Urinary Tract Stones

(Urolithiasis)
Dr. Yasser Al-Hakeem
 Learning Objectives (pt 1)
— By the end of this lecture, you should:
— Describe the pathophysiology and risk factors (intrinsic and
extrinsic) for urinary tract stones.
— Classify stones based on their composition.
— Classify stones based on their radio-density.
— List which stones form in (acidic, alkaline) urine.
— Describe the neural pathway by which renal and ureteral
stones cause loin→groin pain.
 Clinical Problem
— Your relative, a 35-year-old male, has history of recurrent
renal stones. He is currently asymptomatic. He is asking
you:
— Why do stones occur in the urinary tract?
— Are there any risk factors that I should be aware of?
— Are there any lifestyle advices that you can give me?
— When my stones were symptomatic, I often had pain from
my flank to the genitals, why does pain happen in that way?
 Y
I T EAS
E
TAK
!?How do we form stones (calculi) ‫شرح وملخص الساليد البعده‬

like calcium, oxalate,

phosphate, uric acid, cystine

concentration of a substance
is >Ksp but still <Kf

due to the action of stone-

inhibitory substances (like
citrate and magnesium)
 How do we form stones (calculi)?!
‫تشبع زائد‬

— The driving force for stone formation is the supersaturation of

urine with stone-promoting substances (like calcium, oxalate,
phosphate, uric acid, cystine).
— We need to understand these terms:
1. Solubility product (Ksp) of a substance: below this concentration
the urine is called undersaturated and no crystals will form.
2. Formation product (Kf) of a substance: above this concentration
the urine is called supersaturated and crystals will form
(nucleation), these crystals will clump together (aggregation) to
form a stone.
3. If the concentration of a substance is >Ksp but still <Kf: the urine is
‫سِتْقرار‬
ْ ‫ُمت َبَِّدُل اال‬

called metastable and no crystals will form due to the action of

stone-inhibitory substances (like citrate and magnesium).
 Epidemiology & Risk Factors
— The prevalence of stone disease is ↑ in all western societies.
— In US, the lifetime prevalence is 19% (men) & 9% (women).
— Patients with stones have ↑ risk of recurrence (up to 50%
will form another stone in less than 10 years).

— FACTORS AFFECTING STONE FORMATION:

A combination of intrinsic (related to the individual)+
extrinsic (environmental) factors:
 Epidemiology & Risk Factors
Intrinsic factors:
— Obesity: ↑ risk due to 2 causes: Rich In Lethogenic Sub 5* /Egts .

Cobese
1. ↑ urinary secretion of stone-promoting substances like calcium
(Ca), oxalate (Ox), uric acid (UA) + ↓ urinary secretion of stone
Cho date &
.
5 9..

preventing-substances like citrate.

2. More acidic urine (↓pH) which predispose to uric acid stones. why? ·
6,189
— Gender:si
-= s
~ 1.5 more in men, due to 2 possible causes:
=*/
-
. - Els ,
In

1. Testosterone ↑ oxalate production in the liver.

.

2. Women secrete more citrate in urine. stone-inhibitory substance

— Genetics:
white
Caucasians>Asians>Africans (♂).
Certain types of stones like cystine (in children) and calcium
phosphate (in renal tubular acidosis RTA) are inherited.
— Renal Anatomy: PUJO, medullary sponge kidney, horseshoe
kidney: all ↑ risk for stone formation
 Epidemiology & Risk Factors
Intrinsic factors (cont’d):
— Diseases: can predispose to specific stone types:
1. Hypercalcemia (e.g. hyperparathyroidism)→ Ca stones.
2. Gout and myeloproliferative disorders→ uric acid stones
3. Intestinal malabsorption (inflammatory bowel diseases,
bypass surgery)→ ↑oxalate absorption→ oxalate stone.
4. UTI due to urease-producing bacteria: Proteus, Providencia
(urease hydrolyzes urea to ammonium and OH-)→ alkaline
urine→ struvite (MAP) stone.
5. Distal renal tubular acidosis (RTA): inability to excrete H+ in
urine → systemic acidosis with paradoxically alkaline
urine→ calcium phosphate stones.
 Epidemiology & Risk Factors
Extrinsic factors:
— Climate: peak incidence ~1month after peak summer temperature
due to 2 factors:
1. Dehydration → ↑ urine concentration → ↑ crystallization.
2. Sunlight → ↑vit D synthesis → ↑ Ca in urine (hypercalciuria).

— ↓Water intake: <1200 ml/day→ ↑ stone formation.

— Diet: ↑risk in the following:

q ↑ animal protein due to the following changes in urine:
- ↑ (calcium, uric acid).
- ↓ (pH, citrate).
q ↑ salt: Na → co-transport ↑ Ca excretion in urine.
q ↓ dietary calcium! will increase the risk since less calcium in diet
will cause more oxalate absorption from the bowel.
 Epidemiology & Risk Factors
Extrinsic factors (cont’d):
— Drugs: some drugs might promote stone formation, e.g.
1. corticosteroids: ↑ bone resorption → hypercalciuria.
Resorption is the absorption of cells or tissue into the circulatory system,
usually by osteoclasts.

2. Vit D & Ca: ↑ enteric absorption of Ca → hypercalciuria.

3. Vit C: large doses ↑ hepatic production of oxalate.
4. Chemotherapy: breakdown of cells→ hyperuricosuria.
5. Carbonic anhydrase inhibitors→ ↑urine pH→ CaPO4 stone.
6. Loop diuretics (furosemide)→hypercalciuria
hypercalciuria

— Occupation: sedentary work & immobility increase the risk

since both promote bone demineralization→ hypercalciuria.
 Classification of stones
Stones can be classified based on:
§ Composition
§ Appearance on plain x-rays (radio-density).
§ Size.
§ Shape.
§ Location (kidney, ureter, bladder).
Classification: composition ‫شرح عن الساليد القادم‬
 Classification: composition
— 1. Calcium-containing stones:
(a) calcium oxalate (monhydrate or dihydrate): most
common type, insensitive to urinary pH.
(b) calcium phosphate (apatite ˃ brushite) pure or in
combination with (a), seen in alkaline urine (e.g. RTA)
— 2. Infection stones (struvite or MAP= magnesium-
ammonium-phosphate): due to infection by urea-splitting
bacteria leading to alkaline urine.
— 3. Uric acid: in acidic urine which promote uric acid
crystallization
— 4. Cystine: in acidic urine, common in children, autosomal
recessive disease →↑ cystine excretion in urine (insoluble).
Classification: composition
 Classification: radio-density
— Based on appearance on abdominal plain x-ray (K.U.B)
— Accurate only in ~40% of cases.
— (1) Radio-opaque: due to calcium content:
- calcium oxalate.
- calcium phosphate (most radio-dense, similar to bone)
— (2) Faintly (relatively) radio-opaque:
- cystine: due to sulfur that binds cystine crystals.
- infection stones (MAP)
— (3) Radio-lucent: not visible on x-ray:
- uric acid
- drug stones: rare, due to deposition of insoluble drug
particles in urine, e.g. indinavir (HIV), triamterene
(diuretic), some antibiotics.Radio-lucent
Classification: radio-density

Radio-opaque right lower pole renal stone (calcium oxalate)

Classification: radio-density

cystine
infection stone

Faintly radio-opaque left renal stone (cystine)

 Classification: size and shape
— Size is measured by mm or cm.
— Shape: renal stone that grow to occupy (the renal
pelvis + one or more calyces) is called a staghorn ‫قرون الغزالن‬
stone (resembles the horns of the male deer)
‫غزالة أيل‬

Bilateral staghorn renal

stones
 Clinical features
Depend on:
1.Stone size.
2.Stone location (kidney, ureter, bladder).
3.The presence or absence of obstruction.
4.The presence or absence of infection
‫واسع‬
N.B. The renal pelvis is capacious, while the ureter is
narrow and can be obstructed easily by a small stone.
Thus, a large unobstructing renal stone may be
asymptomatic or cause mild pain, while a small
obstructing ureteric stone may cause severe pain.
‫كالم وشرح الدكتور آلخر ساليدين ?‪why loin→groin‬‬
LOCATION
 General Tips: why loin→groin?
Kidneys:
— Pain from the kidney is due to capsule distention
(obstruction or inflammation) travels via (T8-L1) afferent
autonomic nerves to the celiac ganglia (innervate the
stomach causing nausea and vomiting) and then reach the
spinal cord where it is referred to efferent somatic nerves
(T8-L1).
— L1 segment is the origin of 2 somatic nerves:
1. iliohypogastric: causing referred pain from loin to
suprapubic area
2. ilioinguinal: causing referred pain from loin to groin (testis
in male and labia majora in female).
 General Tips: why loin→groin?
Ureter:
— Pain afferents from ureter travel via (T10-L2) afferent autonomic
nerves to the celiac ganglia (innervate the stomach causing
nausea and vomiting) and then the spinal cord where it is
referred to somatic nerves (T10-L2) and is usually described as
(loin to groin) .
— In case of acutely obstructing stone the pain is due to both
(distension of renal capsule + ureteric peristalsis).
— Pain due to chronic or incomplete obstruction (very small stone)
may be less severe or even asymptomatic!
— The site of stone in the ureter (upper, middle, lower) is poorly
correlated with the site and radiation of pain except when the
stone is in the vesico-ureteric junction (VUJ) which will cause
frequency, urgency and pain referred to the tip of the penis.
 References
1- Campbell Walsh Urology, 20th edition.
2- European Association of Urology (EAU) guidelines 2023.
3- Oxford Handbook of Urology, 4th edition.
4- UpToDate website.

THANKS
A LOT