Urinary lithiasis
The 3rd most common disorder of urinary tract after UTI & prostate disorders.
Without medical intervention stone recurrence rate after surgery can be as high as
50% within 5yr
*Stone occurrence is relatively uncommon before age 20 but peaks in incidence in the
fourth to sixth decades of life
*men are affected 2-3 times more frequently than women
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Etiology
If urinary constituents are similar in each kidney
and if there is no evidence of obstruction, why do most stones present in a unilateral
fashion?
Why don’t small stones pass uneventfully down the ureter early in their development?
Why do some people form one large stone
and others form multiple small calculi?
The etiology remain speculative
The physical process of stone formation is a complex cascade of events that occurs
as the glomerular filtrate traverses the nephron.
It begins with urine that becomes supersaturated with respect to stone-forming salts
lead to crystal formation.
crystals may flow out with the urine or become retained in the kidney at anchoring
sites that promote growth and aggregation, ultimately leading to stone formation
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pure aqueous solution of a salt is considered saturated when it reaches the point at
which further added salt crystals will not dissolve
In urine, despite concentration products of stone-forming salt components, such as
calcium oxalate, that exceed the solubility product, crystallization does not
necessarily occur because of the presence of inhibitors and other molecules
Nucleation and Crystal Growth, Aggregation, and Retention
Crystal
components are the main component of urinary stone
the noncrystalline part or
Matrix
component only
2-10% of the weight. (mainly protein)
*Nuclei are the earliest crystal structure that will not dissolve
Magnesium and citrate inhibit crystal aggregation. Nephrocalcin, an acidic glycoprotein
made in the kidney, inhibits calcium oxalate nucleation, growth, and aggregation
1- Mass precipitation theory
suggests that the distal tubules or collecting ducts, or both, become plugged with
crystals, thereby establishing an environment of stasis, & further
stone growth.
This explanation is unsatisfactory; tubules are conical in shape and enlarge as they
enter the papilla, thereby reducing the possibility of ductal obstruction.
2- Randalls hypothesis
(fixed particle theory)
formed crystals are somehow retained within cells or beneath tubular epithelium.
Randall noted whitish-yellow precipitations of crystalline substances occurring on the
tips of renal papillae as submucosal plaques.
3- Carr hypothesis
calculi form in obstructed lymphatics and then rupture into adjacent fornices of a calyx.
Arguing against Carr’s theory are the grossly visible early stone elements in areas
remote from fornices.
Urinary Ions
A. CALCIUM
major ion present in urinary crystals
over 95% of the calcium filtered at the glomerulus is reabsorbed at both the proximal
and distal tubules and limited amounts in the collecting tube.
Less than 2% is excreted in the urine.
B. OXALATE
10–15% of oxalate found in the urine originates from the diet; the vast majority is a
metabolic by product
C. PHOSPHATE
important buffer and complexes with calcium in urine. It is a key component in calcium
phosphate and magnesium ammonium phosphate stones.
The excretion of urinary phosphate in normal adults is related to the amount of dietary
phosphate (especially in meats, dairy products, and vegetables)
D. URIC ACID
Uric acid is the by-product of purine metabolism
E. SODIUM
sodium plays an important role in regulating the crystallization of calcium salts in urine
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F. CITRATE
key factor affecting the development of calcium
urinary stones. A deficiency commonly is associated with stone formation in those with
chronic diarrhea or
renal tubular acidosis type I (distal tubular defect) and in patients undergoing chronic
thiazide therapy
G. MAGNESIUM
lack of dietary magnesium is associated with increased calcium oxalate stone
formation and calcium oxalate crystalluria
H. SULFATE
They can complex with calcium & may help prevent urinary calculi.
stone varieties
A-Calcium calculi.
Calcification either orthtopic in normal places or heterotopic in abnormal places which
(dystrophic normal s. calcium or meastatic elevated s calcium)
*80-85% of urinary stones are calcareous.
Usually due to elevated urinary calcium, uric acid or oxalate or decreased level of
urinary citrate.
Approximately 1/3rd of pt. undergo metabolic evaluation have no identifiable metabolic
defect.
Nephrocalcinossis.
Calcification within renal parenchyma, rarely cause symptoms & not amenable to
traditional therapy for urinary stone disease.
May associated with nephrolithaiasis.
Causes;
RTA, hyperparathyrodism, medullary sponge kidney, sarcoidosis, milke alkali
syndrome, & multiple myeloma.
Types of calcium stone
1-absorptive hypercalciuric nephrolithiasis
Due to increase calcium absorption from small bowel predominantly the jejunum
resulting in hypercalciuria (>4mg/kg) or (>150-200mg/24hr).
Its of 3types;
type1-dietary independent (15%)
*Cellulose phosphate- binding ca. in bowel prevent its absorption.
*hydrochlorothiazides-reduce renal excretion
of ca.
Type 2- dietary dependent
common cause calcium restricted diet (no specific therapy)
Type3-phosphate renal leak (5%)
lead to decrease serum phosphate—increase V D3
synthesis—increase ca absorption &excretion.
2-resorptive hypercalciuria;
hyperparathyrodism 50% presented with renal stone. suspected in Pt. with ca. phosphate
stone, women with
recurrent ca. stones & those with both nephrocalcinosis & nephrolithiasis .
Hypercalcemia is most consistent sign.
3-Renal induced hypercalciuria.
Intrinsic renal tubular defect in ca. excretion. lead to secondary hyperparathyroidism
effectively treated by hydrochlorthiazide.
4-Hyperuricosuric calicium nephrolithiasis:
Due to either excessive dietary intake of purines or increase endogenous uric acid
production
*Monosodium urate absorb & adsorb urinary inhibitors & facilitate heterogeneous
nucleation.
*pt. have elevated urinary uric acid >600-750 mg/24hr. & consistently ph >5.5. The
urinary ph help to differentiate hyperuricosuric calcium from hyperuricosuric uric acid
nephrolithiasis.
-Effectively treated by low purine diet
pot.cit. & allopurinol (xanthine oxidase inhibitor) for both exogenous &endogenous
respectively.
5-Hyperoxaluric calcium nephrolithiasis:
Increase urinary oxalate >40mg/24hr
In pt. with inflammatory bowel disease & chronic diarrheal state —malabsorption increase
luminal fat & bile, ca bind fat (saponification) no more ca ready to bind oxalate– increase
absorption of oxalate (enteric hyperoxaluria) treated by oral ca. or magnesium.
Primary hyperoxaluria
.
rare hereditary disease (enzyme deficiency) ase ca. oxalate stone
& nephrocalcinosis. need combined liver &renal transplant.
6-Hypocitrateuric ca.nephrolithiasis.
Increase metabolic demand on the renal cell mitochondria decrease the excretion of
citrate (hypocitraturia <320mg/24hr) like metabolic acidosis (in RTA), hypokalemia
(thiazide therapy), fasting, hypomagnesemia UTI & androgens.
In contrast alkalosis, estrogen ,growth h. & V D increase urinary citrate. It complex with
ca. ion decreasing energy for crystallization.
Treated by potassium citrate.
B. Non calcium calculi.
1- Struvite.
composed of MAP (magnesium, ammonium, & phosphate). Infection stone ase urea
splitting organisms (proteus, pseudomonas providencia, klebsiella, staph. &
mycoplasma.)
Most commonly in women & may recur rapidly.
usually staghorn calculus. The high ammonium
concentration derived from urea splitting lead to alkaline urinary ph ranges from 6.8-8.3
*normal urinary ph=5-7 in which MAP crystal
soluble.
2- Uric acid stone
Less than 5% of all urinary stones usually in men. Specially pt. with gout,
myeloproliferative disease, rapid weight loss, & those treated with cytotoxic drugs.
Most of them have no hyperuricemia.
Urinary ph consistently < 5.5, in contrast to pt.
with hyperuricosuric calcium nephrolithiasis.
as urinary ph increase >5.75 it dissociates to soluble urate ion.
Treated by increase fluid intake >2L/d & urinary
Ph > 6.0 (alkalinization) allopurinol also help reduce uric acid excretion.
3-cystine
Secondary to inborn error of metabolism.
Resulting in an abnormal intestinal & renal absorption of amino acid cystine, ornithine,
lysine, & arginine. Cystine lithiasis is the only clinical manifestation of this defect.
The solubility of cystine is ph dependent with dissociation constant pka of 8.1so treated
by increase fluid intake >3L & alkalinization.
there is no known inhibitor for cystine stone.
penicillamine can reduce urinary cystine level it complexes with amino acid—more
soluble.
4-Xanthine.
Are secondary to congenital deficiency of xanthine oxidase. This enzyme normally
catalyzes the oxidation of hypoxanthine to xanthine & xanthine to uric acid.
Treatment: high fluid intake, alkalinization
trial of allopurinol xanthine oxidase inhibitor??
5-Other rare
indinavir (protease inhibitor) used in treatment of AIDS .
Long term used of antacid—silica stone.
Triamterene stone ase antihypertensive contain triamterene such as diazyde.
DIAGNOSTIC EVALUATION OF NEPHROLITHIASIS
Any evaluation should be able to identify associated metabolic disorders responsible
for recurrent stone disease. These metabolic problems include
-distal renal tubular acidosis,
-primary hyperparathyroidism,
-enteric hyperoxaluria,
-cystinuria, and
-gouty diathesis.
medical therapy is indicated not only to prevent further stone formation but also to
correct the underlying physiologic disturbance
Indications for a Metabolic Stone Evaluation
Recurrent stone formers
Strong family history of stones
Intestinal disease (particularly chronic diarrhea)
Pathologic skeletal fractures
Osteoporosis
History of urinary tract infection with calculi
Personal history of gout
Solitary kidney
Anatomic abnormalities
Renal insufficiency
Stones composed of cystine, uric acid, or struvite
Protocol for Low-Risk Single Stone Formers
medical history
any underlying conditions that may have contributed to the stone disease
patient's dietary habits, including fluid consumption and excessive intake of certain
foods as well as all medications taken
blood screen
calcium, sodium, potassium, chloride, carbon dioxide, blood urea nitrogen, creatinine,
PTH, uric acid
Urinalysis pH, crystalluria, urine culture
Radiography
Stone analysis
Extensive Diagnostic Evaluation
History and physical examination,
diet history,
radiologic evaluation,
two 24-hour urine specimens on random diet, and dietary instruction for restricted diet
Urine for pH, Total Volume, Oxalate, Citrate, Qualitative Cystine
Blood for PTH, Calcium, Uric Acid, Creatinine, Sodium
CONSERVATIVE MEDICAL MANAGEMENT
Fluid Recommendations
increase in fluid intake to achieve a daily urine output of 2 liters
Lemonade and orange juice increase urine volume as well as increase urinary citrate
excretion
Increase intake of soda can confer an increased risk of subsequent stone recurrence
Protein Restriction
-the incidence of renal stones is higher in populations in which there is an increased
animal protein intake
-Protein intake increases urinary calcium, oxalate, and uric acid excretion and increase
probability of stone formation even in normal subjects
-ingestion of protein is second only to ingestion of vitamin D in enhancing intestinal
absorption of calcium
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Sodium Restriction
-Sodium restriction has been widely recommended as an important element of dietary
prevention of recurrent nephrolithiasis
-The net effect of a high sodium diet was an increased propensity for the
crystallization of calcium salts in urine
-In combination with animal protein restriction and moderate calcium ingestion, a
reduced sodium diet will decrease stone episodes by approximately 50%
Obesity
-increased body mass index, larger waist size, and weight gain correlated with an
increased risk of stone episodes. This increased stone risk was still more pronounced
for women than for men
-urine pH appears to be directly correlated with body size so the increased incidence of
uric acid stone formation in obese stone formers may be secondary to the production of
more acidic urine than in “normal-sized” patients
-weight-reducing diet (low-carbohydrate) delivers a marked acid load to the kidney &
predispose to increased stone risk
Dietary Calcium
Older recommendations to significantly restrict calcium intake probably led to an
increase in available intestinal oxalate. As a result, increase oxalate absorption,
thereby raising the supersaturation of calcium oxalate
Oxalate Avoidance
Since less than 10% to 15% of urinary oxalate is usually derived from dietary sources,
it is unclear how helpful it is to promote the strict avoidance of oral oxalate loading
-avoid foodstuffs that are rich in oxalate, such as spinach, beets, chocolate, nuts, and
tea
1-patient with regional ileitis, colitis and post operative
intestinal bypass excrete excessive amount of
a. calcium in the urine
b. cystine in the urine
c. uric acid in the urine
d. oxalate in the urine
2-hyperuricosuria can also cause calcium oxalate stone
by
a. causing reduction of monosodium urate
b. hetrogenous nucleation of calcium oxalate by
monosodium urate
c. inducing hypercalciuria
d. homogenous nucleation of calcium oxalate
3-patients with enteric hyperoxaluria are more likely to
form stones composed of
a. uric acid
b. calcium oxalate
c. cystine
d. magnesium ammonium phosphate
4-the primary abnormality of renal hypercalciuria is
considered to be
a. hyperabsorption of calcium in small bowel
b. increase vitamin D3 level
c. impairment of renal tubular reabsorption of calcium
d. excessive mobilization of calcium from bone
5-renal tubular acidosis may be associated with urinary
calculi because of
a. hyperoxaluria and hypercalcemia
b. hypermagnesiuria and hypocitraturia
c. hypercalciuria and hypocitraturia
d. hyperuricosuria
6-the primary defect in absorptive hypercalciuria type 1 is
considered to be
a. renal leak of calcium
b. calcium mobilization from bone
c. excessive calcium intake
d. primary hyperabsorption of intestinal calcium
7- urinary PH plays an important role in the formation of
all the following types of urinary calculi except
a. uric acid
b. cystine
c. struvite
d. calcium phosphate
8-sodium cellulose phosphate would be contraindicated in
patient with renal hypercalciuia since it might cause
a. hypercalcemia
b. negative calcium balance
c. secondary hyperuricosuria
d. precipitation of calcium apatite