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www.wjpps.com Vol 8, Issue 7, 2019.
236
Husain. World Journal of Pharmacy and Pharmaceutical Sciences
UROLITHIASIS, PATHOPHSIOLOGY AND ITS CAUSES STUDIS IN
TWO HOSPITALS 2017-2018
Adnan Zair Husain*
Khanaqin General Hospital.
ABSTRACT
The process of forming stones in the kidney, bladder, and/or urethra
(urinary tract) is called as Urolithiasis. Stones form twice as often in
men as women. The hallmark of stones that obstruct the ureter or renal
pelvis is excruciating, intermittent pain that radiates from the flank to
the groin or to the genital area and inner thigh. The stone type is named
after its mineral composition. The most common stones are struvite
(magnesium ammonium phosphate), calcium oxalate, urate, cysteine
and silica. The most common type of kidney stones worldwide contains calcium. Preventative
measures depend on the type of stones.
KEYWORDS: Urethra, Struvite, Calcium Oxalate, Urate, Silicate, Cystine.
INTRODUCTION
enal calculi mean kidney stone and having a stone in any location of urinary tract is referred
to as urolithisis. It is consider one of the oldest diseases which occur in the urinary tract and it
rarely happens in children, it takes various in shapes and sizes and may be very small or as
large as the orange size, it is the most painful urologic disorder.[1,2]
An estimated 1.3 million
Americans seek medical help for kidney stone each year .At the same time, studies suggest
kidney stone affects over (5%) of Americans and that the prevalence has increased over the
past three decades.[1-3]
It may be recurrent and can be easily diagnosed through X-ray.
Formation of renal calculi may occur in kidneys, the ureters or the bladder leading to the
damage of the kidneys and block the flow of urine, impair kidneys function in getting rid of
body waste products and finally cause renal failure. Many literatures and studies mentioned
that there is no exact cause of urinary calculi but there are a number of genetic body reaction
to certain metabolic and chemical conditions and life style risks that contribute to renal
WORLD JOURNAL OF PHARMACY AND PHARMACEUTICAL SCIENCES
SJIF Impact Factor 7.421
Volume 8, Issue 7, 236-267 Research Article ISSN 2278 – 4357
*Corresponding Author
Adnan Zair Husain
Khanaqin General Hospital.
Article Received on
05 May 2019,
Revised on 26 May 2019, Accepted on 19 June 2019
DOI: 10.20959/wjpps20197-14169
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Husain. World Journal of Pharmacy and Pharmaceutical Sciences
calculi formation.1, 4- 6 Understanding such factors can help those at risk for developing
urinary calculi in preventing this condition.
Risk factors are factors that do not seem to be direct causes of the disease, but they may be
associated in some way.
Having a risk factor for urinary calculi makes the chance of getting a condition higher but
does not always lead to urinary calculi.
However, the reason why it occurs in some people and not in others facing the same factors is
unknown.[7-9]
Nurses have an important role in teaching people about how to avoid the risk factors of
urinary calculi and how to prevent them, therefore, the researcher intended to find out the
most common risk factors which may cause urinary calculi and to find out if there is a
significant relation between those factors and other variables.
Supersaturation of urine
When the urine becomes supersaturated (when the urine solvent contains more solutes than it
can hold in solution) with one or more calculogenic (crystal-forming) substances, a seed
crystal may form through the process of nucleation. Heterogeneous nucleation (where there is
a solid surface present on which a crystal can grow) proceeds more rapidly than
homogeneous nucleation (where a crystal must grow in liquid medium with no such surface),
because it requires less energy. Adhering to cells on the surface of a renal papilla, a seed
crystal can grow and aggregate into an organized mass. Depending on the chemical
composition of the crystal, the stone-forming process may precede more rapidly when the
urine pH is unusually high or low.[21]
Supersaturation of the urine with respect to a calculogenic compound is pH-dependent. For
example, at a pH of 7.0, the solubility of uric acid in urine is 158 mg/100 ml. reducing the pH
to 5.0 decreases the solubility of uric acid to less than 8 mg/100 ml. The formation of uric
acid stones requires a combination of hyperuricosuria (high urine uric acid levels) and low
urine pH; hyperuricosuria alone is not associated with uric acid stone formation if the urine
pH is alkaline. Supersaturation of the urine is a necessary, but not a sufficient, condition for
the development of any urinary calculus. Supersaturation is likely the underlying cause of
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uric acid and cystine stones, but calcium-based stones (especially calcium oxalate stones)
may have a more complex etiology.[32]
Inhibitors of stone formation
Normal urine contains chelating agents such as citrate that inhibit the nucleation, growth and
aggregation of calcium-containing crystals. Other endogenous inhibitors include calgranulin
(an S-100 calcium binding protein), Tamm-Horsfall protein, glycosaminoglycans, uropontin
(a form of osteopontin), nephrocalcin (an acidic glycoprotein), prothrombin F1 peptide, and
bikunin (uronic acid-rich protein). The biochemical mechanisms of action of these substances
have not yet been thoroughly elucidated. However, when these substances fall below their
normal proportions, stones can form from an aggregation of crystals. Kidney stones often
result from a combination of factors, rather than a single, well-defined cause. Stones are more
common in people whose diet is very high in animal protein or who do not consume enough
water or calcium. They can result from an underlying metabolic condition, such as distal
renal tubular acidosis, Dent's disease, hyperparathyroidism, primary hyperoxaluruia or
medullary sponge kidney. In fact, studies show about 3% to 20% of people who form kidney
stones have medullary sponge kidney. Kidney stones are also more common in people with
Crohn's disease. People with recurrent kidney stones are often screened for these disorders.
This is typically done with a 24-hour urine collection that is chemically analyzed for
deficiencies and excesses that promote stone formation.[33]
II. Human Urinary System and Kidney Function
The two kidneys, parts of the urinary tract system, regulate the mineral composition, water
content and acidity of the body (National Kidney and Urologic Diseases Information
Clearinghouse (2009) The kidneys and how they work. Retrieved 2009 from http://
kidney.niddk.nih.gov/kudiseases/pubs/pdf/yourkidneys.pdf) Fig. 1. Shows the human urinary
system they are also involved in the excretion of metabolic waste products and chemicals, are
responsible for the production of certain hormones and vitamins, and also have a key role in
blood pressure regulation. Removal of wastes occurs in tiny units inside the kidney known as
nephrons; inside each nephron is a glomerulus which acts as a sieve-like filtering unit
keeping proteins and cells in the bloodstream while allowing wastes to pass through. These
wastes and any extra water become urine, which passes through tubes called the ureters into
the bladder where it is stored until released during urination. Damage to the working units of
the kidneys results in a reduction in the filtering capacity of one or both kidneys (National
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Kidney and Urologic Diseases Information Clearinghouse (2009) The kidneys and how they
work. Retrieved 2009 from http://
kidney.niddk.nih.gov/kudiseases/pubs/pdf/yourkidneys.pdf)(Kidney Health Australia (2009)
Chronic kidney disease (CKD) management in general practice. Melbourne, Vic: Kidney
Health Australia)A critical function of the urinary system is the maintenance of normal
composition and volume of body fluid, this is accomplished by glomerular filtration, tubular
reabsorption, and tubular secretion of soluble and filterable plasma components, By such
means, urine contains water, electrolytes, minerals, and hydrogen ions, end products of
protein metabolism such as urea, uric acid, and creatinine. (Sasha Stumpers et al., 2013).
IV. Pathogenesis of Renal Stone Formation
The physical process of stone formation is a complex cascade of events, result from the
growth of crystals leads to stones formation (Kok 2002). The process of stone formation is
depend on volume of urine, comprise concentrations of calcium, phosphate, oxalate and
sodium ions (Mandel 1989). High ion levels, low urinary volume, low pH, and low citrate
levels privilege the formation of urinary calculi. The pathogenesis of urinary calculi
formation is the end result of the fundamental multi-step physicochemical processes
Fig.2.The genetic, metabolic, environmental and dietetic factors are involved in the
pathogenesis of urolithiasis, all of them privilege the crystallization of salts, formed in inside
renal tubules. Crystalluria is often observed in normal individual, but if crystals remain apart
from each other. They are washed away by urine flow; however, some chemical and
electrical forces trigger the process of aggregation. The crystals aggregate and attaches to
epithelium, which allows them to growing and forming the stones (Khaskhali et al., 2009).
Fig. 2: Pathogenesis of renal stone formation.
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The kidney stone formation in the three broad conceptual categories requires
Excessive concentration of solutes in excess of their solubility in the urine.
Imbalance of modifiers (promoters and inhibitors) and crystallization in the urine.
Epithelial abnormalities that allow attachment and subsequent growth of these crystals in
to stone.
Above the factors act in concert and eventuating in the formation of the kidney stones
(Moe et al., 2010).
Moreover, calcium oxalate (Caox) crystals, the main constituent of human urinary calculi
may adhere in the plasma membrane of epithelial cells by a specific manner and followed by
endocytosis of the crystals resulting to cell damage or death. Damaged cells exhibit a
proliferation response and increase the fibrogentic synthesis, it substance promoting
additional stimulus for crystal growth (Mirian et al., 2010). Calcium stone formation involves
different phase of increasing accumulation of Caox and cap-nucleation, crystal growth,
crystal aggregation and crystal retention (Lingenman 1986).The physico-chemical analysis
describes stone formation as a supersaturated solution in which homogenous or
heterogeneous nucleation can lead to initiation of crystal formation, which can then aggregate
and growth (Bhuskute et al., 2009).
Crystal growth: After the nucleation process, the micro crystals can mature by epitaxially
mediated crystal growth. Epitaxy is oriented overgrowth of one crystalline material on to a
substrate crystalline lattice. Monoepitaxial growth refers to the adsorption of the molecules or
ions one by one on the crystal surface from supersaturated urine and heteroepitaxial growth
refers to direct growth of one crystal on a surface of different composition and the surfaces of
crystal and substrate (Nirlep Chhiber et al., 2014). Several atoms or molecules in a super-
saturated liquid start forming clusters. The total free energy of the cluster is increased by the
surface energy; however, this is significant only when the cluster is small. Crystal growth is
determined by the molecular size and shape of the molecule, the physical properties of the
material, pH, and defects that may form in the crystal‟s structure. Crystal growth is one of the
prerequisites for particle formation. (Qiu et al., 2004.
Dietary role in lithiasis: Modern lifestyle, dietary habits and obesity emerge to be the
promoters of idiopathic stone disease. Modern diets containing a lot of animal protein,
refined carbohydrates and salts act on the metabolism like an acid concentration. To
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overcome this disadvantage, a sufficient supply of potassium and alkali is required. It is
important to know that calcium should not be restricted. Usually the body does not absorb
more calcium, certain conditions, can be absorbed leading to excessive passage in the kidneys
(Borghi et al., 2002).Recent studies report that actual protein consumption in children in
Europe and North America are 3-5 times higher than recommended (Prentice et al., 2006).
The decreased urinary pH may potentiate uric acid lithiasis, it enhance citrate reabsorption in
the proximal tubules, thus decreasing the excretion of this important inhibitor of
crystallization (Trinchieri et al., 2006).A nutritionally poor diet that is low in animal protein
and calcium, which is the main factor that leads to the development of bladder stones in
children in undeveloped countries. This leads to the formation of urine with a relatively high
content of ammonium and urate ions and consequently to the formation of ammonium acid
urate stones (Rizvi et al., 2002). Recent studies have suggested an increased prevalence of
urolithiasis and recurrence associated with obesity with elevated urinary excretion of calcium,
sodium, uric acid and oxalate (Lee, 2008).
Vitamins
Despite a widely held belief in the medical community that ingestion of vitamin C
supplements is associated with an increased incidence of kidney stones28; the evidence for a
causal relationship between vitamin C supplements and kidney stones is inconclusive. While
excess dietary intake of vitamin C might increase the risk of calcium oxalate stone formation,
in practice this is rarely encountered. The link between vitamin D intake and kidney stones is
also tenuous. Excessive vitamin D supplementation may increase the risk of stone formation
by increasing the intestinal absorption of calcium, but there is no evidence that correction of
vitamin D deficiency increases the risk of stone formation.[19]
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Medical management of kidney stones There are a number of practices for treatment of
urinary calculi, including surgery, and endoscopic procedures such as ureterscopy
percutaneous nephlithotomy and extracorporeal shock wave lithotripsy. Medical management
of urolithiasis is still a challenge for modern medical practice (Mohanty et al., 2010, Nabi et
al., 2007, Seitz et al., 2009). Doctors can usually diagnose kidney stones by asking about
symptoms and examining patient. Further tests may be done to confirm the diagnosis and to
reveal the size, location and type of stone (Cox and Coupland, 2010).
``Blood tests These are done to identify excess amounts of certain chemicals related to the
formation of stones and to check the presence of infection by blood cell counts.
Urine analysis It helps to look for signs of infection and estimation of values of various
contributing factors viz. oxalates, calcium, cystine, citrates, magnesium, phosphates, etc.
Taking an X-ray image Stones that contain calcium are usually seen as white spots on X-ray
images (Miller et al., 2007).
An intravenous urogram (IVU) This involves an injection of a special dye that shows up
the whole urinary system on X-ray images, revealing stones that can't usually be seen.
Traditional intravenous pyelography is no longer the primary method of investigation in
patients with renal colic (Shokeir, 2002).
Abdominal Ultrasonography
Abdominal ultrasonography has limited use in the diagnosis and management of urolithiasis.
Although ultrasonography is readily available, quickly performed and sensitive to renal
calculi, it is virtually blind to ureteral stones (sensitivity: 19 percent), which are far more
likely to be symptomatic than renal calculi (Yilmaz et al., 1998).
Plain Film Radiography Less radiopaque calculi, such as pure uric acid stones and stones
composed mainly of cystine or magnesium ammonium phosphate, may be difficult, if not
impossible, to detect on plain-film radiographs. Although 90 percent of urinary calculi have
historically been considered to be radiopaque, the sensitivity and specificity of KUB
radiography alone remain poor (sensitivity: 45 to 59 percent; specificity: 71 to 77 percent)
(Levine et al., 1997).
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Non-contrast helical computerized tomography It produces pictures from a series of X-ray
images taken at different angles - it is sometimes used to diagnose kidney stones and is
thought to be the most accurate diagnostic test. It has become the first-line investigation in a
number of centers (Masarani et al., 2007). This imaging modality is fast and accurate and it
readily identifies all stone types in all locations. Its sensitivity (95 to 100 percent) and
specificity (94 to 96 percent) suggest that it may definitively exclude stones in patients with
abdominal pain (Chen et al., 1999; Vieweg et al., 1998; Dalrymple et al., 1998; Boulay et al.,
1999).
Shock wave lithotripsy Shock wave lithotripsy is an external source to the patient that
propagates through the body before being focused on kidney stone waves that cause stone
fragmentation directly by producing mechanical stresses or indirectly by the collapse of
cavitation bubbles. This is the most common treatment for urolithiasis, which can have
slightly side effects (Evan et al., 2005).
Extracorporeal Shockwave Lithotripsy (ESWL) ESWL is a non-invasive procedure which
uses shock waves to fragment calculi. This proficiency is the most widely used method for
dealing renal and ureteral stones. However, intervention success rates depend on stone
composition, size, properties and location of the stone as well as the orchestration type and
frequency of shock (Knoll, 2007, Tombolini et al., 2010, Coe, 2005). Some oral medicinal
drug have positive effects, they are not effective in all patients, but citrate is one of the
majority widely used medical therapies for preventing urinary stone disease (Serhat and
Kupeli, 2006, Mattle and Hess, 2005). The medical treatment of urolithiasis is aimed at
assisting the patient from further growth of existing stones and development of new stones,
thus decreasing morbidity and the need for surgical intervention hence, under these
circumstances medical treatment Stone incidence depends on geographical, climatic, ethnic,
dietary and genetic factors. The recurrence risk is basically determined by the disease or
disorder causing the stone formation. Accordingly, the prevalence rates for urinary stones
vary from 1% to 20%.[4]
In countries with a high standard of life such as Sweden, Canada or
the US, renal stone prevalence is noteably high (> 10%). For some areas an increase of more
than 37% over the last 20 years is reported.[5]
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Table. Prevalence and incidence of urolithiasis from two European countries.
Spain 2007 (%) Germany 2000 (%)
5.06 4.7 Prevalence
NA 4.0 Females
NA 5.5 Males
0.73 1.47 Incidence
NA 0.63 Females
NA 0.84 Males
Stones can be classified into those caused by: infection, or non-infectious causes (infection
and non-infection stones); genetic defects[8]
; or adverse drug effects (drug stones) (Table
KK).
Table KK: Stones classified by aetiology
Non-infection stones
• Calcium oxalate
• Calcium phosphate,
• Uric acid
Infection stones
• Magnesium ammonium phosphate
• Carbonate apatite
• Ammonium urate
Genetic causes
• Cystine
• Xanthine
• 2,8-dihydroxyadenine
Drug stones
Stone composition
Stone composition is the basis for further diagnostic and management decisions. Stones are
often formed from a mixture of substances. Table BB lists the clinically most relevant
substances and their mineral components.
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Table. BB: Stone composition.
Risk groups for stone formation: The risk status of stone formers is of particular interest
because it defines the probability of recurrence or regrowth, and is imperative for
pharmacological treatment. About 50% of recurrent stone formers have just one lifetime
recurrence.[6,9]
Highly recurrent disease is observed in slightly more than 10% of patients.
Stone type and disease severity determine low or high-risk of recurrence.
High-risk stone formers
General factors
Early onset of urolithiasis (especially children and teenagers).
Chemical formula Mineral name Chemical name
CaC2O4.H2O Whewellite Calcium oxalate monohydrate
CaC2O4.2H2O Wheddelite Calcium oxalate dihydrate
Ca10(PO4)6.(OH)2 Apatite Basic calcium phosphate
Ca5(PO3)3(OH ) Carbonite apatite Calcium hydroxyl phosphate
Ca3(PO4)2 Whitlockite b-tricalcium phosphate
Ca5(PO4)3OH Dahllite Carbonate apatite phosphate
PO4.2H2O Brushite Calcium hydrogen phosphate
CaCO3 Aragonite Calcium carbonate
Ca8H2(PO4)6.5H2O Octacalcium phosphate
C5H4N4O3 Uricite Uric acid
C5H4O3-2H20 Uricite Uric acid dihydrate
NH4C5H3N4O3 Ammonium urate
NaC5H3N4O3.H2O Sodium acid urate monohydrate
MgNH4PO4.6H2O Struvite Magnesium ammonium phosphate
MgHPO4.3H2O Newberyite Magnesium acid phosphate trihydrate
MgNH4(PO4).1H2O Dittmarite Magnesium ammonium phosphate monohydrate
[SCH2CH(NH2)COOH]2 Cystine
CaSO4.2H2O
Zn3(PO4)2.4H2O
Calcium sulphate dihydrate
Zinc phosphate tetrahydrate
Gypsum
Xanthine
2,8-Dihydroxyadenine
Proteins
Cholesterol
Calcite
Potassium urate
Trimagnesium phosphate
Melamine
Matrix
• Active compounds
crystallising in urine
• Substances impairing urine
composition (Section 4.11)
Drug stones
Foreign body calculi
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Familial stone formation.
Brushite-containing stones (CaHPO4.2H2O).
Uric acid and urate-containing stones.
Infection stones.
Solitary kidney (the kidney itself does not particularly increase the risk of stone formation,
but prevention of stone recurrence is of more importance).
Diseases associated with stone formation
Hyperparathyroidism.
Metabolic syndrome.[17]
Nephrocalcinosis.
Gastrointestinal diseases (i.e., jejuno-ileal bypass, intestinal resection, Crohn’s disease,
malabsorptive.
conditions, enteric hyperoxaluria after urinary diversion) and bariatric surgery.[16]
Sarcoidosis.
Genetically determined stone formation
Cystinuria (type A, B and AB)
Primary hyperoxaluria (PH)
Renal tubular acidosis (RTA) type I
2,8-Dihydroxyadeninuria
Xanthinuria
Lesch-Nyhan syndrome
Cystic fibrosis
Drugs associated with stone formation
Anatomical abnormalities associated with stone formation
Medullary sponge kidney (tubular ectasia)
Ureteropelvic junction (UPJ) obstruction
Calyceal diverticulum, calyceal cyst
Ureteral stricture
Vesico-uretero-renal reflux
Horseshoe kidney
Ureterocel-
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Classification of stones
Urinary stones can be classified according to size, location, X-ray characteristics, aetiology of
formation, composition, and risk of recurrence.[6,18-20]
A- Stone size
Stone size is usually given in one or two dimensions, and stratified into those measuring up to
5, 5-10, 10-20, and > 20 mm in largest diameter.
B- Stone location
Stones can be classified according to anatomical position: upper, middle or lower calyx; renal
pelvis; upper, middle or distal ureter; and urinary bladder. Treatment of bladder stones is not
discussed here.
C- X-ray characteristics
Stones can be classified according to plain X-ray appearance [kidney-ureter-bladder (KUB)
radiography] (Table), which varies according to mineral composition.[20]
Non-contrast-
enhanced computed tomography (NCCT) can be used to classify stones according to density,
inner structure and composition, which can affect treatment decisions.
Table. QQ: X-ray characteristics.
Radiolucent Poor radiopacity Radiopaque
phosphate Uric acid Magnesium ammonium Calcium oxalate dihydrate
Ammonium urate Apatite Calcium oxalate monohydrate
Xanthine
2,8-Dihydroxyadenine
Drug-stones (Section 4.11)
Cystine Calcium phosphates
Diagnostic evaluation
1 Diagnostic imaging
The clinical situation will inform on the most appropriate imaging modality, which will differ
for suspected ureteral stone or suspected renal stone.
Standard evaluation includes a detailed medical history and physical examination. Patients
with ureteral stones usually present with loin pain, vomiting, and sometimes fever, but may
also be asymptomatic.[21]
Ultrasound (US) should be used as the primary diagnostic imaging tool, although pain relief,
or any other emergency measures should not be delayed by imaging assessments. US is safe
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(no risk of radiation), reproducible and inexpensive. It can identify stones located in the
calices, pelvis, and pyeloureteric and vesicoureteric junctions, as well as in patients with
upper urinary tract dilatation. US has a sensitivity of 45% and specificity of 94% for ureteric
stones and a sensitivity of 45% and specificity of 88% for renal stones.[22]
The sensitivity and specificity of KUB radiography is 44-77% and 80-87%, respectively.[23]
KUB radiography should not be performed if NCCT is considered[24]
, however, it is helpful
in differentiating between radiolucent and radiopaque stones and for comparison during
follow-up.
Recommendation LE GR
With fever or solitary kidney, and when diagnosis is doubtful, immediate imaging is
indicated. 4 A*
*Upgraded following panel consensus
Evaluation of patients with acute flank pain: NCCT has become the standard for diagnosing
acute flank pain, and has replaced intravenous urography (IVU). NCCT can determine stone
diameter and density. When stones are absent, the cause of abdominal pain should be
identified. In evaluating patients with suspected acute urolithiasis, NCCT seems to be
significantly more accurate than IVP.[25]
GR LE Recommendation
A 1a Following initial US assessment, NCCT should be used to confirm stone
diagnosis in patients with acute flank pain, because it is superior to IVU.
IVU = intravenous urography; NCCT = non-contrast enhanced computed tomograpy.
NCCT can detect uric acid and xanthine stones, which are radiolucent on plain films, but not
indinavir stones.[26]
NCCT can determine stone density, inner structure of the stone and skin-
to-stone distance; all of which affect extracorporeal shock wave lithotripsy (SWL)
outcome.[20, 27-29]
The advantage of non-contrast imaging must be balanced against loss of
information on renal function and urinary collecting system anatomy, as well as higher
radiation dose Radiation risk can be reduced by low-dose CT.[30]
In patients with body mass
index (BMI) < 30, low-dose CT has been shown to have a sensitivity of 86% for detecting
ureteric stones < 3 mm and 100% for calculi > 3 mm.[31]
A meta-analysis of prospective
studies[32]
has shown that low-dose CT diagnosed urolithiasis with a pooled sensitivity of
96.6% (95% CI: 95.0-97.8) and specificity of 94.9% (95% CI: 92.0-97.0).
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Table. YY: Radiation exposure of imaging modalities.[33-36]
Method Radiation exposure (mSv)
KUB radiography 0.5-1
IVU 1.3-3.5
Regular-dose NC T 4.5-5
Low-dose NCCT 0.97-1.9
Enhanced CT 25-35
Recommendation LE GR
If NCCT is indicated in patients with
BMI < 30, use a low-dose technique.
1b A
NCCT = non-contrast enhanced computed tomograpy.
Radiological evaluation of patients for whom further treatment of renal stones is planned.
Recommendations LE GR
A contrast study is recommended if stone removal is planned and the
anatomy of the renal collecting system needs to be assessed.
3 A*
Enhanced CT is preferable in complex cases because it enables 3D
reconstruction of the collecting system, as well as measurement of stone
density and skin-to-stone distance. IVU may also be used.
4 C
*Upgraded based on panel consensus.
CT – computed tomograpy; IVU = intravenous urography.
Diagnostics - metabolism-related: Each emergency patient with urolithiasis needs a succinct
biochemical work-up of urine and blood besides imaging. At that point, no distinction is
made between high- and low-risk patients for stone formation.
Recommendations: basic laboratory analysis - emergency urolithiasis patients[11,12,37,38]
Urine GR
Dipstick test of spot urine sample A*
• red cells
• white cells
• nitrite A
• approximate urine pH
Urine microscopy and/or culture
Blood
Serum blood sample A*
• creatinine
• uric acid
• (ionised) calcium
• sodium
• potassium
• Blood cell count A*
• CRP
If intervention is likely or planned: Coagulation test (PTT and INR). A*
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*Upgraded based on panel consensus.
CPR = C-reactive protein; INR = international normalised ratio; PTT = partial
thromboplastin time.
Basic laboratory analysis - non-emergency urolithiasis patients
Biochemical work-up is similar for all stone patients. However, if no intervention is planned,
examination of sodium, potassium, CRP, and blood coagulation time can be omitted.
Only patients at high-risk for stone recurrence should undergo a more specific analytical
programme.[11]
Stone-specific metabolic evaluation is described in Chapter 4.
The easiest means to achieve correct diagnosis is by analysis of a passed stone using a valid
method as listed below (2). Once mineral composition is known, the potential metabolic
disorders can be identified.
Analysis of stone composition
Stone analysis should be performed in all first-time stone formers.
In clinical practice, repeat stone analysis is needed in the case of:
• Recurrence under pharmacological prevention;
• Early recurrence after interventional therapy with complete stone clearance;
• Late recurrence after a prolonged stone-free period.[39]
Patients should be instructed to filter their urine to retrieve a concrement for analysis. Stone
passage and restoration of normal renal function should be confirmed.
The preferred analytical procedures are infrared spectroscopy (IRS) or X-ray diffraction
(XRD).[40-42]
Equivalent results can be obtained by polarisation microscopy, but only in
centres with expertise. Chemical analysis (wet chemistry) is generally deemed to be
obsolete.[40]
Recommendations LE GR
Always perform stone analysis in first-time formers using a valid
procedure (XRD or IRS).
2 A
Repeat stone analysis in patients: 2 B
• Presenting with reccurent stones despite drug therapy;
• With early recurrence after complete stone clearance;
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• With late recurrence after a long stone-free period because stone composition may change
IRS = infrared spectroscopy; XRD = X-ray diffraction.
Diagnosis in special groups and conditions
1--Diagnostic imaging during pregnancy
In pregnant women diagnostic imaging (exposure to ionising radiation) might be associated
with teratogenic risks and development of (childhood) malignancies. The risk for the child
crucially depends on gestational age and amount of radiation delivered. X-ray imaging during
the first trimester should be reserved for diagnostic and therapeutic situations in which
alternative imaging methods have failed.[43,44]
Ultrasound (when necessary using change in renal resistive index and
transvaginal/transabdominal US with a full bladder) has become the primary radiological
diagnostic tool when evaluating pregnant patients suspected of renal colic.[45]
Statement LE
Normal physiological changes in pregnancy can mimic ureteral obstruction,
therefore, US may not help to differentiate dilatation properly and has a limited
role in acute obstruction.
3
Magnetic resonance imaging (MRI) can be used, as a second-line procedure, to define the
level of urinary tract obstruction, and to visualise stones as a filling defect.[46,47]
Low dose CT protocols, or low dose CT scans reduce the radiation exposure and are currently
recommended to be used judicially in pregnant women as a last-line option.[48,49]
Recommendations LE GR
In pregnant women, ultrasound is the imaging method of choice. 1a A*
In pregnant women, MRI should be used as a second-line imaging modality. 3 C
In pregnant women, low-dose CT should be considered as a last-line option.
The exposure should be less than 0.05 Gy.
3 C
*Upgraded following panel consensus.
CT = computed tomograpy; MRI = magnetic resonance imaging.
Paediatric patients with urinary stones have a high risk of recurrence, therefore, standard
diagnostic procedures for high-risk patients apply ().
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Statement LE
In paediatric patients, the most common non-metabolic disorders
are vesicoureteral reflux, ureteropelvic junction obstruction,
neurogenic bladder, and other voiding difficulties.[50]
4
Recommendations GR
In all paediatric patients, efforts should be made to complete a
metabolic evaluation based on stone analysis.
A
All efforts should be made to collect stone material that should
then be analysed to classify the stone type.
A*
*Upgraded following panel consensus.
2-Diagnostic imaging
When selecting diagnostic procedures to identify urolithiasis in paediatric patients, it should
be remembered that these patients might be uncooperative, require anaesthesia, or be
sensitive to ionising radiation.[51-53]
Again, the principle of ALARA (As Low As Reasonably
Achievable) should be observed.
3-Ultrasound: Ultrasound (US) is the primary imaging technique[51]
in paediatrics. Its
advantages are absence of radiation and no need for anaesthesia. Colour Doppler US shows
differences in the ureteric jet[54]
and resistive index of the arciform arteries of both kidneys,
which are indicative of the grade of obstruction.[55]
Nevertheless, US fails to identify stones in > 40% of paediatric patients[56-59]
(LE: 4), and
provides no information on renal function.
Statement LE
US is the first choice for imaging in children and should
include the kidney, filled bladder, and adjoining portions of
the ureter.[54-57, 60]
2a
3.3.3.2.3 Plain films (KUB radiography)
KUB radiography can help to identify stones and their radiopacity, and facilitate follow-up.
4--Intravenous urography (IVU)
The radiation dose for IVU is comparable to that for voiding cystourethrography (0.33
mSV).[61]
However, the need for contrast medium injection is a major drawback.
5- Helical computed tomography (CT)
Recent low-dose CT protocols have been shown to significantly reduce radiation exposure.[36]
The principle of ALARA (as low as reasonably achievable) should always be observed. In
adults it has a sensitivity of 94-100% and specificity of 92-100%.[62]
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In children, only 5% of stones escape detection by NCCT.[54,62,63]
Sedation or anaesthesia is
rarely needed with modern high-speed CT apparatus.
6-Magnetic resonance urography (MRU)
Magnetic resonance urography cannot be used to detect urinary stones. However, it might
provide detailed anatomical information about the urinary collecting system, the location of
an obstruction or stenosis in the ureter, and renal parenchymal morphology.[64]
Recommendations GR
In children, US is the first-line imaging modality when a stone is suspected. B
If US does not provide the required information, KUB radiography (or
NCCT) should be performed.
B
US = ultrasound; KUB = kidney, ureter, bladder; NCCT = non-contrast enhanced computed
tomography.
Disease management: Management of patients with renal or ureteral stones Treatment
decisions for upper urinary tract calculi are based on several general aspects such as stone
composition, stone size, and symptoms.
1 Renal colic Pain relief
Pain relief is the first therapeutic step in patients with an acute stone episode.[65,66]
Non-steroidal anti-inflammatory drugs (NSAIDs) are effective in patients with acute stone
colic[67,68]
, and have better analgesic efficacy than opioids. Patients receiving NSAIDs are
less likely to require further analgesia in the short-term.
Opioids, particularly pethidine, are associated with a high rate of vomiting compared to
NSAIDs, and carry a greater likelihood of further analgesia being needed[69,70]
(see below). If
an opioid is used, it is recommended that it is not pethidine. Prevention of recurrent renal
colic Facilitation of passage of ureteral stones is discussed in Section 3.4.3.1.2.
For patients with ureteral stones that are expected to pass spontaneously, NSAID tablets or
suppositories (e.g., diclofenac sodium, 100-150 mg/day, 3-10 days) may help reduce
inflammation and the risk of recurrent pain.[70-72]
Although diclofenac can affect renal
function in patients with already reduced function, it has no functional effect in patients with
normal kidney function[73]
(LE: 1b).
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In a double-blind, placebo-controlled trial, recurrent pain episodes of stone colic were
significantly fewer in patients treated with NSAIDs (as compared to no NSAIDs) during the
first 7 days of treatment *72+. Daily α-blockers reduce recurrent colic (LE: 1a) (Section
3.4.3.1.2).
If analgesia cannot be achieved medically, drainage, using stenting or percutaneous
nephrostomy, or stone removal, should be performed.
Statement and recommendations for analgesia during renal colic
Statement LE
For symptomatic ureteral stones, urgent stone removal as first-
line treatment is a feasible option.
1b
Recommendations GR
In acute stone episodes, pain relief should be initiated
immediately.
A
Whenever possible, an NSAID should be the first drug of
choice. e.g. diclofenac*, indomethacin or ibuprofen**.
A
Second choice: hydromorphine, pentazocine or tramadol. C
Use α-blockers to reduce recurrent colics. A
*Affects glomerular filtration rate (GFR) in patients with reduced renal function (LE: 2a).
**Recommended to counteract recurrent pain after ureteral colic.
Management of sepsis in obstructed kidney
The obstructed kidney with all signs of urinary tract infection (UTI) is a urological
emergency. Urgent decompression is often necessary to prevent further complications in
infected hydronephrosis secondary to stone-induced, unilateral or bilateral renal obstruction.
Decompression
Currently, there are two options for urgent decompression of obstructed collecting systems:
placement of an indwelling ureteral stent; percutaneous placement of a nephrostomy tube.
There is little evidence to support the superiority of percutaneous nephrostomy over
retrograde stenting for primary treatment of infected hydronephrosis. There is no good-
quality evidence to suggest that ureteric stenting has more complications than percutaneous
nephrostomy.[74,75]
Only one RCT[76]
assessed decompression of acute infected
hydronephrosis. The complications of percutaneous nephrostomy insertion have been
reported consistently, but those of ureteric stent insertion are less well described.[74]
Definitive stone removal should be delayed until the infection is cleared following a complete
course of antimicrobial therapy.
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Statement LE
For decompression of the renal collecting system, ureteral stents
and percutaneous nephrostomy catheters are equally effective.
1b
Recommendations
For sepsis with obstructing stones, the collecting system should be urgently decompressed,
using percutaneous drainage or ureteral stenting. Definitive treatment of the stone should be
delayed until sepsis is resolved.
Further measures
Following urgent decompression of the obstructed and infected urinary collecting system,
both urine- and blood samples should be sent for culture-antibiogram sensitivity testing, and
antibiotics should be initiated immediately thereafter. The regimen should be re-evaluated in
the light of the culture-antibiogram test. Intensive care might become necessary.
Recommendations GR
Collect urine for antibiogram test following decompression.
A* Start antibiotics immediately thereafter (+ intensive care if necessary).
Re-evaluate antibiotic regimen following antibiogram findings.
*Upgraded based on panel consensus.
3.4.2 Specific stone management in Renal stones
The natural history of small, non-obstructing asymptomatic calculi is not well defined, and
the risk of progression is unclear. There is still no consensus on the follow-up duration, and
timing and type of intervention. Treatment options are observation, chemolysis or active
stone removal.
Types of treatments
1---Conservative treatment (Observation)
Observation of renal stones, especially in calices, depends on their natural history.
Statement LE
It is still debatable whether renal stones should be treated, or
whether annual follow-up is sufficient for asymptomatic caliceal
stones that have remained stable for 6 months.
4
Recommendations GR
If renal stones are not treated, periodic evaluation is recommended
(after 6 months and yearly follow- up of symptoms and stone status
[US, KUB or CT]).
A*
*Upgraded based on panel consensus.
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Pharmacological treatment
1 Percutaneous irrigation chemolysis
Today, percutaneous chemolysis is rarely used. Percutaneous irrigation chemolysis may be an
option for infection- and uric acid stones.[77,78]
For dissolution of struvite stones, Suby’s G
solution (10% hemiacidrin; pH 3.5-4) can be used.[79]
2 -Oral chemolysis
Stones composed of uric acid, but not sodium or ammonium urate, can be dissolved by oral
chemolysis. Prior stone analysis may provide information on stone composition. Urinary pH
measurement and X-ray characteristics may provide information on the type of stone.
Oral chemolitholysis is based on alkalinisation of urine by application of alkaline citrate or
sodium bicarbonate.[78,80]
The pH should be adjusted to 7.0-7,2. Within this range, chemolysis
is more effective at a higher pH, which might lead to calcium phosphate stone formation.
Monitoring of radiolucent stones during therapy is the domain of US, however, repeat NCCT
might be necessary. In the case of uric acid obstruction of the collecting system, oral
chemolysis in combination with urinary drainage is indicated.[81]
A combination of
alkalinisation with tamsulosin seems to achieve the highest SFRs for distal ureteral stones.[81]
Recommendations GR
The dosage of alkalising medication must be modified by the patient
according to urine pH, which is a direct consequence of such medication.
A
Dipstick monitoring of urine pH by the patient is required three times a day
(at regular intervals). Morning urine must be included.
A
Specific diseases[30,31]
Intestinal diseaseFluid loss due to chronic diarrhea modifies pH levels andalters the
absorption of different substances, which can leadto the alteration of urine pH in a sustained
manner, changingurine balance. This causes the formation of an inner nucleusto which stone-
forming ions adhere. Thus, acidic urine con-tributes to the formation of uric acid calculi, and
alkalineurine favors the appearance of calcium stones, while a pHabove 7.5 is associated with
struvite calculi.
3 Diabetes There are several mechanisms by which diabetes melli-tus increases the incidence
of urolithiasis. First, chronichyperglycemia may cause a low-grade inflammation in gas-
trointestinal epithelium by altering the balance betweenintestinal flora and circulatory defense
mechanisms; later,this inflammation leads to an increased absorption ofoxalate, as seen in
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chronic diarrheal illnesses, where diar-rheal fluid losses induced low pH and citrate levels
increaseurinary calcium oxalate and uric acid supersaturations.[32]
Secondly, chronic
hyperglycemia may alter the epithelialfunctions of both gastrointestinal and urinary tracts
forabsorption and excretion of elements, thereby directly facil-itating the formation of
calculus.[32]
Thirdly, immunosuppression secondary to diabetes melli-tus and chronic
glycosuria induce urinary tract infections,which may cause urolithiasis, since some bacteria
canprovoke urinary supersaturation and modify the environ-ment, thus leading to the
formation of crystal deposits whichmay be a factor that promotes urolithiasis; in fact, 10%
ofurinary calculi are struvite stones which are built by magne-sium ammonium phosphate
produced during infection withbacteria that possess the enzyme urease.[32]
Finally, diabetic
nephropathy induced glomerular dys-functions can alter urinary content, which
facilitatesurolithiasis.32Daudon et al., in a study to evaluate whether the risk ofuric acid
calculi increases with type 2 DM, also mention keyfactors for an increased incidence of
urolithiasis in peoplewith diabetes; this is due to insulin resistance, characteristicof the
metabolic syndrome and type 2 DM, which leads t to alower pH urinary through impaired
kidney ammoniagenesisbecause a low urine pH is the main factor of uric acid
stoneformation[37,38]
Gout Patients with hyperuricemia can form uric acid kidney stonesand
calcium oxalate calculi, pure or a mixture of both, dueto urinary acidification.[39]
In cases of
primary gout, 39% of patients have urinarystones, of which 30% are asymptomatic and
diagnosed onlyby ultrasonography.[20]
Pregnancy There are pathophysiological changes that make pregnantwomen more
susceptible to urolithiasis; among them,urinary stasis caused by increased progesterone
andmechanical compression, in addition to increased glomeru-lar filtration rate, the intake of
calcium supplements, andincreased circulating levels of vitamin D leading to highurine pH,
hypercalciuria, and hyperuricosuria; the increasedglomerular filtration rate leads to an
increase in tubular flowfollowed by decreased tubular reabsorption and increasedexcretion of
calcium and/or uric acid. It has also been foundthat placental formation of 1,25-
dihydroxycholecalciferolpromotes intestinal reabsorption of calcium and mobiliza-tion of
bone calcium.40However, it is generally accepted that pregnancy is nota state of increased
stone formation; it has been foundthat pregnant women present hypercitraturia; citrate is
aninhibitor of crystal growth and aggregation, therefore it canbe considered a clinically
significant protective factor dur-ing pregnancy, compensating the effects of hypercalciuriaand
hyperuricosuria.40The incidence of urolithiasis in pregnancy is observedin 1/200---1500
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pregnancies, it is much more common inCaucasians than in African Americans, and about
75% ofpregnant patients with nephrolithiasis have calcium phos-phate stones.[41,42]
Regarding
complications, there is a greater risk of pre-mature birth which may occur in up to 67% of
cases,43anda higher percentage of premature rupture of membranesin pregnant women with
than without nephrolithiasis (7 vs.2.9%; p < 0.05),42in addition to a greater need for
cesareansection.
Obesity A body mass index greater than 30 is associated withan increased risk of kidney
stone formation, since urineoxalate, uric acid, sodium, and phosphate excretion ishigher in
people with a similar index than those with a lowerBMI.20Urolithiasis is more common in
obese people than innormal-weight individuals (11.2 vs. 6.1%, respectively); thatis, obese
people are 1.55 times more likely to suffer from this disease.
PATIENTS AND METHOD: Two hundred patients out of (270) patients were diagnosed
with renal stone after several investigations, such as urine analysis Ultrasonography and X-
ray for kidneys ureters and bladder (K.U.B). Patients were chosen from the baquba teaching
hospital and khanaqin hospital in iraq and in order to know these risk factors were unique for
formation of urinary calculi (200) normal subjects were chosen as a control group after
getting their agreement to participate in this study. A comparative group 200 normal subjects
were selected to match patients with renal stone regarding their age, sex, marital status
educational level and place of residence. The patients were selected according to the
following criteria:
A. Diagnosed with renal stone.
B. Didn’t have any acute disease and had no history of or chronic diseases such as, diabetes
mellitus or heart disease.
C. Their ages 18 years or older.
The study was carried out during the period between 2017 –2018(.taken 2 years) After
reviewing the literatures related to this disease, a questionnaire format was designed includes
the following.
1. General information comprised sociodemogrphic data including, age, sex, marital, status,
educational level, and area of residency.
2. Items related to factors concerning the medical history of patients and control group.
3. Items related to risk factors concerning the diet and drugs in patients group and control
group.
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The questioner was revised by 5 expertises in this field for validity and the result showed
(96%) agreement. Onthe basis of their feedback 3 items were changed and 2 items were
added.
An Interview technique was used as a method for gathering data, the researcher and her
assistants completed the questionnaires and all patients with renal stone from the two
hospitals agreed to participate in this study after getting the permission from the two
hospitals.
In addition, patient's files were checked for urine analysis to find out if the patients had
increases in uric a cid and calcium, their x-ray (K.U.B) were checked too.
Data analysis was done through frequency, percentage, t test and chi square.
RESULTS
To find out the differences between the sample patients and the control group (normal
subjects) a comparison between the two groups was done. Table (1) represented the socio-
demographic characteristics of the sample patients and the control group. (38%) of the
samples age was between 36 and 45 years old and most of the samples were married. Male
patients constituted (68%) of the sample and female (32%), moreover, Regarding the area of
residency, (75%) of the sample lived in the city, while (27%) of them came from rural areas.
Table. 1. The Socio-demographic Characteristics of 100 patients and the normal
subjects.
Normal
subjects
Normal
subjects
Patients
Patients
Characteristic of the
sample
% No % No
20
40
25
15
20
40
25
15
23
3 8
24
15
23
3 8
24
15
25-35
36 – 45
46– 55
56-65
1-Age
100 100 100 100 Total
66
34
66
34
68
32
68
32
Male
Female 2- sex
100 100 100 100 Total
12
88
12
88
8
92
8
92
Single
Married 3- Marital status
100 100 100 100 Total
6
70
6
70
2
68
2
68
Students
Employee 3-Occupation
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18
6
18
6
20
10
20
10
Housewife
Retired
100 100 100 100 Total
30
30
34
6
30
30
34
6
32
28
30
10
32
28
30
10
Read & Write
Primary school
Secondary school
College graduate &
4 -Level of
education
100 100 100 100 Total
60
40
60
40
65
35
65
35
City
Rural area
100 100 100 100 Total
Table 2 illustrated that there was a statistical difference between the mean and the standard
deviations for male and female patient p<0.01.
The highest percentage of the patients and the control group were employee and high
secondary school graduation was achieved in (30%) of the patients enrolled.
Table. 2. The means and standard deviations for both male and female patients and
comparison between them by using t-test.
p D.F. t MS S.D No. Sex
‹ 98 13.43 2.52 5.72 68 male
0.001 2.09 3.84 32 Female
Table (3) declared the risk factors of stone formation related to health history in patients
group and control group.There were significant differences (p‹0.01) between the two groups
regarding all the risk factors except for the parathyroid disorders, however , about half of the
patients were complaining from urinary tract infections.
(48 %) and (44%) of them had family history of stone formation, in addition (26%) of
patients had previously bilharziasis, while only (2%) of control group had the same disorders.
Moreover,(26%) of those patients had gout, and( 22%)were complaining from other diseases
leading them to confined in bed for along time as showed in table 3.
There were no significant differences between the two groups related to the risks factors
which were displayed.
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Table. 3. Risk factors related to health history in patients group and control group.
Relati
on
Chi-square
(X2) Control group Patients Patients
% No % No. % No. % No. Risk factors
Factors related to others
disease such
0.34* 12.84 98 98 2 2 74 74 26 26 1-Gout
N.S 3.77 98 98 2 2 90 90 10 10 2-Parathyroid disorders (over
active)
0.39* 14.86 78 78 22 22 52 52 48 48 3-Urinary tract infection
0.40* 15.8 82 82 18 18 56 56 44 44 4-Family history in stone
formation
0.89* 79.78 100 100 0 0 82 82 18 18 5-Previous catherization
0.32* 10.04 86 86 14 14 67 67 33 33 6-Dehydrations and sweating
0.44* 18.91 98 98 2 2 78 78 22 22 7-Long time bed rest
0.34* 11.48 98 98 2 2 74 74 26 26 8-Bilhaziasis
Intable (4) except for the risk factors of taking green vegetables and taking antacids (p<0.01).
The highest percentages of patients (58%) were taking a large a mount of green vegetables in
their diet, while (39%) of control group also did. However the percentage of patients who ate
meat is very low (9%), and (10%) for the control group.
The current study revealed that more than half of patients enrolled in this study ate a large
amount of potatoes (55%) and (75%) were taking tomatoes, while patients taking antacids
were (%30) and (%13) of control group also did. Moreover, 35% of the patients receiving
Aspirin tablets.
Table. 4. Risk factors related to diet and drugs in patients group and control group.
Relation Chi-square
(X2)
Control group Patients Risk factors
No Yes No Yes
NS 0.47 90 180 10 20 91 182 9 18 1-Meats
NS 1.8 74 148 26 52 65 130 35 70 2-Milk
0.27* 7.22 61 122 39 78 42 84 58 116 3-Green Vegetables
NS 0.98 52 104 48 96 45 90 55 110 4-Potatos
NS 0.88 32 64 68 136 26 52 74 148 5-Tomatoes
NS 0.37 68 136 32 64 71 142 29 58 6-Orange juice
NS 2.71 30 60 39 78 72 144 28 56 7-Water
NS 1.8 74 148 28 52 65 130 35 70 8-Aspirin
NS 0.48 88 176 12 24 91 182 9 18 9-Vitamine C.
0.29* 8.56 87 174 13 26 70 140 30 60 Antacids 10-
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DISCUSSION
The current study results indicated that male expose to renal stone formation than female, this
finding is similar to other studies,1,3,4 they found that most of the patients with renal stones
were males. This could be due to anatomical differences in urinary tract between males and
females; in male the urethra is longer than in female which may cause accumulation and
stagnation of urine in the bladder for longer times.
Regarding the area of residency, the majority of sample lived in the city, while (27%) of them
came from rural areas. This could be because the hospitals were in the centre of the city while
the patients who lived in the rural areas may visit the health centres near them.
The present study indicated that about half of patients were complaining from urinary tract
infections, this is in consistent with other studies1,3,8,9 which mentioned that a person prone
to urinary tact infection may be at risk of developing urinary calculi.
Bacteria in the urine may alter the pH level (acid –base balance) and this can trigger the
formation of urinary calculi. In addition urinary tract infection disturbs the flow of fluid in the
body.
The current study showed that (44%) of the patients whose relative have been afflicted with
urinary calculi in comparison with control group is (18%) This finding is in agreement with
other studies, which mentioned that hereditary genetic disorder could increase the risk of
developing renal stone.4,5,10 This could result in the body’s inability to properly absorb
substance ,such as calcium. Consequently a build –up of calcium can lead to the formation of
urinary calculi. In addition, this factor is probably one of the few factors which is not
preventable.4,5,11
Kavanagh12 in his study about renal stone found that most of renal stones were composed of
calcium oxalate (CaOx), which had commonly been attributed to the presence of high urinary
oxalate output. Bilharziasis may cause bladder calcification and formation of urinary calculi.
WHO report and other studies13-16 found that people with this disease are more liable to
urinary calculi than other people because female ova deposits 300 to 400 eggs a day. Those
move across tissues by action of their prolytic enzymes and enter the bladder, causing severs
inflammation, tissue reaction, fibroses and calcification.
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The current study supports the literatures finding that there were significant differences
between the patients group and the control group P < 0.01, (26%) of the patients had
previously bilharziasis, while only (2%) of the control group had the same disease.
The present study indicated that (33%) of patients had dehydration due to decrease fluid
intake and sweating, while (14%) of control group had the same condition, this is supported
by other findings9,10,17 which stated that low fluid intake will decrease urine output, it will
concentrate urine and allow solutes to precipitate and during summer the body lose a lot of
fluid through perspiration and urine output decrease. This will increase the possibility of
developing urinary calculi. Moreover, rise in the urine concentration, typically occurring in
the hot climate, speeds up the process of crystal growth and increases the chance for urinary
calculi formation. Gout is a medical condition that can affect the normal balance and increase
in uric acid secretion and may be a risk of urinary calculi.4-6 In the current study (26%) of
patients had Gout, while only (2%) of the control group had the same disease.
Okada et al., 18 mentioned in their study that Long-term bed-rest induced renal stone
formation. In addition, other various studies found that complete bed rest for long time and
reduction of physical activity may be a risk factor for urinary calculi formation,1,16,17 the
present study is in agreement with those previous studies,(22%) of the sample patients were
complaining from other diseases leading them to confine in bed for a long time, while (2%)
of control group had the same condition.
Dalton19 Khanna et al.,20, Ja Heon et al., 21 reported that many patients developed urinary
calculi after the insertion of a Foley catheter. The presence of a foreign body within the
urinary tract can develop urinary calculi even in the absence of infection, they concluded that
renal stone is more common in patients with urethral catheterization than for those voiding
spontaneously, in the present study (18%) of the sample patients were previously catheterized
,this finding is consistent with the results of the previous studies More than half of the sample
patients were taking a large a mount of green vegetables in their diet and very low (9%) ate
meat , although a diet high in animal protein affects certain minerals in the urine, that may
promote the formation of renal stone.[1,2,9]
Many studies found those who ate the most animal protein had a 33 percent higher risk of
developing urinary calculi.1,2,22 However, most of the people in Iraq prefer to eat vegetables
and beans because they are cheaper than meat.
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Vegetables contain a large a mount of oxalate which may cause renal stone. This result is
supported by other literatures which mentioned that oxalate should be restricted in people
who are at risk of urinary calculi formation.[1,3,6]
The current study revealed that (30%) of the patients were taking antacids, while (13%) of
control group also did. This is in agreement with other studies who mentioned that there is
evidence that certain types of medication may increase the risk of developing urinary
calculi.1, 2, 5,16 Moreover,[35]
percent of the patients were receiving Aspirin tablets this is in
consistent with other literatures1-3,16 who mentioned that this drug may increase the
likelihood of stone formation.
CONCLUSION
Evidence show that many factors may influence urolithiasis,either as a protective or a risk
factor. The main inheren t human biological factors, with a poor probability for
change,include: testosterone, white or Caucasian race, anatomicalabnormalities, and genetic
diseases.There are also modifiable factors such as diet, exer-cise, stress, and drugs, which
enable timely interventionslike in the lifestyle of a person. In concordance with theliterature,
for the prevention of urolithiasis we suggest:adequate calcium intake, taking more than 3 l of
water aday, and reducing salt and animal protein intake, such as red meat. Also The present
reassessment conveys entropy about the pathophysiology of kidney stone stone, types and
treatments of urolithiasis. Kidney stone disease remains a major public health burden. Its
pathophysiologic mechanisms are complex, majorly because it is polygenic disorder Dietary
agents play a essential part in urinary calculus formation, and dietary alteration can reduce
the risk of stone recurrence. Treatment is successful if attended in early stage itself. Surgical
treatment is more effective. Stone disease is a significant burden on the health care budget in
a country. Patient education, healthy lifestyle practice and prevention with early diagnosis
will aid in improving the health of the nation and reduce spending of the precious health
dollar.
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