RENAL STONES

EPIDEMIOLOGY Solubility Product Constant (Ksp)

If A (aq) + B (aq) = AB (s) then [A] [B] = Ksp
(NEPHROLITHIASIS) **calculations is more complicated in urine than in water
 US data: (develop stone during their lifetime) If A x B >Ksp then precipitates form
-13% of men Once crystals forms, it can act as a nidus for more precipitate
- 7% of women formation as long as the solution continues to be supersaturated
 Peak incidence: 30-50 yrs. old Urinalysis: Crystalluria
 2-3% of population will experience acute renal colic
 Adult: incidence in men 3x more than in women TYPES OF STONES
 Children: incidence is equal among male and female Stone composition:
 Rates of nephrolithiasis declines with age - most consist of 95% crystalline materials and 5% non crystalline
 13% of men matrix
 7 % of women - matrix materials: protein, cellular debris and other organic materials
40-50% recur within 5 years
50-60% recur within 10 years Type of Stones
75% recur within 20-30 years CALCIUM Uric acid Struvite Cystine
(75-85%) (5-10%) (5%) (1%)
No History Incidence Age of > males ; 3:1 > men > female; 1:3 Equal
rd th
of stones cases/1000/yr occurence (3 -4 decade)
Men 3-4 30-60 Slowly declines Calcium oxlate infection
with age and calcium
Women 2 20-30 Declines to phosphate
1/1000
women/yr for A. CALCIUM STONES
next 4 decades (dark brown, small, ovoid, hard with granular surface)
1. Idiopathic Hypercalciuria (50-55%)
 hereditary (?), 2:1 (M:F)
MECHANISM OF STONE FORMATION  normocalcemia, unexplained hypercalciuria
 Urinary stones usually arise because of the breakdown  raises urine saturation with respect to Ca oxalate and calcium
of a delicate balance between solubility and precipitation of salts phosphate
 The kidneys must conserve water, but they must excrete materials  Dx: urine Ca: > 300 mg/ 24hr (men)
that have low solubility >250 mg/24 hr (women)
- balanced during adaptation to diet, climate, and activity 4 mg/kg/24 hr
- mitigated to some extent by the fact that urine contains
 rule out:
substances such as pyrophosphate, citrate, and glycoproteins
- hyperthyroidism
that inhibit crystallization which are less than perfect
- cushing’s syndrome
Supersaturation
- sarcoidosis
 when concentration of a substance in a solution is above the
- malignant tumors
saturation point
- vitamin D intoxication
 Supersaturated urine is due to excessive excretion rates and/or
- rapidly progressive bone disease
because water conservation is extreme, crystals form and may grow
- Paget’s disease
and aggregate to form a stone
 Treatment: Low sodium, low protein diet, thiazides
 Excess can promote spontaneous development of new crystals
 Reduction in ligands such as citrate can increase ion activity and
2. Hyperuricosuria (20%)
therefore supersaturation.
 4:1 (M:F), dietary indiscretion (excessive intake of purine from meat
 Urine supersaturation can be increased by dehydration or by
and fish)
overexcretion of calcium, oxalate, phosphate, cystine, or uric acid.
 phosphate and uric acid are acids that dissociate readily  mech. Of stone formation: salting out calcium oxalate by urate
over the physiologic range of urine pH.  Dx: urine uric acid: > 750mg/ 24 hr (women)
 Alkaline urine contains more dibasic phosphate, favoring deposits > 800 mg/24 hr (men)
of brushite and apatite.  Treatment: allopurinol and low purine diet
 Below a urine pH of 5.5, uric acid crystals predominate
3. Primary Hyperparathyroidism (3-5%)
Crystallization  3:10 (M:F), neoplasia
 when urine supersaturation is excessive, crystals begin to nucleate  Dx: hypercalcemia with nonsuppressed PTH
 crystal nuclei will grow in size if urine is supersaturated with respect  Treatment: Surgery
to that crystal phase 4. Distal RTA (rare)
 multiple crystals can then aggregate to form a kidney stone  1:1 (M:F)
 hereditary/ acquired
 Dx: hyperchloremic metabolic acidosis
urine pH > 5.5

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RENAL STONES
 Treatment: alkali replacement MANIFESTATIONS
(NEPHROLITHIASIS)
5. Hypocitraturia (20-40%)
1. Stone growth (renal papillae, collecting system, parenchyma)
2. Stone passage (obstructive)
 1:1 or 2:1 (M:F)
 hereditary (?), diet ASYMPTOMATIC
 Dx: urine citrate: < 320 mg/ 24 hr
 Treatment: alkali supplements SYMPTOMATIC
 Usually causes PAIN:
B. URIC ACID STONES - begins gradually
(smooth, yellow, brown, hard,low urinary pH, radiolucent stone) - usually in the flanks
1. Metabolic Syndrome (30%) - increases in the next 20-60 min
 1:1 (M:F), diet - pain may remain in the flank
 Dx: glucose intolerance, obesity and hyperlipidemia - spread downward to ipsilateral groin, testis or vulva
 Treatment: alkali and allopurinol
 Stone size of <5mm = spontaneous passage
 Urine UAE: >1,000 mg/24 hr  give allopurinol
BLEEDING: gross/microscopic hematuria
2. Gout (30%)
 3:1 to 4:1 (M:F), hereditary, DIAGNOSIS
 Dx: clinical diagnosis
 Treatment: alkali and allopurinol
3. Idiopathic (30%)
 1:1 (M:F), hereditary (?)
 Dx: uric acid stones, no gout
 Treatment: alkali and allopurinol if urine UAE: >1,000 mg/24 hr

4. Dehydration: (?)
 1:1 (M:F), intestinal/ habit
 Dx: history, fluid losses via GIT
 Treatment: alkali, fluid replacement, reversal of cause

C. CYSTINE STONES
(small, rounded, multiple and smooth, yellowish and waxy)
 1:1 (M:F)
 Hereditary, AR (autosomal recessive) disorder of defective proximal CT stonogram (axial view) (sagittal view)
renal tubular reabsorption of filtered dibasic AA
 Poor solubility in the urine, normal urine cystine excretion 1. Helical CT scan without radiocontrast (CT STONOGRAM)
<18mg/day • gold standard diagnostic test for detection of kidney stones
•Most sensitive radiologic examination for the detection, localization,
 Stone type of elevated cystine excretion
and characterization of urinary calcifications
 Visible in plain radiograph (STAGHORN)/(BILATERAL MULTIPLE
ADVANTAGES:
STONE)
1. Detection of uric acid stones
 Treatment: Massive fluid alkali and D-PENICILLAMINE IF NEEDED
2. No exposure to the risk of contrast medium
3. Possible diagnosis of other causes of abdominal pain
D. STRUVITE
 For follow-up monitor stones formation and growth: STANDARD
(soft, friable and irregular, yellow white or gray)
ABDOMINAL X-RAYS
 <1:3 (M:F)
 Infection of triple phosphate stones
2. Intravenous Pyelogram (IVP)
 Form only when the upper urinary tract is infected with urease-
producing bacteria (Proteus mirabilis, Klebsiella pnenumonia, or
 IV iodinated contrast media
Providencia sp.)
 Renal fumction NORMAL
 Hydrolysis of urea  supraphysiologic urine pH >8 -> formation of
 AKI (Contrast Nephropathy)
struvite
 If incomplete treatment  struvite stone grows quicKly and fill the
renal collecting system (STAGHORN CALCULI)

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RENAL STONES
MEDICAL MANAGEMENT OF URETERAL STONES
(NEPHROLITHIASIS)
Medical Expulsive Therapy (MET)
1. SIZE OF STONE
(5-8mm 15%, <5mm 90%)
within 4weeks
Tx: α-adrenoreceptor blockers (TAMSULOSIN)
Ca channel blockers (NIFEDIPINE)
2. DEGREE OF OBSTRUCTION
(submucosal edema, and associated inflammation)
Tx: steroids, antibiotics, analgesics, and hydration

TYPE OF STONE/ STONE CRYSTAL SHAPE

INCIDENCE/ SEX CHARACTERISTICS
PREDOMINANCE
CALCIUM dark brown - Staghorns
Intravenous pyelogram OXALATE small rare
(75-85%) ovoid - Randall’s
OTHER SYNDROMES > male hard with palques
granular surface envelope
1. STAGHORN CALCULI
 Struvite, cystine, and uric acid URIC ACID smooth -low urinary
 Fill up the renal pelvis and extend outward through the yellow or brown pH,
infundibulum to the calyces (5-10%) hard - ONLY
 May have few symptoms and can lead to eventual loss of kidney > male radiolucent
function stone
- possible
2. NEPHROCALCINOSIS diamond/ rhomboid staghorns
 Calcium stones grown in the papillae, may break loose and cause STRUVITE Soft - infection
colic friable and -Staghorns
 Some stay and lead to multiple papillary calcification (5%) irregular common
--> nephrocalcinosis > female yellow white or
Papillary nephrocalcinosis gray
 Is common in distal RTA
 Can lead to: severe hypercalciuria, medullary sponge kidney
and calcification at the dilated distal collecting tubules
coffin-lid
CYSTINE Small -Staghorns
EVALUATION AND MANAGEMENT OF PATIENTS Rounded common
WITH NEPHROLITHIASIS (1%) multiple - Inherited
1. Metabolic condition equal smooth (insolubility of
 Do blood works; 24 hr urinalysis yellowish cystine)
2. Composition of the stone waxy
3. Hydration status, diet, activity, and environment hexagonal
*staghorn calculi
The need to operate: (Urological)
- formed by struvute, cystine or uric acid
1. Intractable pain - fills renal pelvis and may extend outward through infundibula to
2. Bleeding
calyces
3. Infection
4. Severity of obstruction

FACTORS TO CONSIDER FOR SPECIFIC TREATMENT

1. Location of the stone
2. Extent of obstruction
3. Nature of stone
4. Function of the affected/unaffected kidney
5. Presence of infection
6. Progress os tone passage
7. Risk of operation/anesthesia

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