NEPHROLITHIASIS
Half a million Americans suffer from stone episodes every
year. Environmental and metabolic risk factors exist, for example, the incidence
of stone disease in the USA is highest in the southeastern USA, which is
referred to as the stone belt. In most patients stone disease is preventable.
Surgical removal of stones should be followed by a long term management to
identify the predisposing factors and to design a prophylaxis plan.
How do stones form?
Stones are most likely to form when one or more factors
which promote the precipitation of calcium salts are
present .
These include
1. an increase in excretion of calcium oxalate or presence
of uric acid crystals
2. low urine volume.
What are the inhibitors of stone formation?
Urine contains potent inhibitors of stone growth and
aggregation for calcium oxalate and calcium phosphate. These substances include Urine
glycoprotein, citrate, and pyrophosphates. Nephrocalcin is a glycoprotein inhibitor of calcium oxalate
crystal growth that is present in normal urine.
What are the symptoms of kidney stones?
Patients may have no symptoms although they have kidney
stones for many years. Microscopic Hematuria or blood in the urine may be
present. Some times the stones cause obstruction to the urine flow which if left
untreated can cuase damage to the kidney and renal failure.
The most dramatic symptom of kidney stones is severe
colicky pain described as renal colic. it usually starts suddenly and can be
very severe. It originates in the flank areas and tends to radiate towards the
groin area. It indicates that the body is trying to get rid of the stone as it
has moved and is probably in the ureter causing the pain.
What are the various types of Stone Types?
Most stones are calcareous (contain calcium.). Stones may
be formed of calcium oxalate, calcium phosphate, cysteine, uric acid or struvite.
Calcium stones are more common in men and the condition is strongly familial
.
What are Stag horn stones?
Stag horn stones are very rapidly growing stones. They may
affect both kidneys in which case renal failure can occur. Kidneys can be
damaged as a result of the presence of stag horn stones. The stones may be
formed of uric acid, Cysteine or Struvite. Cysteine is an amino acid which if excreted in excess as
a result of hereditary disorder of its metabloism, can cause kidney stones at an
early age. Infection is another important cause of rapid growth of kidney
stones. the stones are usually described as struvite stones
How often can one forms stones?
Patients may form stones every 2 or three years.
Can you detect stones on an X ray of the abdomen?
Calcium and cysteine based stones can be viewed on a plain
film. Uric acid stones are radiolucent
What are CYSTINE STONES
Some patients with kidney stones have a condition called cystinuria and form
stones made of the amino acid cystine. The cystine is an amino acid which is
normally abosrbed by the kidney. When there is defective absorption, large
amounts of this amino acids are excreted in the urine and may crystallize and
form large stones. The condition is rather uncommon affecting 1 per 10000 persons.
The crystals of cystine can be seen on microscopic
examination of the urine and appear as Flat hexagonal plates
If cystinuria is suspected, the
cyanide nitroprusside test is a simple and effective means of screening. Stone formation occurs in homozygous individuals. Positive
nitroprusside test is seen in both heterozygotes who will not form stones and
homozygous who do.
The only effective therapies include induction of polyuria
and urinary alkalinization.(pH greater than 7.5)_.
What are STRUVITE
stones ?
These are Magnesium- ammonium phosphate stones. They are
seen commonly in patients with recurrent urinary tract infection. They can grow
rapidly and may lead to formation to
stag horn stones. The Crystal appear as coffin lid crystals under the
microscope. They are more common in women
Can some Drugs cause renal stones?
Yes the prolonged use of some drugs may rarely result in
stone formation. For instance Allopurinol which is often used in the treatment
of gout may cause formation of xanthine
stones. Other medications associated with stone formation include Oxypurinol,, Triamterene
and Crixivan.
What is HYPERCALCIURIA?
This is a relatively common condition which predisposes to stone formation.
The urine in these patients contains higher concentration of calcium. The cause
is not clear , but the condition is often familial and is called hypercalciuria.
I have calcium stones in the kidney, do I need to decrease my calcium
intake?
Decreasing calcium intake may lead to excess of oxalate
absorption as well as bone disease, thus this is usually not recommended.
How can one prevent recurrence of kidney stones?
Low sodium intake and a diuretic may be the treatment of
choice in patients with active stone disease. 90% reduction in risk of new stone
formation was obtained by this modality of therapy versus 60% in a placebo
treated group.
Thiazides and/or potassium citrate is the treatment if
hypercalciuria persist on this regimen.
Amiloride can be added.
Amiloride favorable effect is related to its correction of hypokalemia
which can induce intracellular acidosis which can decrease citrate excretion and
it also increase calcium reabsorption in the distal tubule. Citrate normally
form a non dissociable but soluble compounds with calcium.
Potassium citrate and not sodium citrate should be used
since sodium will cause intravascular expansion and increase calcium excretion.
Potassium citrate will have two indirect effects. most of the exogenous citrate
is converted to bicarbonate thus correcting any degree of acidosis that may be
contributing to stone formation and secondly the correction of hypokalemia.
Avoidance of high protein diet is important to prevent
recurrence.
nephrolithiasis. This results in high content of
undissociated uric acid. Once a uric acid stone is formed, it could induce
formation of calcium oxalate stones by epitaxy, heterogeneous nucleation.
Evaluation of patients with kidney stones
Limited Evaluation
Full workup is probably not indicated in patients with a
single calcium stone. If there is evidence of active bone disease full work up
is recommended. This is best done as outpatient, when patient is on his regular
diet. Plasma Calcium concentration should be measured on 2 or 3 occasion as well
as a 24 hours urine collections for calcium. Since calcium excretion parallels
that of sodium, a low sodium intake may mask hypercalciuria. Urinary sodium
should always be determined.
Three 24 hours urine collections made and analyzed for uric
acid, calcium, oxalate, and citrate content (citrates are more difficult to
measure, may be only determined in patients who is negative for both
hyperoxaluria and hyperuricosuria).
Oxalates are usually measured if there is suspicion of
hyperoxaluria secondary to intestinal causes or of primary type. Corresponding
serum values obtained.
Any stones passed should be analyzed.
All patients should avoid dehydration
No metabolic disturbance may be found in 10 to 15% of
patients
Extensive evaluation
Two 24 hour urine samples
These samples should be collected on the regular diet
One urine sample should be obtained after one week
adherence on a diet restricted in calcium (400 mg/day), sodium (100 mEq/day) and
oxalate.
Samples are analyzed for
Calcium (Hypercalciuria is defined as calcium excretion
greater than 300 mg per day in men and 250 mg per day in women)
Oxalate (greater than 40 mg per day of oxalate in the urine
should prompt a search for enteric hyperoxaluria which can be treated with oral
calcium supplements)
Phosphate
Uric acid
citrate
pH
total volume
Magnesium
Fasting venous blood sample obtained for PTH
Fasting urinary calcium
used to detect renal calcium leak and calciuric response to
oral calcium load
How to prevent recurrent kidney stones?
General measures
Goal is to prevent recurrence.
Fluid intake sufficient to assure a minimum urine output of
2L/day
Dietary sodium restriction (100 mEq/d)
A high sodium intake increases urinary calcium, lowers
citrate and promotes sodium urate induced calcium oxalate crystallization and
blunts the hypocalciuric response to thiazide
Oxalate restriction in all patients with oxalate stones,
also useful in patients with intestinal hyperabsorption of oxalate and in
patients taking sodium cellulose phosphate
Dietary calcium restriction recommended in patients with
intestinal hypercalciuria
Restriction of proteins useful in presence of
hyperuricosuria or hypocitraturia
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