Transcript Uric Acid Stones

KIDNEY STONES
nephrolithiasis (kidney calculi or stones) is welldocumented common occurrences in the
general population
The etiology of this disorder is multifactorial and
is strongly related to dietary lifestyle habits or
practices.
Urinary calculi or stones are the most common
cause of acute ureteral obstruction.
The term nephrolithiasis (kidney calculi or
stones) refers to the entire clinical picture of the
formation and passage of crystal agglomerates
called calculi or stones in the urinary tract
Activity means:
Formation of new stones
Enlargement of old stones
Passage of gravel
Despite attempted dietary modification
over a 3 to 6 month period.
Nephrocalcinosis: calcification of renal
papilla that if break loose cause colic
Sludge: sufficient uric acid or cystine in
the urine may plug both ureters with
precipitate
Staghorn calculi: struvite, cystine, and
uric acid
Epidemiology
3:1 M:F (~7% men/ 3% women) Women typically excrete
more citrate and less calcium than men
Ethnic Background Stones are rare in Native
Americans, Africans, American Blacks, and Israelis
3rd-5th decade most common (70%)
predispositicve diseases: (RTA type 1, Hyperparathyroidism, cysteinuria, milk-alkali syndrome,
sarcoidosis, Crohn's disease)
Family History produce excess amounts of a
mucoprotein in the kidney or bladder allowing crystallites
to be deposited and trapped forming calculi or stones
Climate (mountainous, desert, or tropical)
Time of year (warmest three months)
Lifestyle (sedentary)
Medications: protease inhibitors, carbonic anhydrase
inhibitors
10% of all people will have a kidney stone in
their lifetime
1 in 1,000 adults are hospitalized annually in
the United States for renal calculi
50% of those who develop a renal stone will
have a recurrence within the next 5-7 years
Urinary calculi found in 1% of all autopsies
Types of Renal Calculi
Calcium Stones
Calcium Oxalate (60%)
Calcium Phosphate (10%)
Calcium Oxalate and Calcium Phosphate (10%)
Struvite Stones (10-15%)
Uric Acid Stones (5-10%)
Cystine Stones (1-2%)
Any factor that reduces urinary flow or causes
obstruction, which results in urinary stasis or
reduces urine volume through dehydration and
inadequate fluid intake, increases the risk of
developing kidney stones.
Low urinary flow is the most common
abnormality, and most important factor to correct
with kidney stones. It is important for health
practitioners to concentrate on interventions for
correcting low urinary volume in an effort to
prevent recurrent stone disease
Pathophysiology
Formation requires four key elements
1.Supersaturation of urine with solutes
2.Relative lack of the inhibitors citrate &
pyrophosphate
3.Nucleation
4.Stasis or lack of urine flow
Clinical Presentation
Symptoms may vary and depend on the location and
size of the kidney stones or calculi within the urinary
collecting system. In general, symptoms may include
acute renal or ureteral colic, hematuria (microscopic or
gross blood in the urine), urinary tract infection, or vague
abdominal or flank pain. A thorough history and physical
examination, along with selected laboratory and
radiologic studies, are essential to making the correct
diagnosis. Small nonobstructing stones or "silent stones"
located in the calyces of the kidney are sometimes found
incidentally on x-rays or may be present with
asymptomatic hematuria. Such stones often pass
without causing pain or discomfort
Area of impaction
UPJ
where ureter passes over pelvic brim and
iliac vessels
UVJ: smallest diameter of the urinary tract
In FM the posterior pelvis: ureter is
crossed anteriorly by the pelvic blood
vessels and broad ligament
Consequences of urinary tract
obstruction
Reduced glomerular filtration rate
Reduced renal blood flow (after initial rise)
Impaired renal concentrating ability
Impaired distal tubular function
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Nephrogenic diabetes insipidus
Renal salt wasting
Renal tubular acidosis
Impaired potassium concentration
Postobstructive diuresis
Phase A
Phase B
Intraluminal
pressure
RBF
GFR
... due to
... due to
... due to
obstruction
h Peristalsis
Vasodilation
-Prostacyclin
-Prostraglandin
E2
h Intratubular
pressure
... due to
... due to
... due to
Disorganised
peristalsis dilation
of tubules and
ureter
Vasoconstriction -Continuing
obstruction
-Angiotensin II
-Thromboxane A2 -vasoconstrictio
Acute urinary tract obstruction
Functional consequences
Ureteric and tubular pressure
Renal blood flow (RBF)
GFR
0
6
Hours
12
baseline
18
Calcium Stones
Hereditary Hypercalciuria condition
Main risk factor for calcium stone development
in the United States
Mean value of calcium in urine in excess of:
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300 mg/day (7.5 mmol/day) for males
250 mg/day (6.25 mmol/day) for females
30-40% patients with calcium stones have
hypercalciuria
Struvite Stones
Triple phosphate or infection stones
Occur twice as often in women than in men
Form only with presence of bacteria that have
urea-splitting enzyme urease
Proteus mirablis, Kelbsiella, Serratia, Mycoplasma,
Psuedomonas, Urealyticum
Alkaline urine promotes struvite calculi formation
Urea-splitting organisms break down urea
 Carbon dioxide and ammonia are produced
 Urine pH increases
 Carbonate levels rise
Uric Acid Stones
Uric Acid: end product of purine metabolism
 Derived from exogenous sources
 Produced endogenously during cell turnover
Contributing disease states to uric-acid stones:
 Inflammatory bowel disease,
lymphoproliferative and myeloproliferative
disorders due to increased cellular breakdown
which causes purines to be released and so
increases uric acid load
Cystine Stones
Autosomal recessive trait
 Inborn dysfunction in reabsorption of dibasic amino
acids like cystine, ornithine, lysine, arginine (sometimes
seen as COLA) from renal tubules
1 in 15,000 people in U.S are affected
Normal cystine excretion: < 20 mg/day
> 7.0 urine pH promotes cystine solubility
Medical Nutrition Therapy: increase fluid intake >4 L/day,
decrease sodium, may restrict protein since methionine is
precoursor to cystine
Standard Medical Practice: with medications, keep pH
alkaline 24 hrs/day
Preventive therapy
It is limited to recurrent stone formers, which
includes patients in whom helical CT on
initial symptoms presentation shows
evidence of more than one stone.
MONITORING
24 hour urine collection: 4 to 8 weeks after
recommendation, if negative every year.
Ultrasonography at one year if negative
every 2 to 4 years thereafter.
Calcium Oxalate Stones
MANAGEMENT
Lifestyle Change
Dietary modification
High fluid intake
Reduced protein intake
Limiting sodium intake
Calcium intake
Foods and drinks containing oxalate
beets
chocolate
coffee
cola
nuts
rhubarb
spinach
strawberries
tea
wheat bran
Drug therapy indicated if the stone
disease remains active
Activity means:
Formation of new stones
Enlargement of old stones
Passage of gravel
Despite attempted dietary modification
over a 3 to 6 month
period.
MEDICATION
Thiazide duretics for hypercalciuria
Allopurinol or potassium citrate for hyperuricosuria
potassium citrate for hypocitraturia
potassium citrate for type 1 renal tubular acidosis