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Urinary Lithiasis
Urinary Lithiasis
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
Why don’t small stones pass uneventfully down the ureter early in their development?
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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
pure aqueous solution of a salt is considered saturated when it reaches the point at which
further added salt crystals will not dissolve
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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
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
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
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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;
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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