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Recurrent urinary tract infections

MedGen UID:
500878
Concept ID:
CN000011
Finding
Synonyms: Frequent urinary tract infections; Urinary infection; Urinary tract infection; Urinary tract infections
 
HPO: HP:0000010

Definition

Repeated infections of the urinary tract. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews
  • CROGRecurrent urinary tract infections

Conditions with this feature

Afibrinogenemia
MedGen UID:
7919
Concept ID:
C0001733
Disease or Syndrome
Hereditary deficiency of complement factor I is associated with a propensity to pyogenic infection and follows an autosomal recessive pattern of inheritance (Vyse et al., 1996). See also complement factor H deficiency (609814), which shows overlapping clinical features.
Cystinuria
MedGen UID:
8226
Concept ID:
C0010691
Disease or Syndrome
Cystinuria is an autosomal disorder characterized by impaired epithelial cell transport of cystine and dibasic amino acids (lysine, ornithine, and arginine) in the proximal renal tubule and gastrointestinal tract. The impaired renal reabsorption of cystine and its low solubility causes the formation of calculi in the urinary tract, resulting in obstructive uropathy, pyelonephritis, and, rarely, renal failure (summary by Barbosa et al., 2012).
Felty's syndrome
MedGen UID:
4674
Concept ID:
C0015773
Disease or Syndrome
A rare complication of rheumatoid arthritis with autoimmune NEUTROPENIA; and SPLENOMEGALY.
Langer-Giedion syndrome
MedGen UID:
6009
Concept ID:
C0023003
Disease or Syndrome
Langer-Giedion syndrome is a condition that causes bone abnormalities and distinctive facial features. People with this condition have multiple noncancerous (benign) bone tumors called exostoses. Multiple exostoses may result in pain, limited range of joint movement, and pressure on nerves, blood vessels, the spinal cord, and tissues surrounding the exostoses. Affected individuals also have short stature and cone-shaped ends of the long bones (epiphyses). The characteristic appearance of individuals with Langer-Giedion syndrome includes sparse scalp hair, a rounded nose, a long flat area between the nose and the upper lip (philtrum), and a thin upper lip. Some people with this condition have loose skin in childhood, which typically resolves with age. Affected individuals may have some intellectual disability.
Prune belly syndrome
MedGen UID:
18718
Concept ID:
C0033770
Congenital Abnormality
In its rare complete form, 'prune belly' syndrome comprises megacystis (massively enlarged bladder) with disorganized detrusor muscle, cryptorchidism, and thin abdominal musculature with overlying lax skin (summary by Weber et al., 2011).
Diverticulum of bladder
MedGen UID:
57625
Concept ID:
C0156273
Disease or Syndrome
Williams syndrome
MedGen UID:
59799
Concept ID:
C0175702
Disease or Syndrome
Williams syndrome (WS) is characterized by cardiovascular disease (elastin arteriopathy, peripheral pulmonary stenosis, supravalvar aortic stenosis, hypertension), distinctive facies, connective tissue abnormalities, intellectual disability (usually mild), a specific cognitive profile, unique personality characteristics, growth abnormalities, and endocrine abnormalities (hypercalcemia, hypercalciuria, hypothyroidism, and early puberty). Feeding difficulties often lead to failure to thrive in infancy. Hypotonia and hyperextensible joints can result in delayed attainment of motor milestones.
X-linked agammaglobulinemia
MedGen UID:
65123
Concept ID:
C0221026
Disease or Syndrome
X-linked agammaglobulinemia (XLA) is characterized by recurrent bacterial infections in affected males in the first two years of life. Recurrent otitis is the most common infection prior to diagnosis. Conjunctivitis, sinopulmonary infections, diarrhea, and skin infections are also frequently seen. Approximately 60% of individuals with XLA are recognized as having immunodeficiency when they develop a severe, life-threatening infection such as pneumonia, empyema, meningitis, sepsis, cellulitis, or septic arthritis. S pneumoniae and H influenzae are the most common organisms found prior to diagnosis and may continue to cause sinusitis and otitis after diagnosis and the initiation of gammaglobulin therapy. The prognosis for individuals with XLA has improved markedly in the last 25 years as a result of earlier diagnosis, the development of preparations of gammaglobulin that allow normal concentrations of serum IgG to be achieved, and more liberal use of antibiotics.
SCID due to absent class II HLA antigens
MedGen UID:
69211
Concept ID:
C0242583
Disease or Syndrome
A hereditary immunodeficiency disorder caused by the absence of major histocompatibility complex class II expression. Signs include upper and lower respiratory tract bacterial infections, malabsorption, diarrhea, and mucocutaneous candidiasis.
Distichiasis-lymphedema syndrome
MedGen UID:
75566
Concept ID:
C0265345
Congenital Abnormality
Lymphedema-distichiasis syndrome is characterized by lower-limb lymphedema and distichiasis (aberrant eyelashes ranging from a full set of extra eyelashes to a single hair). Lymphedema typically appears in late childhood or puberty, is confined to the lower limbs, and is often asymmetric; severity varies within families. Males develop edema at an earlier age and have more problems with cellulitis than females. Distichiasis, which may be present at birth, is observed in 94% of affected individuals. About 75% of affected individuals have ocular findings including corneal irritation, recurrent conjunctivitis, and photophobia; other common findings include varicose veins, congenital heart disease, and ptosis. About 25% of individuals are asymptomatic.
Adenine phosphoribosyltransferase deficiency
MedGen UID:
82772
Concept ID:
C0268120
Disease or Syndrome
Adenine phosphoribosyltransferase (APRT) deficiency is characterized by excessive production of 2,8-dihydroxyadenine (DHA), which is excreted in the urine, where it is poorly soluble and leads to kidney stone formation and chronic kidney disease (CKD). Kidney stones, the most common clinical manifestation of APRT deficiency, can occur at any age; in at least 50% of affected individuals symptoms do not occur until adulthood. In a significant number of individuals, intratubular and interstitial precipitation of DHA crystals can result in kidney failure (i.e., DHA crystal nephropathy).
Purine-nucleoside phosphorylase deficiency
MedGen UID:
75653
Concept ID:
C0268125
Disease or Syndrome
Purine nucleoside phosphorylase deficiency is a rare autosomal recessive immunodeficiency disorder characterized mainly by decreased T-cell function. Some patients also have neurologic impairment (review by Aust et al., 1992).
Ehlers-Danlos syndrome, classic type
MedGen UID:
78660
Concept ID:
C0268335
Disease or Syndrome
Ehlers-Danlos syndrome (EDS), classic type is a connective tissue disorder characterized by skin hyperextensibility, abnormal wound healing, and joint hypermobility. It includes two previously designated subtypes (EDS type I and EDS type II) that are now recognized to form a continuum of clinical findings. The skin is smooth, velvety to the touch, and hyperelastic; i.e., it extends easily and snaps back after release (unlike lax, redundant skin, as in cutis laxa). The skin is fragile, as manifested by splitting of the dermis following relatively minor trauma, especially over pressure points (knees, elbows) and areas prone to trauma (shins, forehead, chin). Wound healing is delayed, and stretching of scars after apparently successful primary wound healing is characteristic. Complications of joint hypermobility, such as dislocations of the shoulder, patella, digits, hip, radius, and clavicle, usually resolve spontaneously or are easily managed by the affected individual. Other features include hypotonia with delayed motor development, fatigue and muscle cramps, and easy bruising. Less common findings include mitral and tricuspid valve prolapse, aortic root dilatation, and spontaneous rupture of large arteries.
Ehlers-Danlos syndrome, type 2
MedGen UID:
120628
Concept ID:
C0268336
Disease or Syndrome
Ehlers-Danlos syndrome (EDS), classic type is a connective tissue disorder characterized by skin hyperextensibility, abnormal wound healing, and joint hypermobility. It includes two previously designated subtypes (EDS type I and EDS type II) that are now recognized to form a continuum of clinical findings. The skin is smooth, velvety to the touch, and hyperelastic; i.e., it extends easily and snaps back after release (unlike lax, redundant skin, as in cutis laxa). The skin is fragile, as manifested by splitting of the dermis following relatively minor trauma, especially over pressure points (knees, elbows) and areas prone to trauma (shins, forehead, chin). Wound healing is delayed, and stretching of scars after apparently successful primary wound healing is characteristic. Complications of joint hypermobility, such as dislocations of the shoulder, patella, digits, hip, radius, and clavicle, usually resolve spontaneously or are easily managed by the affected individual. Other features include hypotonia with delayed motor development, fatigue and muscle cramps, and easy bruising. Less common findings include mitral and tricuspid valve prolapse, aortic root dilatation, and spontaneous rupture of large arteries.
Cutis laxa, X-linked
MedGen UID:
82793
Concept ID:
C0268353
Congenital Abnormality
Menkes disease, occipital horn syndrome (OHS), and ATP7A-related distal motor neuropathy (DMN) are disorders of copper transport caused by mutations in the copper-transporting ATPase gene (ATP7A). Infants with classic Menkes disease appear healthy until age two to three months, when loss of developmental milestones, hypotonia, seizures, and failure to thrive occur. The diagnosis is usually suspected when infants exhibit typical neurologic changes and concomitant characteristic changes of the hair (short, sparse, coarse, twisted, and often lightly pigmented). Temperature instability and hypoglycemia may be present in the neonatal period. Death usually occurs by age three years. Occipital horn syndrome is characterized by "occipital horns," distinctive wedge-shaped calcifications at the sites of attachment of the trapezius muscle and the sternocleidomastoid muscle to the occipital bone. Occipital horns may be clinically palpable or observed on skull radiographs. Individuals with OHS also have lax skin and joints, bladder diverticula, inguinal hernias, and vascular tortuosity. Intellect is normal or slightly reduced. ATP7A-related distal motor neuropathy, an adult-onset disorder resembling Charcot-Marie-Tooth disease, shares none of the clinical or biochemical abnormalities characteristic of Menkes disease or OHS.
Primary hypomagnesemia
MedGen UID:
120640
Concept ID:
C0268448
Disease or Syndrome
Familial hypomagnesemia with hypercalciuria and nephrocalcinosis is a progressive renal disorder characterized by excessive urinary Ca(2+) and Mg(2+) excretion. There is progressive loss of kidney function, and in about 50% of cases, the need for renal replacement therapy arises as early as the second decade of life (summary by Muller et al., 2006). A similar disorder with renal magnesium wasting, renal failure, and nephrocalcinosis (HOMG5; 248190) is caused by mutations in another tight-junction gene, CLDN19 (610036), and is distinguished by the association of severe ocular involvement. For a discussion of phenotypic and genetic heterogeneity of familial hypomagnesemia, see HOMG1 (602014).
Congenital defect of folate absorption
MedGen UID:
83348
Concept ID:
C0342705
Disease or Syndrome
Hereditary folate malabsorption (HFM) is characterized by folate deficiency with impaired intestinal folate absorption and impaired folate transport into the central nervous system (CNS). Findings include poor feeding and failure to thrive, anemia often accompanied by leukopenia and/or thrombocytopenia, diarrhea and/or oral mucositis, hypoimmunoglobulinemia, and other immunologic dysfunction resulting in infections with unusual organisms. Neurologic manifestations include developmental delays, cognitive and motor impairment, behavioral disorders and, frequently, seizures.
Microcephaly, normal intelligence and immunodeficiency
MedGen UID:
140771
Concept ID:
C0398791
Congenital Abnormality
Nijmegen breakage syndrome (NBS) is characterized by progressive microcephaly, intrauterine growth retardation and short stature, recurrent sinopulmonary infections, an increased risk for cancer, and premature ovarian failure in females. Developmental milestones are attained at the usual time during the first year; however, borderline delays in development and hyperactivity may be observed in early childhood. Intellectual abilities tend to decline over time and most children tested after age seven years have mild to moderate intellectual disability. Recurrent pneumonia and bronchitis may result in respiratory failure and early death. Approximately 40% of affected individuals have developed malignancies before age 20 years, with the risk being highest for T-cell (55%) and B-cell lymphomas (45%). Other tumors include T-cell lymphoma and solid tumors (e.g., medulloblastoma, glioma, and rhabdomyosarcoma). Note, however, that much of what is reported about NBS is based on individuals who are homozygous for the single most common Eastern European pathogenic variant, 657_661del5.
Ochoa syndrome
MedGen UID:
98015
Concept ID:
C0403555
Disease or Syndrome
Urofacial syndrome (UFS) is characterized by prenatal or infantile onset of urinary bladder voiding dysfunction, abnormal facial movement with expression (resulting from abnormal co-contraction of the corners of the mouth and eyes), and often bowel dysfunction (constipation and/or encopresis). Bladder voiding dysfunction increases the risk for urinary incontinence, megacystis, vesicoureteric reflux, hydroureteronephrosis, urosepsis, and progressive renal impairment.
X-linked agammaglobulinemia with growth hormone deficiency
MedGen UID:
141630
Concept ID:
C0472813
Disease or Syndrome
Isolated growth hormone deficiency is a condition caused by a severe shortage or absence of growth hormone. Growth hormone is a protein that is necessary for the normal growth of the body's bones and tissues. Because they do not have enough of this hormone, people with isolated growth hormone deficiency commonly experience a failure to grow at the expected rate and have unusually short stature. This condition is usually apparent by early childhood. There are four types of isolated growth hormone deficiency differentiated by the severity of the condition, the gene involved, and the inheritance pattern. Isolated growth hormone deficiency type IA is caused by an absence of growth hormone and is the most severe of all the types. In people with type IA, growth failure is evident in infancy as affected babies are shorter than normal at birth. People with isolated growth hormone deficiency type IB produce very low levels of growth hormone. As a result, type IB is characterized by short stature, but this growth failure is typically not as severe as in type IA. Growth failure in people with type IB is usually apparent in early to mid-childhood. Individuals with isolated growth hormone deficiency type II have very low levels of growth hormone and short stature that varies in severity. Growth failure in these individuals is usually evident in early to mid-childhood. It is estimated that nearly half of the individuals with type II have underdevelopment of the pituitary gland (pituitary hypoplasia). The pituitary gland is located at the base of the brain and produces many hormones, including growth hormone. Isolated growth hormone deficiency type III is similar to type II in that affected individuals have very low levels of growth hormone and short stature that varies in severity. Growth failure in type III is usually evident in early to mid-childhood. People with type III may also have a weakened immune system and are prone to frequent infections. They produce very few B cells, which are specialized white blood cells that help protect the body against infection (agammaglobulinemia).
Hardikar syndrome
MedGen UID:
208652
Concept ID:
C0795969
Disease or Syndrome
A syndrome of multiple abnormalities comprising obstructive liver disease with cholestasis, hydroureter and hydronephrosis, cleft lip and palate, retinal pigmentation, and gastrointestinal obstructive disorders. Mental development is usually normal or moderately retarded. Initial growth delay is a constant feature. This and Kabuki make-up syndrome share many common characteristics.
Currarino triad
MedGen UID:
323460
Concept ID:
C1531773
Disease or Syndrome
Posterior column ataxia with retinitis pigmentosa
MedGen UID:
324636
Concept ID:
C1836916
Disease or Syndrome
Posterior column ataxia with retinitis pigmentosa is an autosomal recessive neurologic disorder characterized by childhood-onset retinitis pigmentosa and later onset of gait ataxia due to sensory loss (summary by Ishiura et al., 2011).
Exstrophy of the bladder
MedGen UID:
374033
Concept ID:
C1838703
Disease or Syndrome
Bladder exstrophy and epispadias complex (BEEC) is an anterior midline defect with variable expression involving the infraumbilical abdominal wall including the pelvis, urinary tract, and external genitalia (Gearhart and Jeffs, 1998). BEEC is one of the most severe urologic birth defects because of its profound impact on continence, sexual function, and morbidity due to the effect of chronic and recurrent infections on renal function. The term 'exstrophy,' derived from the Greek work ekstriphein, which literally means 'turn inside out,' was first used by Chaussier in 1780. Martinez-Frias et al. (2001) emphasized that exstrophy of the cloaca and exstrophy of the bladder are 2 different expressions of a primary developmental field defect. Cloacal exstrophy is a feature of the OEIS (omphalocele-exstrophy-imperforate anus-spinal defects) complex (258040). Exstrophy of the cloaca includes the persistence and exstrophy of a common cloaca that receives ureters, ileum, and a rudimentary hindgut and is associated with failure of fusion of the genital tubercles and pubic rami, incomplete development of the lumbosacral vertebrae with spinal dysraphism, imperforate anus, cryptorchidism and epispadias in males and anomalies of the mullerian duct derivatives in females, and a wide range of urinary tract anomalies. Omphalocele is common, and most patients have a single umbilical artery.
Hand foot uterus syndrome
MedGen UID:
331103
Concept ID:
C1841679
Disease or Syndrome
Hand-foot-genital syndrome (HFGS) is characterized by limb malformations and urogenital defects. Mild bilateral shortening of the thumbs and great toes, caused primarily by shortening of the distal phalanx and/or the first metacarpal or metatarsal, is the most common limb malformation and results in impaired dexterity or apposition of the thumbs. Urogenital abnormalities include: abnormalities of the ureters and urethra and various degrees of incomplete Müllerian fusion in females; hypospadias of variable severity with or without chordee in males. Vesicoureteral reflux, recurrent urinary tract infections, and chronic pyelonephritis are common; fertility is normal.
ATR-X syndrome
MedGen UID:
337145
Concept ID:
C1845055
Disease or Syndrome
Alpha-thalassemia X-linked intellectual disability (ATRX) syndrome is characterized by distinctive craniofacial features, genital anomalies, severe developmental delays, hypotonia, intellectual disability, and mild-to-moderate anemia secondary to alpha-thalassemia. Craniofacial abnormalities include small head circumference, telecanthus or widely spaced eyes, short nose, tented vermilion of the upper lip, and thick or everted vermilion of the lower lip with coarsening of the facial features over time. Although all affected individuals have a normal 46,XY karyotype, genital anomalies range from hypospadias and undescended testicles to severe hypospadias and ambiguous genitalia, to normal-appearing female external genitalia. Global developmental delays are evident in infancy and some affected individuals never walk independently or develop significant speech.
Hypomagnesemia 5, renal, with ocular involvement
MedGen UID:
344503
Concept ID:
C1855466
Disease or Syndrome
Keratoconus posticus circumscriptus
MedGen UID:
340922
Concept ID:
C1855645
Disease or Syndrome
Scalp ear nipple syndrome
MedGen UID:
357183
Concept ID:
C1867020
Disease or Syndrome
Scalp-ear-nipple syndrome is characterized by aplasia cutis congenita of the scalp, breast anomalies that range from hypothelia or athelia to amastia, and minor anomalies of the external ears. Less frequent clinical characteristics include nail dystrophy, dental anomalies, cutaneous syndactyly of the digits, and renal malformations. Penetrance appears to be high, although there is substantial variable expressivity within families (Marneros et al., 2013).
Stevenson-Carey syndrome
MedGen UID:
383183
Concept ID:
C2677763
Disease or Syndrome
Chromosome 22q11.2 deletion syndrome, distal
MedGen UID:
395634
Concept ID:
C2678480
Disease or Syndrome
Beaulieu-Boycott-Innes syndrome
MedGen UID:
462289
Concept ID:
C3150939
Disease or Syndrome
Beaulieu-Boycott-Innes syndrome (BBIS) is an autosomal recessive neurodevelopmental disorder characterized by delayed development, moderate intellectual disability, and dysmorphic facial features. Other developmental anomalies, such as cardiac and renal defects, may also occur (summary by Beaulieu et al., 2013).
Chromosome 17q12 deletion syndrome
MedGen UID:
482768
Concept ID:
C3281138
Disease or Syndrome
Urofacial syndrome 2
MedGen UID:
767434
Concept ID:
C3554520
Disease or Syndrome
Urofacial syndrome (UFS; Ochoa syndrome) is an autosomal recessive disorder characterized by congenital urinary bladder dysfunction associated with an abnormal facial expression upon smiling, laughing, and crying. Affected individuals have an overactive detrusor muscle that fails to fully expel urine because of concomitant internal sphincter contraction, and patients may experience lifelong urinary incontinence, recurrent urosepsis, vesicoureteral reflux, and renal failure. In addition, some patients have severe constipation, indicating a generalized elimination defect (summary by Stuart et al., 2013). For a discussion of genetic heterogeneity of UFS, see UFS1 (236730).

Recent clinical studies

Etiology

Flower A, Bishop FL, Lewith G
BMC Fam Pract 2014 Sep 26;15:162. doi: 10.1186/1471-2296-15-162. [Epub ahead of print] PMID: 25260870Free PMC Article
Milosević D, Batinic D, Vrljicak K, Skitarelić N, Potkonjak AM, Turudić D, Bambir I, Roić AC, Spajić M, Spajić B
Coll Antropol 2014 Mar;38(1):151-4. PMID: 24851610
Lin WH, Kao CY, Yang DC, Tseng CC, Wu AB, Teng CH, Wang MC, Wu JJ
Eur J Clin Microbiol Infect Dis 2014 Sep;33(9):1533-9. Epub 2014 Apr 23 doi: 10.1007/s10096-014-2100-4. [Epub ahead of print] PMID: 24756209
Nseir W, Taha M, Nemarny H, Mograbi J
Int J Infect Dis 2013 Dec;17(12):e1121-4. Epub 2013 Aug 2 doi: 10.1016/j.ijid.2013.06.007. [Epub ahead of print] PMID: 23911156
Beerepoot MA, Geerlings SE, van Haarst EP, van Charante NM, ter Riet G
J Urol 2013 Dec;190(6):1981-9. Epub 2013 Jul 15 doi: 10.1016/j.juro.2013.04.142. [Epub ahead of print] PMID: 23867306

Diagnosis

Milosević D, Batinic D, Vrljicak K, Skitarelić N, Potkonjak AM, Turudić D, Bambir I, Roić AC, Spajić M, Spajić B
Coll Antropol 2014 Mar;38(1):151-4. PMID: 24851610
Lin WH, Kao CY, Yang DC, Tseng CC, Wu AB, Teng CH, Wang MC, Wu JJ
Eur J Clin Microbiol Infect Dis 2014 Sep;33(9):1533-9. Epub 2014 Apr 23 doi: 10.1007/s10096-014-2100-4. [Epub ahead of print] PMID: 24756209
Geerlings SE, Beerepoot MA, Prins JM
Infect Dis Clin North Am 2014 Mar;28(1):135-47. Epub 2013 Dec 7 doi: 10.1016/j.idc.2013.10.001. [Epub ahead of print] PMID: 24484580
Wehbi E, Patel P, Kanaroglou N, Tam S, Weber B, Lorenzo A, Pippi Salle JL, Bagli D, Koyle M, Farhat WA
BJU Int 2014 Feb;113(2):304-8. doi: 10.1111/bju.12387. PMID: 24053220
Milošević D, Trkulja V, Turudić D, Batinić D, Spajić B, Tešović G
J Pediatr Urol 2013 Dec;9(6 Pt B):1170-7. Epub 2013 May 30 doi: 10.1016/j.jpurol.2013.04.019. [Epub ahead of print] PMID: 23725853

Therapy

Kanai H, Sato H, Takei Y
J Pediatr Hematol Oncol 2015 Mar;37(2):e131-4. doi: 10.1097/MPH.0000000000000205. PMID: 24942028
Flower A, Bishop FL, Lewith G
BMC Fam Pract 2014 Sep 26;15:162. doi: 10.1186/1471-2296-15-162. [Epub ahead of print] PMID: 25260870Free PMC Article
Geerlings SE, Beerepoot MA, Prins JM
Infect Dis Clin North Am 2014 Mar;28(1):135-47. Epub 2013 Dec 7 doi: 10.1016/j.idc.2013.10.001. [Epub ahead of print] PMID: 24484580
Wehbi E, Patel P, Kanaroglou N, Tam S, Weber B, Lorenzo A, Pippi Salle JL, Bagli D, Koyle M, Farhat WA
BJU Int 2014 Feb;113(2):304-8. doi: 10.1111/bju.12387. PMID: 24053220
Beerepoot MA, Geerlings SE, van Haarst EP, van Charante NM, ter Riet G
J Urol 2013 Dec;190(6):1981-9. Epub 2013 Jul 15 doi: 10.1016/j.juro.2013.04.142. [Epub ahead of print] PMID: 23867306

Prognosis

Kanai H, Sato H, Takei Y
J Pediatr Hematol Oncol 2015 Mar;37(2):e131-4. doi: 10.1097/MPH.0000000000000205. PMID: 24942028
Kochiashvili D, Khuskivadze A, Kochiashvili G, Koberidze G, Kvakhajelidze V
Georgian Med News 2014 Jun;(231):11-6. PMID: 25020163
Wehbi E, Patel P, Kanaroglou N, Tam S, Weber B, Lorenzo A, Pippi Salle JL, Bagli D, Koyle M, Farhat WA
BJU Int 2014 Feb;113(2):304-8. doi: 10.1111/bju.12387. PMID: 24053220
Salonia A, Clementi MC, Graziottin A, Nappi RE, Castiglione F, Ferrari M, Capitanio U, Damiano R, Montorsi F
J Sex Med 2013 Sep;10(9):2265-73. Epub 2013 Jul 22 doi: 10.1111/jsm.12242. [Epub ahead of print] PMID: 23875698
Milošević D, Trkulja V, Turudić D, Batinić D, Spajić B, Tešović G
J Pediatr Urol 2013 Dec;9(6 Pt B):1170-7. Epub 2013 May 30 doi: 10.1016/j.jpurol.2013.04.019. [Epub ahead of print] PMID: 23725853

Clinical prediction guides

Rodrigues P, Hering F, Campagnari JC
Urol Int 2014;93(1):67-73. Epub 2014 Feb 26 doi: 10.1159/000356063. [Epub ahead of print] PMID: 25011551
Bulut IK, Mir S, Berdeli A, Sozeri B
Clin Nephrol 2014 Mar;81(3):152-8. PMID: 24559587
Salonia A, Clementi MC, Graziottin A, Nappi RE, Castiglione F, Ferrari M, Capitanio U, Damiano R, Montorsi F
J Sex Med 2013 Sep;10(9):2265-73. Epub 2013 Jul 22 doi: 10.1111/jsm.12242. [Epub ahead of print] PMID: 23875698
Beerepoot MA, Geerlings SE, van Haarst EP, van Charante NM, ter Riet G
J Urol 2013 Dec;190(6):1981-9. Epub 2013 Jul 15 doi: 10.1016/j.juro.2013.04.142. [Epub ahead of print] PMID: 23867306
Milošević D, Trkulja V, Turudić D, Batinić D, Spajić B, Tešović G
J Pediatr Urol 2013 Dec;9(6 Pt B):1170-7. Epub 2013 May 30 doi: 10.1016/j.jpurol.2013.04.019. [Epub ahead of print] PMID: 23725853

Recent systematic reviews

Eells SJ, Bharadwa K, McKinnell JA, Miller LG
Clin Infect Dis 2014 Jan;58(2):147-60. Epub 2013 Sep 24 doi: 10.1093/cid/cit646. [Epub ahead of print] PMID: 24065333Free PMC Article
Beerepoot MA, Geerlings SE, van Haarst EP, van Charante NM, ter Riet G
J Urol 2013 Dec;190(6):1981-9. Epub 2013 Jul 15 doi: 10.1016/j.juro.2013.04.142. [Epub ahead of print] PMID: 23867306
Grin PM, Kowalewska PM, Alhazzan W, Fox-Robichaud AE
Can J Urol 2013 Feb;20(1):6607-14. PMID: 23433130
Zaffanello M, Malerba G, Cataldi L, Antoniazzi F, Franchini M, Monti E, Fanos V
J Biomed Biotechnol 2010;2010:321082. Epub 2010 Mar 30 doi: 10.1155/2010/321082. PMID: 20379347Free PMC Article
Naber KG, Cho YH, Matsumoto T, Schaeffer AJ
Int J Antimicrob Agents 2009 Feb;33(2):111-9. Epub 2008 Oct 28 doi: 10.1016/j.ijantimicag.2008.08.011. [Epub ahead of print] PMID: 18963856

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