This document discusses urinary lithiasis (kidney stones) in children. It covers the causes, types, and treatment of stones. The most common types are calcium oxalate and calcium phosphate stones, caused by hypercalciuria in 30-60% of cases. Other causes include cystinuria, struvite stones related to urinary tract infections, and uric acid stones. Treatment depends on the stone location and composition but may involve removal procedures like lithotripsy or addressing the underlying metabolic condition through diet, medication, or surgery. The goal is to dissolve or pass existing stones and prevent new stone formation.
Urolithiasis is a common disease that is estimated to
produce medical costs of $2.1 billion per year in the United States alone.
Renal colic affects approximately 1.2 million people
each year in USA and accounts for approximately 1% of
all hospital admissions.
Most active emergency departments (EDs) manage
patients with acute renal colic every day.
This PPT covers the Pathophysiology of Kidney stones.It include the factors responsible for formation of stones, types of kidney stones, Symptoms of kidney stones
Kidney stones (also called renal calculi, nephrolithiasis or urolithiasis) are hard deposits made of minerals and salts that form inside your kidneys. Diet, excess body weight, some medical conditions, and certain supplements and medications are among the many causes of kidney stones.
Urolithiasis is a common disease that is estimated to
produce medical costs of $2.1 billion per year in the United States alone.
Renal colic affects approximately 1.2 million people
each year in USA and accounts for approximately 1% of
all hospital admissions.
Most active emergency departments (EDs) manage
patients with acute renal colic every day.
This PPT covers the Pathophysiology of Kidney stones.It include the factors responsible for formation of stones, types of kidney stones, Symptoms of kidney stones
Kidney stones (also called renal calculi, nephrolithiasis or urolithiasis) are hard deposits made of minerals and salts that form inside your kidneys. Diet, excess body weight, some medical conditions, and certain supplements and medications are among the many causes of kidney stones.
Urinary Stone analysis
A kidney stone is a hard mass developed from crystals that separate from the urine and build up on the inner surfaces of the kidney.
Nephrolithiasis, commonly known as kidney stones, refers to the formation of hard mineral and salt deposits within the kidneys or urinary tract. These stones can vary in size, ranging from tiny grains to larger, more substantial formations. Nephrolithiasis is a relatively common condition and can affect people of all ages, although it is more prevalent in adults.
An illustrative presentation on Microscopic examination of Urine for Medical, Dental, Pharmacology and Biotechnology students to facilitate easy- learning and self-study..
definition of malnutrition, the definition of protein-energy malnutrition , the etiology 0f protein-energy malnutrition, the pathophysiology of malnutrition, features of marasmus, features of kwashiorkor, vitamins and micronutrient deficiencies, signs of micronutrients deficiency, diagnosis, management of malnutrition,prognosis of malnutrition ,prevention of malnutrition
Definition of erythema infectiosum, the causative factor, clinical presentation, the three stages of rash, the slipped cheek, the sequences of the rash, the diagnosis of the fifth disease, the differential diagnosis of fifth disease, the treatment of erythema infectiosum, the prognosis of fifth disease , congenital erythema infectiosum, the complications of fifth disease , Human parvovirus B19
What is kingella kingae bacterium,features of K. kingae,Species of Kingella,epidemiology of k. kingae,Proposed pathogenesis of K. kingae infections,Transmission of k. kingae ,Pathegenesis of k. kingae,diagnosis ,NAAT for k.kingae ,treatment of k.kingae,prevension ,osteomyelitis due to k,kingae.endocarditis due to k.kingae,Septic Arthritis due to k. kingae,Spondylodiscitis due to k. kingae, prevention of k. kingae infection
What is congenital nephrotic syndrome ,what is the definition of congenital nephrotic syndrome,what is the inheritance,what are the responsible genes ,what are the types of congenital nephrotic syndrome,what is the presentation ,diagnosis ,and treatment of congenital nephrotic syndrome, primary type and secondary type of congenital nephrotic syndrome
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What is achondroplasia, definition , etiology ,types of dwarfism , genetic background,clinical presentations ,history and clinical examination , differential diagnosis ,diagnostic tests ,radiological findings ,CT scan and MRI , Medical care and role of growth hormone ,Surgical care and consultation,
Definition of neonatal sepsis,type of neonatal sepsis ,early onset neonatal sepsis,late onset neonatal sepsis,Pathophysiology of neonatal sepsis,,sign and symptoms of neonatal sepsis, diagnosis of neonatal sepsis,management of neonatal sepsis, antibiotic used for neonatal sepsis,prevention of neonatal sepsis, prognosis of neonatal sepsis ,and A summary
What is bronchiolitis and its definition, the age group, signs and symptoms and clinical presentation The clinical practice guidelines, how to diagnosis, clinical criteria, what are the severity degrees and How to assess the severity, what are the investigations that may be needed, Is there any diagnostic test, what is the prognosis
What is the management,
What is your knowledge regarding electrical burn in children,types of electrical burns in children.,characteristic features of each type ,minor electrical burn , high -voltage electrical burn ,lightning electrical burn what are the clinical presentations and management ,cardiac complication of electrical burn,neurological complication of electrical burn , cutaneous and oral complication ,masculoskeletal complication and ocular and renal complications
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definition what is FPIES, what it defers from other food allergy, what are the signs and symptoms ,what are the different types of food allergy ,how to diagnose FPIES ,what are the oral food challenge (OFC) ,what is the treatment , the prognosis of FPIES
What is influenza ,ethology ,types ,presentations signs and symptoms ,epidemic influenza ,laboratory investigations , management , the WHO guidelines in dealing with cases and contact
What is Fifth disease, what is erythema infectiosum What is the causative factor, pathophysiology ,clinical presentation ,diagnosis ,laboratory investigations ,treatment , precautions and prognosis ,
حساسية الجلد ماهي فوائد الجلد ماهي الحساسية ماهي انواع حساسية الجلد ماهي العوامل التي تؤدي لحدوث الحساسية ماهي انواع الحساسية ماهي اعراض الحساسية ماهي طرق الوقاية من الحساسية ماهو علاج الحساسية
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Anti ulcer drugs and their Advance pharmacology ||
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June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...
Urinary lithiasis
1. Urinary LithiasisUrinary Lithiasis
in childrenin children
Prof. Dr. Saad S Al Ani
Senior Pediatric Consultant
Head of Pediatric Department
Khorfakkan Hospital
Sharjah ,UAE
saadsalani@aol.com
2. Urinary LithiasisUrinary Lithiasis
• The wide geographic variation in the
incidence of lithiasis in childhood is related to:
– Climatic
– Dietary
– Socioeconomic
factors
• Approximately 7% of urinary calculi occur
in children <16 yr of age.
22
3. Stone formationStone formation
• Approximately 75% of all stones contain
calcium as a major constituent, and 60% are
composed of calcium oxalate
• Most “spontaneous” stones are composed of
calcium, oxalate, or phosphate crystals(COP)
– Others are due to uric acid, cystine,
ammonium crystals, or phosphate crystals, or
a combination of these substances (UCAP)
33
4. Stone formationStone formation (Cont.)(Cont.)
• The risk of stone formation increases in the
presence of increasing concentrations of these
crystals and is reduced with increasing
concentrations of inhibitors.
44
5. Stone formationStone formation (Cont.)(Cont.)
• Renal calculi develop from crystals that
form on the calyx and aggregate to form a
calculus
• Bladder calculi may be stones that formed
in the kidney and traveled down the ureter, or
they can form primarily in the bladder.
55
6. Stone formationStone formation (Cont.)(Cont.)
• Stone formation depends on four factors:
1. Matrix
2. Precipitation-crystallization
3. Epitaxy
4. Absence of inhibitors of stone formation in
the urine
6
7. Stone formationStone formation (Cont.)(Cont.)
1. Matrix
– Is a mixture of protein , non-amino sugars,
glucosamine, water, and organic ash
– Makes up 2-9% of the dry weight of
urinary stones
– Is arranged within the stones in organized
concentric laminations
7
8. Stone formationStone formation (Cont.)(Cont.)
2. Precipitation-crystallization
– Refers to supersaturation of the urine
with specific ions composing the crystal.
– Crystals aggregate by chemical and
electrical forces.
8
9. Stone formationStone formation (Cont.)(Cont.)
Precipitation-crystallization (Cont.)(Cont.)
– Saturation of urine with respect to the ions
increases:
• Rate of nucleation, crystal growth, and
aggregation
• likelihood of stone formation and growth
9
10. Stone formationStone formation (Cont.)(Cont.)
3. Epitaxy
– Refers to the aggregation of crystals of
different composition but similar
lattice structure, thus forming stones of a
heterogeneous nature.
– e.g. calcium oxalate and monosodium
urate have similar structures and calcium
oxalate crystals can aggregate on a nucleus of
monosodium urate crystals.
10
11. Stone formationStone formation (Cont.)(Cont.)
4. Inhibitors of stone formation
Urine contains inhibitors of stone formation,
including:
i. Citrate
ii. Diphosphonate
iii. Magnesium ion
11
12. Clinical ManifestationsClinical Manifestations
• Gross or microscopic hematuria
• Severe abdominal or flank pain (renal
colic)
( If the calculus is in the renal pelvis, calyx , or
ureter and causes obstruction)
– Typically the pain radiates anteriorly to the
scrotum or labia.
– Often the pain is intermittent
12
15. DiagnosisDiagnosis
• Approximately 90% of urinary calculi are
calcified to some degree and
consequently are radiopaque on a plain
abdominal film
– Struvite (magnesium ammonium phosphate)
stones are radiopaque.
– Cystine, xanthine, and uric acid calculi may
be radiolucent
15
16. DiagnosisDiagnosis (Cont.)(Cont.)
• Some children have nephrocalcinosis,
(which is calcification of the renal tissue itself )
• Unenhanced spiral CT scan of the
abdomen and pelvis is the most accurate study
( if a child with suspected renal colic)
– 96% sensitivity and specificity in:
Delineating the number and location of calculi
Demonstrates whether the involved kidney is hydronephrotic
16
17. DiagnosisDiagnosis (Cont.)(Cont.)
• An alternative is to obtain a plain
radiograph of the abdomen and pelvis
plus a renal ultrasonogram.
• Any material that resembles a calculus
should be sent for analysis by a
laboratory that specializes in identifying
the components of urinary calculi
17
18. Metabolic EvaluationMetabolic Evaluation
• A metabolic evaluation for the most common
predisposing factors should be undertaken in
all children with urolithiasis bearing in
mind that structural, infectious, and metabolic
factors often coexist.
18
19. Metabolic EvaluationMetabolic Evaluation (Cont.)(Cont.)
• Laboratory tests suggested for
evaluation of urolithiasis
19
I. Serum
• Calcium • Electrolytes and anion gap
• Phosphorus • Creatinine
• Uric acid • Alkaline phosphatase
22. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi
1.Calcium1.Calcium Oxalate and Calcium PhosphateOxalate and Calcium Phosphate
CalculiCalculi
•The most common metabolic abnormality in these
patients is normocalcemic hypercalciuria
•Between 30% and 60% of children with calcium
stones have hypercalciuria without
hypercalcemia.
22
23. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi (Cont.)(Cont.)
• Hypercalciuria may be absorptive, renal,
or resorptive
23
Type Serum
Ca++
Restricted
Ca++
(urine)
Fasting
Ca++
(urine)
Ca++
load
(urine)
S.PTH
Absorptive N N or ↑ N ↑ ↑
Renal N ↑ ↑ ↑ N
Resorptive ↑ ↑ ↑ ↑ ↑
S.PTH :serum parathyroid hormone
24. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi (Cont.)(Cont.)
Other metabolic aberrations that
predispose to stone disease include :
24
1.Hyperoxaluria 2.Heterozygous cystinuria
3.Hyperuricosuria 4.Hypomagnesuria
5.Hypocitruria 6.Hyperparathyroidism
7.Renal tubular acidosis
25. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi (Cont.)(Cont.)
2.Cystine Calculi2.Cystine Calculi
•Cystinuria accounts for 1% of renal calculi in
children
•Rare autosomal recessive disorder
•Disorder of the epithelial cells of the renal tubule
that prevents absorption of the 4 dibasic amino
acids (Cystine, Ornithine , Lysine, Arginine,)
(COLA) and results in excessive urinary excretion
of these products.
25
26. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi (Cont.)(Cont.)
3.Struvite Calculi3.Struvite Calculi
•Magnesium ammonium phosphate
•In the kidney, the calculi often have a staghorn
configuration, filling the calyces
•The calculi act as foreign bodies, causing:
- Obstruction
- Perpetuating infection
- Causing gradual kidney damage
26
27. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi (Cont.)(Cont.)
Struvite Calculi (cont.)Struvite Calculi (cont.)
•Patients with struvite stones also can have
metabolic abnormalities that predispose to
stone formation.
•These stones often are seen in children with
neuropathic bladder dysfunction,
particularly those who have undergone an ileal
conduit procedure
27
28. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi (Cont.)(Cont.)
Urea-splitting organisms
(most often Proteus spp, and
occasionally Klebsiella spp ,
Escherichia coli, Pseudomonas
spp, and others)
28
Urinary tract
infections
Urinary alkalinization
and excessive
production of ammonia
Precipitation of magnesium
ammonium phosphate
(struvite) and calcium
phosphate
Struvite CalculiStruvite Calculi
(cont.)(cont.)
29. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi (Cont.)(Cont.)
4. Uric Acid Calculi4. Uric Acid Calculi
•Calculi containing uric acid are more common in
less-developed areas of the world.
•Hyperuricosuria with or without
hyperuricemia is the common underlying
factor in most cases
•The stones are radiolucent
29
30. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi (Cont.)(Cont.)
Uric Acid Calculi (cont.)Uric Acid Calculi (cont.)
• DiagnosisDiagnosis should be suspected in a patient
with persistently acid urine and urate
crystalluria
• Hyperuricosuria can result from various
inborn errors of purine metabolism
30
31. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi (Cont.)(Cont.)
Uric Acid Calculi (cont.)Uric Acid Calculi (cont.)
Causes of urate calculi:Causes of urate calculi:
•Lesch-Nyhan syndrome
•Glucose- 6-phosphatase deficiency
•Short-bowel syndrome( e.g. ileostomies)
•Chronic dehydration and acidosis
•Some tumors and myeloproliferative diseases
31
32. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi (Cont.)(Cont.)
5.Indinavir Calculi5.Indinavir Calculi
•Indinavir sulfate is a protease inhibitor
approved for treating HIV infection.
•Up to 4% of patients acquire symptomatic
nephrolithiasis.
•Most of the calculi are radiolucent and are
composed of indinavir-based monohydrate,
although calcium oxalate and/or phosphate
have been present in some.
32
33. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi (Cont.)(Cont.)
Indinavir Calculi (cont.)Indinavir Calculi (cont.)
• After each dose, 12% of the drug is
excreted unchanged in the urine.
•The urine in these patients often contains
crystals of characteristic rectangles and
fan-shaped or starburst crystals.
33
34. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi (Cont.)(Cont.)
Indinavir Calculi (cont.)Indinavir Calculi (cont.)
•Indinavir is soluble at a pH of <5.5.
•Dissolution therapy by urinary
acidification with :
- Ammonium chloride or
- Ascorbic acid
34
35. Pathogenesis of specificPathogenesis of specific
Renal CalculiRenal Calculi (Cont.)(Cont.)
6.Nephrocalcinosis6.Nephrocalcinosis
• Nephrocalcinosis refers to calcium
deposition within the renal tissue.
• Often nephrocalcinosis is associated with
urolithiasis.
35
37. Treatment
• In a child with a renal or ureteral calculus, the
decision whether to remove the stone
depends on:
- Location
- Size
- Composition (if known)
- Obstruction and/or infection if is present.
37
38. Treatment (cont.)
• If the calculus does not pass or seems unlikely
to pass or if there is associated urinary tract
infection, removal is necessary
• Lithotripsy of bladder, ureteral, and small
renal pelvic calculi using the holmium laser
through a flexible or rigid ureteroscope is quite
effective
38
39. Treatment (cont.)
• In children with hypercalciuriaIn children with hypercalciuria:
- Some reduction in calcium and sodium
intake is necessary
-Thiazide diuretics also reduce renal calcium
excretion.
-Addition of potassium citrate, an inhibitor
of calcium stones, with a dosage of
1-2 mEq/kg/24hr is beneficial.
39
40. Treatment (cont.)
• In patients with uric acid stones:In patients with uric acid stones:
- allopurinol is effective
• In patients with cystine stones:In patients with cystine stones:
- Alkalinization of urine with sodium
bicarbonate or sodium citrate is effective.
• D- penicillamine, which is a chelating
agent that binds to cysteine or homocysteine,
increasing the solubility of the product
40
41. Treatment (cont.)
• Treatment of type 1 RTATreatment of type 1 RTA
-- Involves:
*Correcting the metabolic acidosis
*Replacing lost potassium and sodium
• Treatment of primary hyperoxaluriaTreatment of primary hyperoxaluria
-- Involves:
* Liver transplantation
* Kidney transplantation
41
42. References
• Lottmann H, Gagnadoux MF, Daudan M: Urolithiasis in children. In
Gearhart JP, Rink RC, Mouriquand PDE, editors: Pediatric urology, ed 2,
Philadelphia,2010, Saunders, pp 631–661
• http://emedicine.medscape.com/article/2182757-overview
• http://emedicine.medscape.com/article/983884-overview
• http://emedicine.medscape.com/article/437096-overview
• Nacaroglu HT, Demircin G, Bülbül M, Erdogan O, Akyüz SG, Caltik A.
The association between urinary tract infection and idiopathic
hypercalciuria in children. Ren Fail. 2013;35(3):327-32.
• http://emedicine.medscape.com/article/439127-overview
• http://emedicine.medscape.com/article/444968-overview
• http://emedicine.medscape.com/article/444683-overview
42