Transcript Urinary _stone_diseasex

URINARY STONE DISEASE
By Dr.Aiman AL Solumany (R2)
King Fahd General Hospital
In General

Urinary calculi are the third most common problem
of the urinary tract, exceeded only by urinary tract
Infections and pathologic conditions of the prostate.

1-Renal calculi

2- medical evaluation
EPIDEMIOLOGY OF RENAL CALCULI
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Incidence
The lifetime prevalence of kidney stone disease is
estimated at 1% to 15%, with the probability of having
a stone varying according to age, gender, race, and
geographic location
Recurrence rate – with out ttt 10% at 1 yr, 50% at 10
yrs.
Factors :.
1- intrinsic factor.
2- extrinsic factors
EPIDEMIOLOGY OF RENAL CALCULI

Intrinsic Factors
 genetics: FHx and race
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rare in Natives, blacks
common in Asians and whites
about 25% of patients with kidney stones have a family
history of kidney stones.
Age and Sex
Peak - 20-40 years old
M : F - 3:1
F > M - stones 2nd to infections or abN
EPIDEMIOLOGY OF RENAL CALCULI
Extrinsic Factors:
1. Geography
o The prevalence of urinary calculi is higher in those
who live in mountainous, desert, or tropical areas.
o increased
incidence: US, UK, Scandanavia,
Mediterranean, northern India/Pakistan, northern
Australia, central Europe, and China.
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EPIDEMIOLOGY OF RENAL CALCULI
2-climate and seasonal factors :
o incidence highest in July, Aug, Sep: 1-2 months after
maximal mean annual temperature  dehydration,
increased exposure to sunlight and increased vitamin
D production w/ increased urinary Ca excretion.
3-water intake:
o decreases average time of residence of free crystal
particles in urine and dilutes components.
EPIDEMIOLOGY OF RENAL CALCULI
4-Diet:.
.high protein and Na
ca stones
.high purine
pH
hyperuricosuria
.low Vit B12
formation and excretion of
oxalate.
The risk of stone disease correlates with weight
and body mass index.
EPIDEMIOLOGY OF RENAL CALCULI
5-occupation:
 stones
more likely to be found in pts w/ sedentary
lifestyles
 professional and managerial groups, affluent
countries/regions/societies
6-stress:
 lower
family income, mortgage problems, emotional
life events associated w/ stone disease
PHYSICOCHEMISTRY
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State of Saturation:
The physical process of stone formation is a complex
cascade of events.
It begins with urine that becomes supersaturated with
respect to stone-forming salts, such that dissolved ions
or molecules precipitate out of solution and form
crystals or nuclei. Once formed, 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.
PHYSICOCHEMISTRY
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A solution containing ions or molecules of a soluble
salt is described by the concentration product, which is
a mathematical expression of the product of the
concentrations of the pure chemical components (ions
or molecules) of the salt.
A pure aqueous solution of a salt is considered
saturated when it reaches the point at which no
further added salt crystals will dissolve.
PHYSICOCHEMISTRY
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The concentration product at the point of saturation is
called the thermodynamic solubility product, Ksp,
Ksp, which is the point at which the dissolved and
crystalline components are in equilibrium for a specific set
of conditions.
At this point, addition of further crystals to the saturated
solution will cause the crystals to precipitate unless the
conditions of the solution, such as pH or temperature, are
changed.
PHYSICOCHEMISTRY
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In urine, despite concentration products of stoneforming 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 .
In this state of saturation, urine is considered to be
metastable with respect to the salt.
PHYSICOCHEMISTRY
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As concentrations of the salt increase further, the
point at which it can no longer be held in solution is
reached and crystals form. this point is called the
formation product, Kf.
Ksp and Kf differentiate the three major states of
saturation in urine: undersaturated, metastable, and
unstable.
PHYSICOCHEMISTRY
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Below the solubility product, crystals will not form under any
circumstances.
above the formation product, the solution is unstable and crystals will
form.
In metastable range, in which the concentration products of most
common stone components reside, spontaneous nucleation or
precipitation
does
not
occur
despite
urine
that
is
supersaturated. in this area that modulation of factors
controlling stone formation can take place and therapeutic
intervention is directed.
PHYSICOCHEMISTRY
Nucleation and Crystal Growth, Aggregation, and
Retention:
o In normal urine, the concentration of calcium oxalate is four
times higher than its solubility in water
o calcium oxalate precipitation in urine occurs only when its
supersaturation is 7 to 11 times its solubility.
 Precip occurs due to the following factors :.
1-Low urinary volumes.
2-High rates of calcium, oxalate, phosphate, or urate
excretion.
3- Low citrate and magnesium excretion .
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PHYSICOCHEMISTRY
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Nuclei are the earliest crystal structure that will not
dissolve.
Homogenous nucleation - process of nuclei formation
in pure solution
Heterogenous nucleation - nuclei form on existing
surfaces - eg epithelial cells, cell debris, urinary
casts, crystals - Lower concentration needed
Most of CaOx is heterogenous
PHYSICOCHEMISTRY
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Another concept necessary for understanding the
genesis of urinary calculi is that of aggregation.
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Crystal nuclei cannot grow large enough to attach to
and occlude renal tubular lumens within the 5 to 7
minutes that it takes for them to pass through tubules
and enter the renal pelvis. They can, aggregate into
large clumps within a minute
PHYSICOCHEMISTRY
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Inhibitors:.
Whole urine, when added to a solution of calcium
phosphate, raises the supersaturation level required
to initiate calcium phosphate crystallization.
Citrate, Magnesium, and pyrophosphate together
were account for 20% of the inhibitory activity of
whole urine, with citrate comprising the most
important factor of the three.
no specific inhibitors are known that affect uric
acid crystallization.
PHYSICOCHEMISTRY
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Citrate
acts as an inhibitor of calcium oxalate and calcium
phosphate stone formation by a variety of actions:
1- it complexes with calcium, reducing the
availability of ionic calcium to interact with oxalate
or phosphate
PHYSICOCHEMISTRY
2- It directly inhibits the spontaneous precipitation
of
calcium oxalate and prevents the agglomeration
of
calcium oxalate crystals.
it has limited inhibitory effect on calcium oxalate crystal
growth , more potent activity in reducing calcium
phosphate growth.
3- citrate prevents heterogeneous nucleation of calcium
oxalate by monosodium urate .
PHYSICOCHEMISTRY
Magnesium:.
Its complexe with oxalate, which reduces ionic
oxalate concentration and calcium oxalate
supersaturation. In addition, magnesium reduces the
rate of calcium oxalate crystal growth in vitro.
Inorganic pyrophosphate:.
responsible for 25% to 50% of the inhibitory activity
of whole urine against calcium phosphate
crystallization.
PHYSICOCHEMISTRY
Two urinary glycoproteins, nephrocalcin and TammHorsfall glycoprotein, are potent inhibitors of
calcium oxalate monohydrate crystal aggregation .
1-Nephrocalcin is an acidic glycoprotein containing
predominantly acidic amino acids that is synthesized
in the proximal renal tubules and the thick
ascending limb. In simple solution, nephrocalcin
strongly inhibits the growth of calcium oxalate
monohydrate crystals .
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PHYSICOCHEMISTRY
2. Tamm-Horsfall glycoprotein:
. syn - thick ascending limb & distal tubule
. inhibits aggregation CaOx- most potent
. Under specific condition, THP can promote
aggregation (high ionic strength, high calcium and
low pH)
. Citrate can increase THP and its inhibitory effect
PHYSICOCHEMISTRY
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3. Osteopontin (uropontin):
Osteopontin has been shown to inhibit nucleation,
growth, and aggregation of calcium oxalate
crystals as well as to reduce binding of crystals to
renal epithelial cells in vitro
PHYSICOCHEMISTRY
Matrix:
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Renal calculi consist of both crystalline and
noncrystalline components.
The noncrystalline component is termed matrix,
which typically accounts for about 2.5% of the
weight of the stone In some cases reached up
to 65%.
PHYSICOCHEMISTRY
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chemical analysis reveals a heterogeneous mixture
consisting of 65% protein, 9% non-amino sugars,
5% glucosamine, 10% bound water, and 12%
organic ash .
Non–urease-producing bacteria such as E. coli may
play a role in stone formation by increasing the
production of urinary matrix substances, thereby
increasing crystal adherence to the renal epithelium.
MINERAL METABOLISM
Calcium:.
30% to 40 % of dietary calcium is absorbed from
small intestine (the jejunum and the proximal portion of the
ileum) and only approximately 10% absorbed in the
colon.
absorption of calcium varies with calcium intake. with
low calcium intake, calcium absorption is enhanced;
during high calcium intake absorption is reduced.
MINERAL METABOLISM (Calcium)
Calcium in Plasma in three form :
1) combined with plasma proteins (40%)
2) combined with other substances but diffusible
through capillaries (10%)
3) Ca++ (50%) active
MINERAL METABOLISM (Calcium)
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the net absorption of calcium 100 to 300 mg/Day.
Calcium is absorbed in the ionic state; therefore,
substances that complex calcium, such as phosphate,
citrate, sulfate, oxalate, and fatty acids, reduce the
availability of ionic calcium for absorption.
The most important factor that mediates active or
transcellular
calcium
absorption
is
1,25dihydroxyvitamin D3, or calcitriol.
MINERAL METABOLISM (Calcium)
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The active form of vitamin D, 1,25(OH)2D3, is the most
potent stimulator of intestinal calcium absorption.
After conversion of 7-dehydrocholesterol in the skin to
previtamin D3 promoted by sunlight,
previtamin D3 is hydroxylated in the liver to 25hydroxyvitamin D3, which is further hydroxylated in the
proximal renal tubule to 1,25(OH)2D3.
The conversion of 25-hydroxyvitamin D3 to 1,25(OH)2D3
is stimulated by parathyroid hormone (PTH) and by
hypophosphatemia.
MINERAL METABOLISM (Calcium)
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A decrease in serum calcium increases secretion of PTH,
which in turn directly stimulates the enzyme 1αhydroxylase, which is located in the mitochondria of the
proximal renal tubule.
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After transport via the bloodstream to the intestine,
1,25(OH)2D3, binds to the vitamin D receptor in the
brush border membrane epithelial cells to enhance
calcium absorption.
MINERAL METABOLISM (Calcium)
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Calcitriol also acts on the bone and kidney in addition
to its action in increasing calcium absorption from the
intestine.
PTH increases renal calcium reabsorption and enhances
phosphate excretion, leading to a net increase in serum
calcium, which ultimately suppresses further PTH
secretion and synthesis of 1,25(OH)2D3.
Only mature PTH is secreted from the parathyroid
gland, and the most potent stimulus for its secretion is a
decrease in serum calcium.
MINERAL METABOLISM (phosphorus)

Phosphorus: is transported across the intestine through
active and passive mechanisms. Approximately 60% of
the phosphate in the diet is absorbed by the intestine.
1,25-Dihydroxyvitamin D3 stimulates phosphorus
absorption in the duodenum and jejunum through a
sodium-dependent active transport process .
 The transport of phosphate is pH dependent: A
decrease in luminal pH inhibits phosphate transport,
and an increase in pH stimulates phosphate transport.
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MINERAL METABOLISM (phosphorus)
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phosphorus is secreted by the ileum and colon.
About 65% of the absorbed phosphate is excreted
by the kidney and the remainder by the intestine.
Under normal conditions, approximately 20% of
the filtered load is excreted, the other 80% being
absorbed by the proximal tubule.
MINERAL METABOLISM (phosphorus)
PTH is the major hormonal regulator of renal
phosphate reabsorption.
 Daily, about 150 to 200 mmol of calcium and
about 100 mmol of phosphorus are filtered:
Only 5 mmol of calcium and 10 mmol of
phosphorus are excreted in the urine. So, 97%
to 99% of calcium and 85% to 90% of
phosphorus are reabsorbed by the kidney.
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MINERAL METABOLISM (Magnesium)
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Magnesium is also absorbed via active and passive
mechanisms by the intestine.
About 35% to 40% of ingested magnesium is
absorbed.
Although magnesium is absorbed mostly in the small
intestine, some is absorbed by the large bowel also.
Both vitamin D and PTH increase magnesium
absorption.
MINERAL METABOLISM (Oxalate)
Oxalic acid is present in many foods and
beverages.
 poorly absorbed in N pts,  with  Ca in diet.
 Oxalate absorption is markedly increased in
patients with small bowel resection and an
intact colon or inflammatory bowel disease .
 stomach and distal bowel may be the primary
sites for oxalate absorption.
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MINERAL METABOLISM (Oxalate)
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Oxalobacter formigenes, utilize oxalate as an
energy source and consequently reduce intestinal
oxalate absorption.
Recent studies have demonstrated that stone
formers have reduced levels or absent
colonization with Oxalobacter compared with
non—stone-forming.
those individuals lacking the bacteria have higher
urinary oxalate levels.
MINERAL METABOLISM (Oxalate)
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Intestinal oxalate absorption is influenced by
luminal calcium, magnesium, and oxalatedegrading bacteria.
Eighty percent of the oxalate found in urine comes
from endogenous production in the liver (40%
from ascorbic acid, 40% from glycine), and 10%
comes from dietary sources.
Pathopysiology of Stone Formation
Stone Composition
Occurrence (%)
Calcium-Containing Stones
Calcium oxalate
60
Hydroxyapatite
20
Brushite
2
Non–Calcium-Containing Stones
Uric acid
7
Struvite
7
Cystine
1-3
Triamterene
>1
Silica
>1
2,8-Dihyroxyadenine
>1
Stone Composition and Relative Occurrence
Pathopysiology of Stone Formation
(calcium stone )
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Hypercalciuria is the most common abnormality
identified in calcium stone formers.
Between 35% and 65% of all patients with calcium
oxalate kidney stones have increased urinary
calcium excretion in the absence of raised serum
calcium levels.
Pak (1987), who defined it as the excretion of
greater than 200 mg of calcium per 24 hours after
1 week's adherence to a 400-mg calcium, 100-mEq
sodium diet.
Pathopysiology of Stone Formation
(calcium stone )
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Parks and Coe (1986) defined hypercalciuria as
excretion of calcium of greater than 4 mg/kg/day
or greater than 7 mmol/day (men) or 6 mmol/day
(women).
Calcium transport is regulated at three sites:
intestine, bone, and kidney. Dysregulation at any of
these sites can lead to hypercalciuria.
Pathopysiology of Stone Formation
(calcium stone )
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hypercalciuria divided into three subtypes:
1- Absorptive hypercalciuria due to increased
intestinal absorption of calcium.
2- Renal hypercalciuria due to primary renal leak of
calcium.
3- Resorptive hypercalciuria due to increased bone
demineralization.
Pathopysiology of Stone Formation
(calcium stone )
Absorptive hypercalciuria:.
 AH is increased intestinal absorption of calcium,
which occurs in approximately 55% of stone
formers ( Menon, 1986 ).
 AH is classified as :.
type I when urinary calcium remains high despite a
low calcium diet (400 mg dietary calcium daily).
type II when urinary calcium normalizes with a
restricted calcium intake.

Pathopysiology of Stone Formation
(calcium stone )
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1,25-dihydroxyvitamin D3levels are elevated in up
to 50% of patients with absorptive hypercalciuria,
suggesting that, at least in some individuals, this
condition is secondary to increased production of or
increased sensitivity to vitamin D metabolites.
Another etiology of AH is renal phosphate wasting
leading to a subsequent increase in active vitamin
D.
Pathopysiology of Stone Formation
(calcium stone )
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Mechanisms of absorptive hypercalciuria :
Pathopysiology of Stone Formation
(calcium stone )
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Renal hypercalciuria:.
The kidney filters approximately 270 mmol of
calcium and must reabsorb more than 98% of it to
maintain calcium homeostasis.
Approximately 70% of calcium reabsorption occurs
in the proximal tubule.
In renal hypercalciuria, impaired renal tubular
reabsorption of calcium results in elevated urinary
calcium
levels
leading
to
secondary
hyperparathyroidism.
Pathopysiology of Stone Formation
(calcium stone )
the underlying abnormality
is primary renal wasting
of calcium.
The consequent reduction in
circulating serum calcium
stimulates PTH production
Pathopysiology of Stone Formation
(calcium stone )
High fasting urinary calcium levels with a
normal serum calcium value are
characteristic of renal hypercalciuria.
 The elevated fasting urinary calcium and
serum PTH levels differentiate renal from
absorptive hypercalciuria.
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Pathopysiology of Stone Formation
(calcium stone )
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Resorptive hypercalciuria:.
is an infrequent abnormality most commonly
associated with primary hyperparathyroidism.
Primary hyperparathyroidism is the cause of
nephrolithiasis in about 5% of cases .
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Excessive PTH secretion from a parathyroid
adenoma leads to excessive bone resorption and
increased renal synthesis of 1,25(OH)2D3.
which in turn enhances intestinal absorption of
calcium.
the net effect is elevated serum and urine calcium
levels and reduced serum phosphorus levels.
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Idiopathic hypercalciuria occurs in 5% to 10% of
healthy people and in about half of patients with
calcium nephrolithiasis.
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Calcium Load Test.
After 7 days of a low-calcium, low-sodium diet,
patients fast for 12 hours from 9 PM.
Distilled water is provided at 9 PM and midnight.
At 7 AM the next day, patients completely empty
the bladder and discard the urine.
They drink an additional 600 mL of distilled water.
Urine is collected from 7 to 9 AM. This is the fasting
sample.
At 9 AM, 1 g of calcium mixed in a liquid synthetic
meal is given orally.
 Urine is collected from 9 AM to 1 PM. This is the
postload sample. Both urine samples are analyzed
for calcium, creatinine, and cAMP .
 cAMP measurements are used as an indirect
estimate of parathyroid function because most PTH
assays are insensitive to rapid changes in serum
calcium.
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Additional, rare causes of resorptive hypercalciuria
include hypercalcemia of malignancy, sarcoidosis,
thyrotoxicosis, and vitamin D toxicity.
Many granulomatous diseases including tuberculosis,
sarcoidosis, histoplasmosis, leprosy, and silicosis
have been reported to produce hypercalcemia.
Sarcoidosis is most commonly associated with
urolithiasis.
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The sarcoid granuloma produces 1,25(OH)2D3,
causing increased intestinal absorption of calcium,
hypercalcemia, and hypercalciuria.
primary hyperparathyroidism is the most common
cause of hypercalcemia in an outpatient setting,
malignancy is the main cause of hypercalcemia in
hospitalized patients.
Lung and breast cancers account for about 60%
of malignancy-associated hypercalcemia, whereas
renal cell (10% to 15%), head and neck (10%).
Primary Hyperparathyroidism
the prevalence of stone disease in hyperparathyroidism
is only about 1%.
 The diagnosis is difficult ,it requires a demonstration
of hypercalcemia in the absence of any other
disorder that elevates serum calcium .
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Glucocorticoid-Induced Hypercalcemia:
Glucocorticoids can alter calcium metabolism through
their actions on bone, intestine, and parathyroid glands.
Their most potent effect is related to calcium
metabolism in bones, where glucocorticoids promote
bone resorption and reduce bone formation, leading to
osteopenia with chronic use.
stimulate release of PTH .
inhibit intestinal absorption of calcium .
common in patients with Cushing's syndrome.
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Hyperoxaluria,
defined as urinary oxalate greater than 40
mg/day, leads to increased urinary saturation of
calcium oxalate and subsequent promotion of
calcium oxalate stones.
oxalate has been implicated in crystal growth and
retention by means of renal tubular cell injury
mediated by lipid peroxidation and the generation
of oxygen free radicals .
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Causes of hyperoxaluria :.
Disorders in biosynthetic pathways (primary
hyperoxaluria).
Intestinal malabsorptive states associated with
inflammatory bowel disease, celiac sprue, or
intestinal resection (enteric hyperoxaluria).
Excessive dietary intake or high substrate levels
(vitamin C) (dietary hyperoxaluria).
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Primary hyperoxaluria is the result of a rare
autosomal recessive disorder in glyoxylate
metabolism by which the normal conversion of
glyoxylate to glycine alanine glyoxylate
aminotransferase (AGT), is prevented, leading to
oxidative conversion of glyoxylate to oxalate, an
end product of metabolism .
mutation of the AGT gene (AGXT) results in a
substitution of glycine by arginine at position 170.
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markedly high levels of urinary oxalate(>100
mg/day), leading to increased saturation of calcium
oxalate, aggressive stone formation, and marked
nephrocalcinosis
untreated, primary hyperoxaluria leads to end-stage
renal failure, which occurs by age 15 in 50% of
affected patients and is associated with an overall
death rate of approximately 30%
Primary hyperoxaluria is treated with pyridoxine
supplements (200 to 400 mg/day), which lower
oxalate production in some patients.
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Enteric Hyperoxaluria:.
The most common cause of acquired hyperoxaluria is
enteric hyperoxaluria.
Malabsorption from any cause, including small bowel
resection intrinsic disease, or jejunoileal bypass
increases the colonic permeability of oxalate as the
result of exposure of the colonic epithelium to bile salts.
Furthermore, loss of calcium in the feces results in the
presence of less calcium in the intestinal lumen, allowing
oxalate to exist in a soluble form.
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Treatment:.
oral hydration and a low-oxalate, low-fat diet.
Calcium carbonate by mouth, 1 to 4 g with each
meal, binds oxalate in the gut so that it cannot be
absorbed
Cholestyramine, a nonabsorbable resin that binds
fatty acids, bile salts, and oxalate, can be used at
doses of 1 to 4 g with each meal and at bedtime.
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Dietary Hyperoxaluria.
In oxalate-rich foods such as nuts, chocolate, brewed
tea, spinach, broccoli and strawberries can result in
hyperoxaluria in normal patients.
Increased animal protein can also increase urinary
levels of calcium and oxalate .
Severe calcium restriction may result in reduced
intestinal binding of oxalate and increased intestinal
oxalate absorption. Ascorbic acid supplementation has
been shown to increase urinary oxalate levels by in vivo
conversion to oxalate.
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Idiopathic Hyperoxaluria :.
Several studies have suggested that mild
hyperoxaluria is as important a factor as
hypercalciuria in the pathogenesis of idiopathic
calcium oxalate stones .
Baggio and associates (1986) detected a higher
rate of oxalate flux across the red blood cell
membrane at steady state in 114 patients with a
history of calcium oxalate kidney stones compared
with control subjects.
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The treatment of mild hyperoxaluria is difficult.
Dietary restriction of oxalate results in decreased
oxalate excretion, but the decrease may not be
significant
Dietary calcium restriction is counterproductive because
urinary oxalate excretion rises.
Pyridoxine decreases urinary oxalate excretion in 50%
of patients with mild metabolic hyperoxaluria.
Administration of thiazides causes a decrease in urinary
oxalate excretion and normalizes erythrocyte oxalate
fluxes
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Hyperuricosuria:.
is defined by urinary uric acid exceeding 600 mg/day.
Up to 10% of calcium stone formers have high urinary
uric acid levels as the only abnormality .
Hyperuricosuria increases urinary levels of monosodium
urate, which in turn promotes calcium oxalate stone
formation.
At pH greater than 5.5, sodium urate formation
promotes calcium oxalate stone formation through
heterologous nucleation .
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Uric acid may reduce the effectiveness of naturally
occurring inhibitors of crystallization.
uric
acid
crystals
can
bind
urinary
glycosaminoglycans such as heparin that inhibit
crystallization of calcium oxalate.
Excessive dietary purine intake is the main cause of
hyperuricosuria .
Between 80% and 90% of patients with
hyperuricosuric nephrolithiasis are men.
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Management of Hyperuricosuric Calcium
Nephrolithiasis:.
Dietary purine restriction, should prevent
hyperuricosuria and nephrolithiasis. This requires
limiting consumption of red meat, poultry, and fish
Allopurinol inactivates xanthine oxidase and
decreases uric acid synthesis
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Hypocitraturia:.
is defined as a urinary citrate level less than 320 mg/day
( Pak, 1987 ) or less than 0.6 mmol (men) or 1.03 mmol
(women) daily
is an important and correctable abnormality associated with
nephrolithiasis that exists as an isolated abnormality in up to
10% of calcium stone formers and is associated with other
abnormalities in 20% to 60%
Citrate is an important inhibitor that can reduce calcium
stone formation by several mechanisms.
First, reduces urinary saturation of calcium salts by
complexing with calcium
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Second, prevents spontaneous nucleation of calcium
oxalate.
Third, citrate inhibits agglomeration and sedimentation
of calcium oxalate crystals as well as the growth of
calcium oxalate and calcium phosphate crystals.
Finally, normal urinary citrate levels can enhance the
inhibitory effect of Tamm-Horsfall glycoprotein
Metabolic acidosis reduces urinary citrate levels
secondary to enhanced renal tubular reabsorption and
decreased synthesis of citrate in peritubular cells
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Renal Tubular Acidosis (RTA) :.
Is a clinical syndrome that results from specific
defects in renal tubular H+ secretion and urinary
acidification.
There are three types of RTA: 1, 2, and 4
Type 1 (distal) RTA is of particular significance to
urologists not only because it is the most common
form of RTA but also because it is the form of RTA
most frequently associated with stone formation,
which occurs in up to 70% of affected individuals.
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the kidney must reabsorb or regenerate nearly all
of
the filtered bicarbonate each day
(approximately 4500 mmol) to maintain its
buffering capacity.
the kidney must excrete excess acid, which
accumulates from the breakdown of carbohydrates,
fats, and proteins and as a result of bicarbonate
loss in the stool .
A defect in either bicarbonate reabsorption or acid
excretion will lead to metabolic acidosis.
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Type 1 (Distal) Renal Tubular Acidosis :.
Distal RTA is characterized by hypokalemic,
hyperchloremic, non–anion gap metabolic acidosis
and a urinary pH consistently above 6.
The primary abnormality is the inability of the
distal nephron to establish and maintain a proton
gradient between tubular fluid and blood.
Profound hypocitraturia, perhaps the most important
factor in stone formation, is due to impaired citrate
excretion as a result of metabolic acidosis

1)
2)
3)
4)
four major pathogenic mechanisms have been
identified:
a permeability defect.
a proton pump secretory defect.
a voltage-dependent defect.
a carbonic anhydrase deficiency.




More than two thirds of patients with distal RTA are
adults; the rest are children, mostly infants.
Infants generally present with vomiting or diarrhea,
failure to thrive, and growth retardation.
Children present with metabolic bone disease and
renal stones.
Adults present with symptoms attributable to
nephrolithiasis and nephrocalcinosis.



Up to 70% of adults with distal RTA have kidney
stones.
up to 80% of the patients are women.
The most common type of stone associated with
distal RTA is calcium phosphate as a result of
hypercalciuria, hypocitraturia, and increased
urinary pH.

o
o
Type 2 (Proximal) Renal Tubular Acidosis:.
The primary defect here is a failure of bicarbonate
resorption in the proximal tubule leading to urinary
bicarbonate excretion.
The defect in proximal tubular bicarbonate
absorption results in increased urinary citrate
excretion. Thus, most individuals believe that
nephrolithiasis and nephrocalcinosis do not occur in
patients with classic proximal RTA.

o
o
o
Type 4 RTA is associated with chronic renal damage,
usually seen in patients with interstitial renal disease
and diabetic nephropathy.
Chronic renal parenchymal damage results in
moderate reductions in glomerular filtration rate,
hyperkalemia, and hyperchloremic metabolic acidosis
with reduced net acid excretion .
Nephrolithiasis and nephrocalcinosis are uncommon.
patients with type 4 RTA do not make uric acid stones
because their uric acid excretion is low, and they do not
make calcium stones because their calcium excretion is
low.

o
o
o
Diagnosis of Type 1 RTA:.
The patient has hypokalemia, hyperchloremia,
metabolic acidosis, and a urine pH of 5.5 or higher.
Urinary citrate is low, usually less than 50 mg per
24 hours.
Hypercalciuria is seen often.
therapy of RTA :.
 Alkali therapy decreases stone growth and new
stone formation,
o delays the development of nephrocalcinosis,
o normalizes retarded growth in children,
o corrects the metabolic changes of hypokalemia



Potassium bicarbonate or citrate (1 to 2 mmol/kg
daily in two to three divided doses) corrects
systemic acidosis and normalizes urinary citrate.
The goal of treatment is to restore urinary citrate to
high normal levels and not simply to correct
metabolic acidosis.
If hypercalciuria persists with alkali therapy, a
thiazide diuretic is added to the therapeutic
regimen.

o
o
o
Hypomagnesuria:.
is a rare cause of nephrolithiasis, affecting less than
1% of stone formers as an isolated abnormality, with
other abnormalities in 6% to 11%.
Magnesium complexes with oxalate and calcium salts,
and therefore such low magnesium levels result in
reduced inhibitory activity.
Low urinary magnesium is also associated with
decreased urinary citrate levels, which may further
contribute to stone formation).



Whether low magnesium is the cause or an effect of
low citrate is not clear.
Low magnesium levels occur with poor dietary
intake or as a result of reduced intestinal
absorption associated with intestinal abnormalities
producing chronic diarrheal syndrome.
magnesium citrate may be the ideal agent for the
treatment of hypomagnesuric calcium nephrolithiasis


two forms: free uric acid and urate salt, which forms
a complex mostly with sodium.
Sodium urate is approximately 20 times more
soluble in water than free uric acid and does not
crystallize under normal conditions.



Predominantly affects middle-aged men
5 - 8% of stones are pure uric acid stone (they are
often orange, small round and smooth) or 30 - 40%
of uric acid stones are mixed with calcium.
The stones are usually radiolucent but can be
opaque if mixed with calcium or if they are very
large (staghom) they can be faintly radiopaque
even if pure uric acid.



Uric acid is the major metabolic end product of
purine metabolism in men.
The three main factors of uric acid stone formation
are low pH, low urine volume, and hyperuricosuria .
The most important pathogenetic factor is low urine
pH, because most patients with uric acid stones have
normal uric acid excretion but invariably
demonstrate persistent low urine pH
three factors are involved in uric acid urolithiasis:.
First, patients tend to excrete excessively acidic urine
at a relatively fixed, low urinary pH.
Second, they may absorb, produce, or excrete more
uric acid than patients without gout or uric acid
stones.
Third, urinary volume is diminished in these patients.
The combination of these factors is ideal for the
crystallization of uric acid in the urine.




The principal cause of uric acid crystallization is the
supersaturation of urine with respect to
undissociated uric acid .
There is no known inhibitor of uric acid
crystallization.
Dissociation proportional to pH





Pts with uric acid stones have prolonged periods of
acidity in urine.
Almost 100% of the UA is dissociated at pH of 6.5
Patients with gout excrete relatively less ammonium
and more titratable acid than do normal subjects
Patients with gout or uric acid stones exhibit two
other metabolic defects—overproduction of uric
acid and impaired renal uric acid excretion.
The exact cause of uric acid overproduction in
primary gout is unknown


The frequency of uric acid stones in gout is about
20%.
Myeloproliferative disorders such as acute leukemia
are an important cause of severe hyperuricosuria,
particularly in childhood.

o
o
o
o
Evaluation:.
observation of daily urinary pH .
determining the serum and urinary uric acid levels,
assessing the degree of ingestion of dietary
purines.
If the patient has evidence of hyperuricemia,
evaluation should include a brief survey to rule out
myeloproliferative or neoplastic disease .
microscopic examination of the urine

o
o
1.
2.
3.
Therapy:.
instructing the patient to drink enough fluids to ensure
urinary output in excess of 1500 to 2000 mL/day
The urine should be alkalinized to a level between 6.5
and 7.
NaHCO3 650mg qid or Kcitrate 30-60 meq qid
Polycitrate K – 15cc qid or crystals 1pk qid
Attempts at alkalinization of the urine to a pH higher
than 7.0 should be avoided. At a higher pH, there is a
danger of increasing the risk of calcium phosphate
stone formation.
o
o
If the patient has hyperuricemia, or if urinary uric
acid excretion is greater than 1200 mg/day, the
patient should be additionally treated with
allopurinol, 300 to 600 mg/day.
Complications of allopurinol include skin rash, drug
fever, and attack of acute gout. Rarely, an
exfoliative skin reaction with hemorrhagic skin
lesions and systemic vasculitis .
Cystine stones


Cystine stones account for about 1% of all urinary
calculi and occur only in patients who have
cystinuria .
Cystinuria is an autosomal recessive disorder
characterized by a defect in intestinal and renal
tubular transport of dibasic amino acids, resulting in
excessive urinary excretion of cystine .
Cystine stones



accumulation of cystine causes crystallization when
concentrations rise above the saturation point
(approximately 250 mg cystine per liter of urine)
Cystine stones are radiopaque.
The stones are yellowish and have a waxy
appearance. They are often multiple, are large,
and may form staghorns. Cystinuria can cause renal
stones in childhood, but the peak of clinical
expression is in the 2nd and 3rd decades of life.
Cystine stones





Diagnosis:.
The first-morning urine specimen should be examined
for the presence of typical benzene ring or hexagonal
cystine crystals
sodium nitroprusside spot test, which turned purple in
the presence of cystine
If the screening test is positive, urinary cystine excretion
should
be
quantitated
with
amino
acid
chromatography.
A level of greater than 250 mg per 24 hours is usually
diagnostic of cystinuria.
Cystine stones



Treatment:.
The goal of therapy is to lower cystine concentration
in urine below its level of solubility
Diet :
Cystine is produced from the essential amino acid
methionine, which is abundant in meat, poultry, fish,
and dairy products. Thus, a low-methionine diet
decreases urinary cystine excretion.
Cystine stones

o
o
o
Oral Hydration and Alkalinization:.
increasing the urinary output to 3 L/day allows
dissolution of existing stones and prevention of new
cystine stones at urinary cystine excretion of up to
750 mg/day.
fruit juices may have a dual benefit because they
provide not only water, but also alkali
Because the pKa of cystine is 8.3, alkalinization
above 7.5 is necessary for the dissolution of cystine
crystals.
Cystine stones



Sodium bicarbonate (15 to 25 g/day) and potassium
citrate (15 to 20 mmol two to three times a day) are
commonly used for alkalinizing urine.
Acetazolamide (250 mg three times a day) increases
urinary bicarbonate excretion by inhibiting carbonic
anhydrase. It can be used to augment the alkalinization
achieved with bicarbonate or citrate
Urinary cystine excretion can be reduced by the
administration of glutamine (2 g/day in three divided
doses)
Cystine stones



Pharmacologic Agents:.
Two agents can be used: D-penicillamine or alphamercaptopropionylglycine (MPG). Both agents bind
cystine, forming a complex that is soluble in urine.
In many patients, cystine stones are so large and so
obstructive that procedural therapy should be used
initially to debulk or remove the stone.
Struvite Stones





Struvite Stones (Infection Stones)
The stone is composed of magnesium, ammonium,
and phosphate, mixed with carbonate.
Struvite calculi have also been commonly referred
to as infection or triple-phosphate stones and
account for 2% to 20% of all stones
60-90% of staghorns
-F:M 2:1
Struvite Stones




Pathogenesis
Two conditions must coexist for the crystallization of
struvite—urine pH of 7.2 or above and ammonia in the
urine.
The driving force behind struvite stones is infection of
the urine with urease-producing bacteria.
the hydrolysis of urea releases both an acid (carbonic
acid) and a base (ammonia). Because two molecules of
ammonia are produced from one molecule of urea,
neutralization of the base is incomplete. As a result, the
urinary pH rises.
Struvite Stones




The most common urease-producing pathogens are
Proteus, Klebsiella, Pseudomonas, and Staphylococcus.
Proteus mirabilis the most common
Bacteria may be involved in stone formation by
damaging the mucosal layer of the urinary tract,
resulting in both increased bacterial colonization and
crystal adherence.
It has been proposed that ammonium, may alter the
glycosaminoglycan layer present on the surface of the
transitional cell layer and significantly increase
bacterial adherence to normal bladder mucosa.
Struvite Stones

1.
2.
3.
4.
5.
6.
Risk Factor:.
Chronic indwelling catheters
Urinary diversion
Neurogenic bladder
Anatomic abnormalities
FB
Female Sex
Struvite Stones


o
o
Clinical Presentation :.
the symptoms of acute pyelonephritis, including
fevers, chills, flank pain, dysuria, frequency,
urgency, and malodorous, cloudy urine.
Women are more often affected with struvite calculi
than are men, probably because of an increased
susceptibility to urinary tract colonization.
This stone type accounts for the majority of all
staghorn calculi.
Struvite Stones
o
o
Xanthogranulomatous pyelonephritis
pure struvite calculi were significantly less likely to
have metabolic anomalies on 24-hour urine
evaluation than were those patients with mixed
compositions of struvite and calcium oxalate.
Struvite Stones



The preferred management of struvite calculi involves
aggressive surgical approaches. followed by supportive
medical therapy to prevent recurrent urinary tract
infection.
The American Urological Association Guidelines
Committee has released updated guidelines that
strongly recommend endoscopy-based therapy (i.e.,
percutaneous nephrolithotomy) as the first-line therapy
for management of complex renal staghorn calculi.
This report noted that complete elimination of all
infected stone material is essential for the prevention of
recurrent struvite stone formation.
Struvite Stones




Procedural Therapy :.
To cure infection stones, needs to remove them
completely.
Percutaneous nephrolithotomy has been used
increasingly for the treatment of staghorn calculi and
has replaced open stone surgery in all but the rarest of
instances.
anatrophic nephrolithotomy is relegated to the few
patients who have a complete staghorn calculus
associated with infundibular stenosis or distortion of
intrarenal anatomy.
Struvite Stones



Extracorporeal shock-wave lithotripsy (ESWL) is a
less invasive procedure than percutaneous
nephrolithotomy.
stone-free results ranging from 30% to 66% have
been achieved
Most clinicians use a combination of percutaneous
nephrolithotomy and ESWL for the treatment of
patients with large staghorn calculi, particularly if
many branches of the collecting system are
involved.
Struvite Stones


o
o
Medical Treatment
Antibiotics
Long-term, culture-specific antimicrobials often
reduce the bacterial burden, even if they do not
completely sterilize the urine
Bacteria are still located on the surface or within the
lattice of the stones, however, and thus reinfection is
common with cessation of antibiotic therapy.
Struvite Stones



The majority of urease-producing infections are
caused by P. mirabilis, more than 90% of which are
sensitive to penicillin or ampicillin
Tetracyclines or fluoroquinolones such as
ciprofloxacin or norfloxacin can be used for the
treatment of patients with Pseudomonas or
Ureaplasma urinary tract infections
Antibiotics are an adjunct to procedural therapy
and should be used to prevent stone recurrences or
growth after operative procedures.
Struvite Stones



o
acetohydroxamic acid potent irreversible inhibitor of
urease and clinically is effective in lowering pH and
ammonia level.
acetohydroxamic acid be used in conjunction with
antibiotic therapy in patients with infection stones in
whom surgical intervention is contraindicated.
Diet :.
A low-calcium, low-phosphorus diet with aluminum
gels was recommended
Struvite Stones

o
o
o
o
Irrigation and Chemolysis:.
Important aspect of medical treatment is the
dissolution of calculi with irrigation.
no irrigation be attempted until the urine is
completely sterile.
nephrostomy tube is left in place postoperatively.
a percutaneous nephrostomy catheter may be
inserted if pt not fit for surg.
Struvite Stones


the renal pelvis is first irrigated with sterile saline
solution at a rate of 120 mL/hr for 24 to 48 hours,
beginning on the fourth or fifth postoperative day.
The patient is observed carefully for development
of fever or any flank discomfort and for elevation
of serum creatinine, magnesium, or phosphate
levels.
Struvite Stones




If, after 48 hours, the patient's condition remains
satisfactory and if there is no infection, no leakage,
and no fever or flank discomfort, irrigation is begun
with an appropriate solution.
Suby’s solution G (pH 4.0)
hemiacidrin (pH 3.9)
The progress of irrigation is followed by
radiographic tomography of the calculi at intervals.
Miscellaneous Stones

o
o
o
o
Xanthine and Dihydroxyadenine Stones
Xanthine stones are a rare stone.
confused with uric acid stones because both are
radiolucent.
result of an inherited disorder in the catabolic enzyme
xanthine dehydrogenase (XDH) or xanthine oxidase,
which catalyzes the conversion of xanthine to uric acid.
Because xanthine is poorly soluble in urine, the high
levels of xanthine that accumulate in XDH deficiency
lead to xanthine stones
Miscellaneous Stones


Allopurinol, which inhibits XDH andwhich is used to
treat hyperuricemia and hyperuricosuria, can, at
very high levels, predispose to xanthine stones. This
side effect is uncommon, because the drug causes
only partial inhibition of the enzyme and rarely
reduces serum uric acid to levels lower than 3
mg/dL.
Children with inherited deficiencies of adenine
phosphoribosyltransferase (APRT) can also present
in infancy with renal complications and stones.
Miscellaneous Stones


Ammonium acid urate stones represent less than 1% of
all stones. Conditions associated with ammonium acid
urate crystallization include laxative abuse, recurrent
urinary tract infection, recurrent uric acid stone
formation, and inflammatory bowel disease.
stone formation due to laxative abuse has been
postulated to be the result of dehydration due to
gastrointestinal fluid loss causing intracellular acidosis
and enhanced ammonia excretion. Because urinary
sodium is very low with laxative use, urate complexes
with abundant ammonia, thereby leading to urinary
supersaturation of ammonium acid urate.
Miscellaneous Stones

o
o
Matrix calculi are found predominantly in
individuals with infections caused by ureaseproducing organisms.
The stones are radiolucent and may be confused
with uric acid calculi.
In most instances, surgical manipulation is required
for their removal because they are not dissolved by
any means yet known.
Miscellaneous Stones





Medications That Directly Promote Stone Formation
Indinavir Stones. Indinavir sulfate is a protease
inhibitor ,effective in increasing CD4+ cell counts and
decreasing HIV-RNA titers in patients infected with (HIV)
,incidence of 4% to 13%.
individuals taking indinavir on a regular basis are at
high risk of producing indinavir stones due to the high
urinary excretion and poor solubility of the drug at
physiologic urinary pH.
may not be visible on plain film radiography or CT.
These calculi can be quite soft and often dissipate
rapidly during endoscopy or shockwave lithotripsy.
Miscellaneous Stones



Guaifenesin and Ephedrine:.Individuals consuming
large quantities of over-the-counter cough medicines
containing ephedrine or guaifenesin are at risk of
developing stones derived mainly from metabolites of
these medicines.
The stones are radiolucent on conventional radiography
but radiopaque on computed tomography (CT).
treated with a variety of methods, including shockwave
lithotripsy, endoscopy, and alkalinization therapy
Miscellaneous Stones



Triamterene stones : triamterene is a potassiumsparing diuretic commonly used for the treatment of
hypertension. It is a very uncommon stone composition,
accounting for only 0.4% of 50,000 calculi in one
report.
Up to 70% of orally administered triamterene appears
in urine, and a few patients have developed either pure
or mixed triamterene stones.
requiring cessation of this medication, triamterene is not
recommended as an adjunct to thiazides during the
treatment of hypercalciuric states.
Miscellaneous Stones




Anatomic Predisposition to Stones:.
(UPJ) obstruction the incidence is nearly 20%
patients with UPJ obstruction and concurrent renal
calculi carry the same metabolic risks as other stone
formers in the general population
hypercalciuria in 46% of patients, hyperuricosuria
in 11%, hypocitraturia in 13%, primary hyperparathyroidism in 13%, and RTA in 3%.
Treatment of patients reduced their rate of
recurrence.
Miscellaneous Stones



Horseshoe kidneys occur with a prevalence of
0.25% but have an associated rate of renal calculi
of 20%
Because of the high insertion of the ureter into the
renal pelvis, there is a relative impairment of renal
drainage, predisposing to UPJ obstruction.
the risk of stone formation due to urinary stasis
rather than to metabolic derangements.
Miscellaneous Stones



Caliceal diverticula are associated with stones in
up to 40% of patients.
Medullary sponge kidney (MSK) is a disorder
characterized by ectasia of the renal collecting
ducts. Nephrocalcinosis and renal calculi are
frequent complications of MSK.
RTA has not been firmly established as a major
cause of stone formation in patients with MSK, and
hypercalciuria and hypocitraturia are likely the
primary risk factors.
Miscellaneous Stones





Stones in Pregnancy
Symptomatic stones during pregnancy occur at a
rate of 1 in 250 pregnant women.
The majority of symptomatic stones occur in the
second and third trimester of pregnancy.
symptoms of flank pain or hematuria.
The diagnosis can be difficult; up to 28% of women
are misdiagnosed.
Miscellaneous Stones




Important physiologic changes in the kidney occur
during pregnancy that modulate urinary stone risk
factors:.
Renal blood flow increases, leading to a 30% to 50%
rise in glomerular filtration rate, which subsequently
increases the filtered loads of calcium, sodium, and uric
acid.
Hypercalciuria is enhanced by placental production of
1,25(OH)2D3, which increases intestinal calcium
absorption and secondarily suppresses PTH.
Hyperuricosuria has also been reported as a result of
increased filtered load of uric acid
CLINICAL PRESENTATION





Acute Stone Episode
A urinary calculus usually presents with an acute
episode of renal or ureteral colic as the result of a
stone obstructing the urinary tract.
There are five locations where stones can be
impacted in the urinary tract.
First, stones may become impacted in a calyx of the
upper urinary tract.
The second area in which a calculus may become
impacted is the ureteropelvic junction.
CLINICAL PRESENTATION



The third area of impaction is at or near the pelvic
brim, where the ureter begins to arch over the iliac
vessels posteriorly into the true pelvis.
The fourth area, especially in females, is the
posterior pelvis, where the ureter is crossed
anteriorly by the pelvic blood vessels and by the
broad ligament.
Finally, the most constricted area through which the
urinary calculus must pass is the ureterovesical
junction, which is the most common site of impaction
CLINICAL PRESENTATION


left: Ureteropelvic stone.
Severe costovertebral angle
pain from capsular and
pelvic distention; acuterenal
and urethral pain from
hyperperistalsis of smooth
muscl of calyces, pelvis, and
ureter, with pain radiating
along the course of the
ureter (and into the testicle,
since the nerve supply to the
kidney and testis is the
same.)
The
testis
is
hypersensitive.
right: Midureteral stone.
Same as abovebut with more
pain in the lower abdominal
quadrant.
CLINICAL PRESENTATION

Low ureteral stone:
Same as above, with
pain radiating into
bladder, vulva, or
scrotum. The scrotal
wall is hyperesthetic.
Testicular sensitivity is
absent. When the
stone approaches the
bladder, urgency and
frequency with
burning on urination
develop as a result of
inflammation of the
bladder wallaround
the ureteral orifice.
CLINICAL PRESENTATION







Renal colic :
Often at night or in morning, starts in flank and
radiates to groin.
If stone lower down often get lower abd pain .
irritative voiding sy if at UVJ.
Often nausea since autonomic N in celiac ganglion
supply stomach and kidney for autonomic nerves
Most pain from partially obstructing moving stones.
Takes 4-6 hrs for initial pain episode to subside.
CLINICAL PRESENTATION

o
o
o
o
Physical Signs:.
Individuals with urinary lithiasis can rarely find
comfort in any position.
Fever is not present unless urinary infection occurs .
Heart rate and blood pressure may be elevated
because of pain.
Examination of the abdomen reveals moderate,
deep tenderness on palpation over the location of
the calculus and the area of the loin.
URINALYSIS




Uncomplicated stone,may reveals RBC with few WBC or
Bacteria .
Infected urine has RBC ,WBC and bacteria ,white cells cast are
diagnostic of pyelonephritis .
Normal does not rule out urological pathology .
Crystals help to know the compostion of calculi.
Scanning electron micrographs of various
urinary crystals. A, Apatite; B, struvite; C,
calcium oxalate dihydrate; D, calcium oxalate
monohydrate; E, cystine; F, ammonium acid
urate; G, brushite.
Radiographic Examination
Plain Abdominal Films:
plain Kidney-Ureter-Bladder radiographs.
o Ca phos - apatite - most radiopaque.
o Nephrocalcinosis : stars on a dark night - in
medulary spounge kidney.
o Staghorn : struvite, cystine, uric acid.
o Radiolucent :pure uric, xanthine, dehydroxyadenine,
matrix, triamteren.

Radiographic Examination




Intravenous pyelography:.
may be obtained to confirm the presence of
radiolucent stones and also to identify any anatomic
abnormalities that may predispose the patient to
stone formation.
Has limitations – radiolucent stones, small stones can
be missed esp at UVJ, filling defect not always a
stone,
risk of dye allergy, x-ray exposure.
Radiographic Examination

o
o
o
Ultrasonography:.
Ultrasound is a noninvasive method of
demonstrating both the urinary stone and the
consequent hydronephrosis.
Color Doppler ultrasound examination may
demonstrate increased resistive index in the
obstructed kidney and asymmetry or absence of
ureteral jets in the urinary bladder.
Edema and small calculi missed on an IVP can be
appreciated with such studies
Radiographic Examination





Computed tomography:.
Spiral CT now investigation of choice in patients
presenting with acute renal colic.
Sens 97-100%, Spec 97-100%
Advantages over IVP – quicker, no contrast, show up
radiolucent calc, low rad dose, potential for other Dx,
don’t need to wait for Cr, no dye to interfere with other
imaging studies, able to measure stone more accurately
Uric acid stones are visualized no differently from
calcium oxalate stones. Matrix calculi have adequate
amounts of calcium to be visualized easily by CT.
Radiographic Examination


Magnetic resonance imaging (MRI) specifically used
to visualize the urinary tract has been termed
magnetic resonance (MR) urography and has been
reported to be effective in detecting urinary tract
dilation .
MRI is a poor study to document urinary stone
disease.
Diagnostic and Treatment Decision Process



After a urolith is diagnosed, the first assessment is
of the degree of seriousness of the disease process
20% to 40% of patients with stone attacks may
need hospital admission.
Most patients with RC pain relief from intramuscular
injection of 50 to 100 mg of meperidine or 10 to
15 mg of morphine.
Admit if:
1. Pain not controlled with Po meds.
2. Calculus Anuria , usualy solitary kidney or bilat
stones.
3. Infection , esp. when there is obstruction.
4. Emesis.
 Most calculi smaller than 4 to 5 mm pass
spontaneously.
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Analysis of Urinary Stones
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Most medical therapy for stone disease is now
based on analysis of calculi, and decisions
about proper procedures for treatment require
knowledge of stone composition
Medical evaluation
History
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Diet and fluid intake
Medications
Infection
Activity level
Systemic disease
Genetics
Anatomy
Previous surgery
Medical evaluation
Evaluation of the Patient with the First Stone
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All patients should have excretory urography,
urinalysis, urine culture, complete blood count, and
SMA-20.
All stones should be analyzed. If the stone cannot
be recovered, a urine cystine screen should be
performed.
The presence of multiple stones or nephrocalcinosis
on IVU indicates the need for a more detailed
metabolic work-up and aggressive medical therapy
Medical evaluation
Evaluation of the Patient with Multiple or Recurrent Stones
Medical evaluation
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Medical therapy for stone disease serves two
purposes: treatment of the acute episode and
prevention of stone recurrences or new stone
formations
Who Needs Medical Therapy?
Between 25% and 75% of all patients who present
with an initial stone develop a recurrent stone over
prolonged follow-up, lasting from 10 to 20 years .
Medical evaluation
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Patients who have had only their first stone episode
do not undergo a formal metabolic evaluation but
rather have a urinalysis, a urine culture, and a
blood chemical profile, including calcium, uric acid,
electrolytes, and creatinine concentration
MEDICAL MANAGEMENT
CONSERVATIVE MEDICAL MANAGEMENT
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Fluid Recommendations:
Patients should be strongly encouraged to consume
enough fluids to produce 2 liters of urine per day.
Water hardness is unlikely to play a significant role in
recurrence risk.
Carbonated water may confer some protective benefit.
Soda flavored with phosphoric acid may increase stone
risk, whereas soda with citric acid may decrease risk.
Citrus juices (particularly lemon juice) may be a useful
adjunct to stone prevention.
MEDICAL MANAGEMENT
CONSERVATIVE MEDICAL MANAGEMENT
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DIETARY RECOMMENDATIONS
Randomized studies have confirmed the advantage of a diet with
moderate animal protein (meat) intake.
In combination with animal protein restriction and moderate
calcium ingestion, a reduced sodium diet will decrease stone
episodes by approximately 50%.
OBESITY
is an independent risk factor for nephrolithiasis, particularly for
women.
Obese patients have a higher propensity for uric acid calculi.
High-protein, low-carbohydrate diets may increase the risk of
stone formation.
MEDICAL MANAGEMENT
CONSERVATIVE MEDICAL MANAGEMENT
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ROLE OF DIETARY CALCIUM:.
Dietary calcium avoidance actually increases stone recurrence risk.
Calcium supplementation is likely to be safest when it is taken with
meals.
Calcium citrate appears to be a more stone-friendly calcium
supplement because of the additional inhibitor action of citrate.
OXALATE AVOIDANCE:.
Avoidance of excess dietary oxalate loading is reasonable
and intuitive.
Vitamin C in large doses may increase the risk of stone
recurrence. Doses should probably be limited to 2 g/day.
Urinary stone disease
Thank you