
Inhibitors :
Nephrocalcin
Uropontin
Tamm-Horsfall protein
Citrate
Magnesium
Promoters :
Calcium phospate
Calcium oxalate

Urinary tract stone

Age
Sex
Profession
Nutrition
Climate
Race
Inheritanc
e

STONE

Abnormal renal
morphology
Disturbed urin flow
UTI
Metabolic
abnormal
Genetic factors

SUPERSA
TURATION

Increase
excretion of :
1.Stone
forming
constituents
2.
Crystallization
promoters
Decrease :
1.Urinary
volume
2. Excretion of
crystallization
inhibitors

Pathogenesis
CALCIUM STONES
1. Hipercalciuria : excretion of Ca > 4
mg/kg/day
a. Absorptive : increased ca excretion (>0.2
mg/mg creatinine) after an oral calcium
load
b. Renal : urinary ca levels >0.11 mg/dL
glomerular filtration with a normal serum
calcium
c. Resorptive : associated with primary

2. Hyperoxaluria : urinary oxalate greater than

40 mg/day
a. Primary Hyperoxaluria (autosomal recessive

disorder )
b. Enteric Hyperoxaluria : associated with

chronic diarrheal states

c. Dietary Hyperoxaluria : oxalate-rich foods

such as nuts, chocolate, brewed tea,

spinach, broccoli, strawberries.
d. Idiopathic Hyperoxaluria

3. Hyperuricosuria
Urinary uric acid exceeding 600 mg/day
The most common cause increase purin
intake
4. Hypocitraturia
Urinary citrate level less than 320 mg/day
Correctable abnormality
Associated with nephrolithiasis in up to
10% of

5. Hypomagnesuria
Rare cause, less than 1%
Magnesium complexes with oxalate and
calcium,
mg levels decrease reduced inhibitory
activity
Poor dietary intake Mg

URIC ACID STONES

5-10% of all stone
3 factors of uric acid stone formation :
1. Low pH, < 5,5
2. Low urine volume
3. Hyperuricosuria urinary uric acid
less
than 600 mg/day
Secondary causes : gout (20%),obesity ,
myeloproliferative cancer and congenital
disorder

STRUVITE STONES
Infection stones comprise 5% to 15% of all

stones
Composed of Mg ammonium phosphate crystals
= infection stones or triple phosphate stone
Staghorn calculi are typically struvite stone
Caused by infection with urease-producing

bacteria :
- proteus is the most common
- urease hydrolized urea to form ammonia
alkalinizes the urine, pH and allows crystals to
form

CYSTINE STONES
1% of all stones
Congenital disorders, autosomal recessive
Caused by a defect in cystine reabsorption
in the proximal tubule
Cystine poorly soluble at normal pH (pKa
8.3)
Crystal form benzene ring on
microscopy

CALCIUM PHOSPHATE STONE

Urine pH > 5.5
Hypocitraturia
70% of adults with type 1 RTA have
stones
80% are women
Associated with renal cyst

Medications That directly

Promote Stone Formation
Indinavir Stones
Triamterene Stones
Guaifenesin and Ephedrine
Silicate Stones

Anatomic
Predisposition
Ureteropelvic Junction Obstruction :
20 %
cases
Horseshoe Kidneys
Caliceal Diverticula

SUMMARY
The most common type is calcium oxalate
Uric acid stones form at pH <5.5
The most important determinant of
uric acid stone formation is low
urinary pH

Struvite stone are composed of

magnesium
ammonium phosphate crystals
- They are classically caused by infection
with
a urease-producing bacterium
- Urinary pH is >7.2 treatment is surgery
&
antibiotics
Cystine stones caused by a congenital
autosomal recessive disorder

Thank You