urolithiasis, pathophsiology and its causes studis …

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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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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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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]


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]


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]


253


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).


254


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.


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*



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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


257


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


258


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.


259


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


260


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.


261


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-


262


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.


263


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.


264


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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