CLASSIFICATION OF CALCULI (Turk C et al.

, 2011)

Accurate classification of calculi is necessary since it will impact medical care formal
judgement and result. Urinary calculi can be classified according to the following features:
calculus location, calculus size, X-ray characteristics of calculus, calculus composition
(mineralogy), aetiology of calculus formation, and risk group for repeatedly calculus
formation.

Classification according to X-ray characteristics of calculus

1. Radiopaque:
Calcium phosphates
CaOx monohydrate
CaOx dehydrate
2. Poor radiopaque:
Cystine
Apatite
3. Radiolucent:
Xanthine
Ammonium urate
Uric acid
Drug-calculi
2,8-dihydroxyadenine

Classification according to calculus composition

1. Chemical composition
CaOx monohydrate
Ammonium urate
Uric acid dehydrate
Magnesium ammonium phosphate
Calcium hydrogenphosphate
Apatite
Xanthine
Cystine
CaOx dehydrate
Drug calculi
2,8-dihydroxyadenine
Unknown composition
2. Mineral
Uricite
Wheddelite
Struvite
Whewellite
Brushite

Classification according to aetiology of calculus formation

1. Noninfection calculi
Uric acid
Calcium phosphates
Calcium oxalates
2. Infection calculi
Ammonium urate
Apatite
3. Genetic calculi
2,8-dihydroxyadenine
Cystine
Xanthine
4. Drug calculi
Indinavir

STONES OF URINARY SYSTEM

Human urine is super saturated through molecules & ions; which can
crystallize into
crystalluria for development of stone. Once a stone has formed in a kidney it
may travel
down in other parts of the urinary system (ureter, bladder). If they are small,
they are excreted
through the urine. The composition of the stone depends on the etiology but
calcium stone is
the most usual kind of calculi. Urinary calculi can vary in dimensions from
grain of sand to a
grape fruit, or even larger. They can be jagged or smooth and are usually
brown or yellow in
colour. Urolithiasis is a disease in which crystals in the urine to form stones,
called uroliths or
calculi. These can be found anywhere in the urinary tract, where they cause
irritation and
secondary infection, especially at the end of bladder or urethra. Renal calculi
are mostly
composed of 35% pure CaOx (COD or COM or both), 1% is CaOx with uric
acid and 40%
are calcium oxalate with hydroxyapatite or carbonate apatite. 1% of all
stones are brushite
(CaHPO42H2O) and 4% are hydroxyapatite or apatite [Ca10 (PO4)6 (OH)2].
The non-calcium-containing crystal types are struvite, 10% of all stones,
although carbonate
apatite is always intermixed in the struvite stone. 1% of all stones are made
up of cystine &
8% is made up of uric acid. (Harrison L, 2004) Rarely, stones composed of
xanthine or acid
ammonium urate or proteinaceous matrixes of potentially insoluble drugs
(especially
ephedrine) are observed.

Ureteral Stones:

A ureteral stone is a kidney stone that has travelled down to the ureter.
Ureteral stones mainly
present with acute urinary colic. Calculi of ureters less than five mm in width
will remove by
the excretory system. In 1788, Desault designed an instrument with a
guarded blade, which
he used to incise the ureter to remove a stone. Before the development of
the cystoscope,
many attempts were made to remove calculi blindly.

Bladder Stones:

Stones are formed as single or complex calculi in bladder which are upto 5
mm in width.
(Tuffery AA, 1966) Foods containing high levels of protein and minerals like
cacium,
magnesium and phosphorus and bacterial infections of the bladder have
been related to
bladder stone formation. Before the Industrial revolution, the bladder was the
most common
site for stones in the urinary system. Techniques of both cystolithotomy and
lithotripsy were practiced even in antiquity. Other lithotomists in ancient
Egypt removed bladder stones by dilating the urethra and sucking out the
stones.

Kidney Stones:

Though stones in the kidney were rare before industrial revolution, the
existence of kidney
stone was famous even to Hippocrates who indicated the sign and symptoms
under the
heading, The first disease of the kidney. It is clear that he advocated an
incision into the
flank for perinephric abscess and that he recommended the lumbar or flank
approach for the
removal of kidney stones. A renal calculus is solid dump formed from crystals
that
distinguish from urine within urinary system. Following are various renal
stones form in
urinary tract.
A) Struvite stone:

The stones are usually developed by calcium, magnesium ammonium phosphates, uric acid or
cystine. (Pak CYC, 1998) It is called as infection calculi or urease calculi. (Maxwell MM and
Stoller L, 2005AMPH (Struvite) {(NH4)MgPO46H2O} is a biomineral. It produces crystals in
urine. There is evidence that bacterial urease (splits urea and release ammonia) commonly from
species of proteus which is necessary for chemically urinary variations which resulting into
struvite stone forming. Further the ammonia is hydrolysed into NH4+ ions and elevates urine pH
& forms alkaline or neutral urine. An increased pH of urine lowers the magnesium ammonium
phosphate solubility & supports struvite crystals precipitation. Elevated intake of magnesium
based food & phosphate from proteins & decreases H2O intake increases phosphate &
magnesium ions in super saturated urine, which results into the conditions of struvite
formation.(Chauhan CK et al., 2008) The stone appearance varies from large solitary stones to
smaller stones. They can undertake the shape of the urethra or bladder. The struvite stones
dissolution depends on urine acidification through urinary acidifiers or diet. Special diets for
dissolution also have decreased phosphorus, magnesium and protein, as well as elevated salt to
raise water onsumption and dilute the urine. Contraindications to this diet include liver failure,
heart failure, kidney failure, hypoalbuminemia, hypertension and pancreatitis.

B) Uric acid stones:

Uric acid precipitation may form at a normal urate excretion if urinary pH &
urinary volume
are low. Uric acid stones are shaped like a sphere with smooth yellowish
orange surface. The
interior of the calculi seem as orange concentric rings when sectioned.
They can be dispersed in liquid by diet with decreased purines that
alkalinizes and also
dilutes the urine. Allopurinol is used with varied purine metabolism to
prevent the uric acid
formation.
C) Calcium phosphate stone:
 Stones have pure CaP which are relatively unusual & develop mostly in patients, who form
constantly alkaline urine. CaP stone is related with dRTA (Backman U, 1980; Hesse A et al.,
1997), primary hyperparathyroidism & during treatment with carboxyanhydrase inhibitors
such as acetazolamide. Hypercalciuria may lead to formation of calcium stone. Often times the
calcium level in blood is normal even though there is increased urinary calcium. Renal leak
hypercalciuria forms when there is impaired calcium reabsorption in the kidney, leading to
hypercalciuria in a fasting state with no calcium intake. Resorptive hypercalciuria is seen in
hyperparathyroidism, is characterized by elevated breakdown of bone and rise in calcium
level in serum. Calcium calculi may form in patients who excrete much uric acid
(hyperuricosuria). Uric acid crystals develop, when urine is less than pH 5.5, then calcium
crystals initiate layering around this type of crystal.

D) Calcium oxalate stone:

CaOx stones are made up of pure CaOx or of combinations of CaOx and CaP. CaOx stone
formation is seemingly more complex than the non-calcium calculi. (Tiselius H et al., 2008)
CaOx stones are of two types

(1) COM:

They are often solid, dark brown in color & dismal gray externally. Under part cut off,
calculi seem to develop in radiating fashion with round wedges at extreme point externally.

(2) COD:

Pure COD calculi are commonly comparatively little, spherical & sharp composed of a
yellow bunch of thrombocytes. The thrombocytes are arranged in different directions

E) Infection Calculi:

Infection stones are developed in presence of urea-splitting micro-organisms produced

infection. Microorganisms present in calculi are Enterobacter, Staphylococcus, Haemophilus,
Providencia, Pseudomonas, Ureaplasma urealyticum (Mycoplasma), Klebsiella,
Corynebacterium, Micrococci and Bacteroides. Infection of urease-producing
microorganisms results in elevated concentrations of NH4+ & CO3-2 ions in urine and forms
an alkaline pH. The most effective treatment must include complete stones removal and
proper antimicrobial therapy. In patients who are not for surgical therapy, randomized
controlled trials have displayed that chronic antibacterial therapy like acetohydroxamic acid
(urease inhibitors) are effective.

F) 2, 8-Dihydroxyadenine calculi:

Dihydroxyadenine is adenine derivative which deposits in 2,8-dihydroxy-adenine urolithiasis.

Patients are homozygous for the uncommon autosomal recessive adenine phosphoribosyl
transferase deficiency; remove high extents of 2,8-dihydroxyadenine. It has low solubility at
normal pH in urine. Treatment with allopurinol produces a total cessation of stone formation.
Two novel mutations are found in APRT gene in patients with 2,8-dihydroxy adenine renal
calculi

G) Urate stones:

Urate (C5H4N4O3) stones, usually sodium urate monohydrate (NaC5H4N4O3H2O) or

ammonium urate (NH4C5H4N4O3), develop in an acidic to neutral urine. They are usually
yellow-brown, small and smooth stones. Urate stones form by an elevated urinary uric acid
excretion. Dogs with liver disease have increased urinary uric acid excretion due to decreased
tranfer of ammonia to urea & uric acid to allantoin. Urate calculi can be dissolved using a diet
with decreased purines that dilutes and alkalinizes the urine. Allopurinol is used in dogs with
altered metabolism of purine to prevent the uric acid formation. Feeding a purines rich diet
while simultaneously administration of allopurinol can result in the xanthine (C5H4N4O2)
stones formation.

H) Cystine stones:

Cystine ((SCH2CHNH2COOH)2) stones are rare. They are formed by a hereditary condition
called cystinuria, which makes the kidneys cause unusually high levels of chemicals. They
are usually round and smooth. Cystinuria is unusual autosomal recessive disease described by
decreased reabsorption of renal tubules of the dibasic aminoacids lysine, cystine, arginine and
ornithine. (Shekarriz B and Stoller ML, 2002) Over cystine excretion leads to formation of stone
because its urinary solubility is much less than pH of urine. Starting therapy is to raise volume of
urine to increase cystine solubility and dietary decrement of protein. Urine alkalinization has few
roles because pH of urine must be > 7.5 to considerably increase the cystine solubility, and
the high pH is problematic to keep up. Medications like 2-MPG and D-penicillamine contain
thiol, which forms a soluble complex with urinary cystine.

I) Miscellaneous stones:

In miscellaneous stones include the drugs crixivan, sulfamethoxazole,

triamterene,
guaifenesin, ciprofloxacin, 5-fluorocytosine and phenytoin, aminophylline,
oxypurinol,
xanthine, silicates and gypsum following antacid therapy.

1) Crixivan stones:
One of the most common protease inhibitors used for the treatment of
AIDS is indinavir sulfate or crixivan. Urinary stones have been related
with the use of crixivan.
2) Xanthine stones:
The medical management of xanthine stone is limited because its
solubility is necessarially
invariable within the range of physiologic pH. So, currently advice
includes intake of fluid of at least 3 liters/day. (Ano CE et al., 2009)

3) Silicate stones:

Silicate (SiO2) stones develop in acidic to neutral urine. Their

appearance is usually
jackstone. There is possibly an elevated incidence related with dogs on
diets that have a large amount of soybean hulls or corn gluten.
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