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Casepres Acute

Casepres Acute

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Published by: globalcollegecity on Jun 25, 2010
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05/19/2012

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Background
Acute pyelonephritis is a potentially organ- and/or life-threatening infection that characteristically causes somescarring of the kidney with each infection and may lead to significant damage to the kidney (any given episode),kidney failure, abscess formation (eg, nephric, perinephric), sepsis, or sepsis syndrome/shock/multiorgansystem failure. More than 250,000 cases occur in the United States each year (1995 estimate), andapproximately 200,000 patients require hospitalization (1997 data). Wide variation exists in the clinicalpresentation, severity, options, and disposition of acute pyelonephritis.Diagnosing and managing acutepyelonephritis is not always straightforward. In the age range of 5-65 years, it typically presents in the context of a symptomatic (eg, dysuria, frequency, urgency, grosshematuria,  suprapubic pain)urinary tract infection(UTI)with classic upper urinary tract symptoms (eg, flank pain, back pain) with or without systemic symptoms (eg, fever, chills, abdominal pain, nausea, vomiting) and signs (eg,fever, costovertebral angle tenderness) with or without leukocytosis. However, it can present with nonspecificsymptoms.A number of studies using immunochemical markers have shown that many women, who initially present withlower tract symptoms, actually havepyelonephritis. This group of young women is often identified when short-course therapy for uncomplicated cystitis fails. In the extremes of age, the presentation may be so atypical thatpyelonephritis is not in the differential diagnosis. In the infant, the presentation may be feeding difficulty or fever. In the elderly, the presentation may be mental status change or fever. Acute pyelonephritis is complex,and there is no consistent set of signs and symptoms that are both sensitive and specific for the diagnosis;therefore, clinicians must maintain a high index of suspicion.In contrast to the plethora of data available for the treatment of lower  UTI, less substantial data are available regarding the appropriate antibiotic choice or duration of therapy for acute pyelonephritis, but usefulrecommendations can be made. An additional cause for concern is the growing antimicrobial resistance toaccepted standards of treatment. The current emphasis on cost effectiveness and the advent of newer antibiotics have led clinicians to reevaluate the benefit of hospitalization to treat patients with acutepyelonephritis; however, if the patient is managed as an outpatient, he or she should have close follow-up care.The first follow-up visit should occur in 1-2 days, depending on the clinician's estimation of the severity of theinfection. Any deterioration or unsatisfactory improvement warrants admission for intravenous antibiotics andevaluation for any complications. Most cases of uncomplicated pyelonephritis in young women can bemanagedsuccessfullyonan outpatient basis.
Recent studies
 In a retrospective study of 206 elderly patients hospitalized for acute pyelonephritis, Kofteridis et al comparedclinical and microbiologic characteristics of members of the cohort who had diabetes mellitus (88 patients) withthose who did not (118 patients). The authors found that 30.7% of patients with diabetes mellitus (27 patients)had bacteremia, compared with 11% of the controls (13 patients). Moreover, patients with diabetes had longer-lasting fevers than did the controls (median, 4.5 vs 2.5 days, respectively), as well as longer hospital stays(median, 10 vs 7 days, respectively). The mortality rate in patients with diabetes was 12.5%, compared with2.5% in the controls. The authors concluded that acute pyelonephritis is linked to bacteremia, long hospitalstays, and mortality in persons with diabetes.
 
Pathophysiology
Acute pyelonephritis results from bacterial invasion of the renal parenchyma. In all age groups, episodes of bacteriuria occur commonly, but most are asymptomatic (ABU) and do not lead to infection. Infection isinfluenced by bacterial factors and host factors.
Most bacterial data are derived from research with
Escherichia coli,
which accounts for 70-90% of uncomplicated UTIs and 21-54% of complicated UTIs. A subset of 
E coli,
the uropathogenic
E coli 
(UPEC),also termed extraintestinal pathogenic
E coli 
(ExPEC), accounts for most clinical isolates from UTIs. UPECderives commonly from the phylogenetic groups B2 and D, which express distinctive O, K, and H antigens.
UPEC 
genes encode several postulated virulence factors (VFs), including adhesins, protectins, siderophores,and toxins, as well as having the metabolic advantage of synthesizing essential substances.Adhesins have specific regions that attach to cell receptor epitopes in a lock-and-key fashion. Mannose-sensitive adhesins (usually type 1 fimbriae) are present on essentially all
E coli 
. They contribute to colonization(eg, bladder, gut, mouth, vagina) and possibly pathogenesis of infection; however, they also attach topolymorphonuclear leukocytes (PMN), leading to bacterial clearance. Mannose-resistant adhesins permit thebacteria to attach to epithelial cells, thereby resisting the cleansing action of urine flow and bladder emptying.They also allow the bacteria to remain in close proximity to the epithelial cell, enhancing the activity of other VFs.The P fimbriae family of adhesins are epidemiologically associated with prostatitis, pyelonephritis (70-90% of strains), and sepsis. This same family of adhesins in associated with less than 20% of ABU strains. TheAFA/Dr family is associated with diarrhea, UTI, and particularly pyelonephritis in pregnancy. The S/F1C familyis associated with neonatal meningitis and UTI. Siderophores are involved iron uptake, an essential element for bacteria, and possibly adhesion. Protectins include lipopolysaccharide (LPS) coatings (resist phagocytosis),Tra T and Iss (both resist action of complement), and Omp T (cleave host defense proteins, such asimmunoglobulins).Toxins, including alpha hemolysin, cytotoxic necrotizing factor-1, cytolethal distending toxin, and secretedautotransporter toxin, affect various host cell functions; LPS shed from a membrane or released by bacteriallysis leads to cytokine release. No single VF is sufficient or necessary to promote pathogenesis. It seems that amultiple VFs are necessary to ensure pathogenesis, although adhesins play an important role.Bacterial strains producing ABU may provide, in some instances (controversial), a measure of protectionagainst symptomatic infections from UPEC and other organisms; but, it may also cause increased morbidityand mortality. Once bacteriuria is established, these strains appear to stop producing adhesins, allowing themto survive and persist without producing an inflammatory reaction. The frequency of ABU in preschool girls isless than 2%; in pregnant women, 2-9.5%; in women aged 65-80 years, 18-43%; in men aged 65-80 years,1.5-15.3%; in women older than 80 years, 18-43%; and in men older than 80 years, 5.4-21%. There isconsiderable morbidity associated with ABU in pregnancy, renal transplantation, and genitourinary surgery (seeTable 1).Table 1. Asymptomatic Bacteriuria: Incidence, Morbidity, Screening, and Treatment
1
 
ClinicalConditionFrequency (%)Morbidity andMortalityScreeningRecommendedTreatmentWithAntibioticBeneficial
2
CommentsFemaleMaleInfants (= 36Months)
0.4-1.80.5-2.5NoneNoNo
Preschool
0.8-1.30.5NoneNoNo
SchoolChildren andAdolescents
1.1-1.8~ 0May persist foyears withoutadverseoutcome.Increasedincidence of symptomaticUTI’s
3
in girlsin absence of treatment.NoNoNo evidence oscar or renalfailureprogression, if untreated. Abxgiven for anyindication in girlsleads toincreasedsymptomaticUTI’s inposttreatmentperiod.
Premenopausal andNonpregnantWomen
0.8-5.2-More frequentUTI’s andsubsequentABU. No other associatedlong-termadverseoutcome.NoNoNo benefits totreatment havebeen identified.
PregnantWomen
2-9.5
4
-Prior UTI olower socio-economicstatusassociatedwith higher frequency of ABU. 20 –30% untreatedABU progressto acutepyelonephritis(AP), usuallyat end of 2
nd
or early 3
rd
trimester. ABUassociatedwithintrauterineYesAt least 1 urineculture,preferably 2consecutive, atend 1
st
trimester 
5
 YesTreatmentof ABUreducesfrequencyof AP to 2 – 3%After treatment of ABU, periodicfollow-up urineculturesrecommended,e.g. once per month. 1 – 2%women withnegative initialurine culturedevelop ABU andexperience APlater inpregnancy.

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