acute pyelonephritis the most frequent of all nephropathies
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ACUTE PYELONEPHRITISThe most frequent of all nephropathies
Experience based on 276 cases over 12 years
Alain MeyrierHôpital Georges Pompidou and Broussais
Université René Descartes, Paris
Pierre Rayer
P. Rayer
Pyelo -- renal pelvis
-- nephritis: renal infection
at autopsy
1836
CT scan
DMSA scintigraphy
2006Pyelonephritis
Ascending renal tissue suppuration and ischemia
Uropathogenic E. coli
Acute Pyelonephritis
Primary = in a normal urinary tract 250 000 cases per year per million in the US
Secondary = complication of:Vesico-ureteral refluxMegaureterPosterior urethral valvesProstatic obstruction
NephrolithiasisMedullary sponge kidneyRenal cystsIndwelling catheter
Major cause of end-stage renaldisease in the third world
Still a cause of chronic renalinsufficiency in Western
countries
Cystitis in normal female
Simple pyelonephritis
in normal female
Complicated pyelonephritis
in normal female
Complicated pyelonephritis
in male with prostatitis
Complicated pyelonephritis(Ureteral stone)
Signs and symptoms
TypicalLomboabdominal pain. Enlarged, tender kidneyHigh fever and shaking chillsCystitis often lackingESR >>> 20 mm CRP >>> 20 mg/LPyuria = leukocytes > 105/ml + bacteria > 106/ml
MisleadingPainless: diabetic, malnourished alcoholic (autonomous
neuropathy), elderlyHypothermia: sepsisAseptic bacteriuria: uroculture following treatment
Acute pyelonephritisEncounter between an aggressor and a host
1) The vulnerable hostChildMaleDiabeticPregnant womanMenopauseAlcoholicTransplant recipient
2) The aggressor: a uropathogenic strain
Enterobacteria, mostly E. coli and ProteusStaphylococcus saprophyticus
Commensal microorganisms responsiblefor community acquired pyelonephritis (%)
E. coli 71-89 E. coli 60
P. mirabilis 1,1-9,7 P. mirabilis 15
Klebsiella,Enterobacter 1-9,2Enterococcus 1-3,2S. saprophyticus 3-7Other 2-6
Klebsiella 20
Other 5
FIRST EPISODEOR REMOTE
RELAPSE
RELAPSEBY SHORT-TERM
REINFECTION
Bacteria responsible for hospital acquired pyelonephritis
Van Poppel & al, Infection, 16:337, 1988
Factors of uropathogenicity
1) Physico-chemical factors• Enterobacteriaceae are electronegative but their charge is insufficient to
be repelled by the electronegativity of the urothelium, and by the ions
adsorbed on their surface
• They require and use other virulence factors to adhere to the epithelial
cells, the renal tubules, Bowman's capsule and vessel walls
2) Factors independent of fimbriae
3) Fimbrial adhesion
UPEC = UPEC = UropathogenicUropathogenic E. ColiE. Coli
CrossCross--sectionsection ofof thethe humanhuman kidneykidney displayingdisplaying UPEC UPEC fimbrialfimbrial adhesinadhesin--bindingbinding sitessites
Source: Source: LaneLane MC & MC & MobleyMobley HLT KI, 2007; 72:19HLT KI, 2007; 72:19--2525
Factors of uropathogenicityE. coli
Factors independent of fimbriae- Serotype O: O1, O2, O4, O6, O7, O16, O18, O75 are
found in 28 % of the intestinal flora sampling and are responsible for 80 % of pyelonephritis, 60% of cystitisand 30% of asymptomatic bacteriuria
- Aerobactin: siderophore that allows acquisition of ironfrom the urothelium and the urine
- Hemolysin: cytotoxic to the urothelial cells- Resistance to serum bactericidal activity, allowing E. coli
encapsulation
Factors of uropathogenicityE. coli
Fimbrial, and bacterial membrane adhesins
Fimbriae (Pili) carry epitopes (adhesins), lectins that bind to oligosaccharide motifs of the urothelial (and other) cell membranes, especially galactose-galactose (Gal-Gal) sequences
They also recognize blood group epitopes such as P (hence: 'P-fimbriae') and M
Women who are non-secretor of some blood group antigens elaborateglycolipid Gal-globoside receptors and are more susceptible to E. coli adhesion
The P epitope is located at the tip of fimbriae and assumes a fibrillarstructure
Uropthogenic E. coli: pili ("fimbriae")
Transmission electron micrographs of UPEC expressing different fimbriae. (a and b) CFT073 fim L-ON, a mutant that constitutively expresses type 1 fimbriae. (c and d) CFT073 fim L-OFF, a mutant that is unable to express type 1 fimbria produces another type offimbriae. a and c are at 34 000 magnification, and b and d are at 64 000 magnification.
Source: Lane MC & Mobley HLT KI, 2007; 72:19-25
UPEC = Uropathogenic E. Coli
UPEC adhesion to epithelial cells
Scanning electronmicroscopy
UPEC
Stick to theurothelial cell
membrane
(Le (Le BouguenecBouguenec C & al, J Clin C & al, J Clin MicrobiolMicrobiol, 39:1738, 2001), 39:1738, 2001)
Fimbriae are not solely pathogenicthrough their adhesive properties
• Type 1 adhesins bind to mannose and elicithemagglutination
• Hemagglutination increases the inflammatoryresponse to infection
• In a murine model of pyelonephritis Dr -fimbriaebind to Bowman's capsule and tubular cellbasement membranes through the complement'Decay accelerating factor' and type IV collagen
Factors of uropathogenicityP. mirabilis
Mobley HLT & al Kidney Int 46:S129-36, 1994
Specific factors
Four types of adhesins. MR/P in the kidney and PMF in the bladder
Non specific factorsFlagellaeHemolysinUrease → NH3 urinary pH → struvite staghorn stones
Lessons from animal modelsRoberts JA AJKD 1991
Model: primate
1) Flushing UPEC into the ureter2) Renal vein blood:
ReninComplementThromboxane A2
3) Renal tissue histology:Edema, PMNs, haemorrhage, tubular necrosis, capillarythromboses
Ischemia
1
2
3
Lessons from animal modelsHill GS & Clark RL Invest Radiol 1972
Model: rabbit. Flushing of UPEC in the ureter
VascularVascular neopreneneoprene injectioninjectionHistologyHistology
Summary
• Gram negative pathogenic bacteria progress from theperineum to the urethra, the bladder and spread from themedulla outwards into the renal tissue
• They induce intense vasoconstriction, PMNs influx, capillary plugging, edema and hemorrhagic suffusions
• The involved areas are ischemic• Ischemia may lead to necrosis and walled off cavity
formation = abscess• Ischemia may induce papillary necrosis• The corresponding cortex may undergo sclerosis leaving
definitive cortical scars
Pyelonephritickidney removedsurgically as a salvage procedure in a diabetic.
Whitish areas * denote suppuration.
Arrows show abscess formation
*
Renal biopsy
Edema, inflammatory infiltrate * leukocyte casts in the tubules
*
Renal biopsy, human. Edema, PMNs, hemorrhagic suffusions
Imaging• Emergency CT enhanced helical CT scan may reveal a ureteral
calculus requiring immediate referral to the urologist. Sensitivity98%, specificity 100% (Fielding JR, Am J Radiol 71:1051-3, 1998). Absolute superiority over IVP
• Ultrasound examination: not for assessing obstruction (dilatation lacks in 20% of cases. Found in only 65%), but shows parenchymallesions and discloses abscesses > 1 cm
• CT scan: hypodense images indicating vasoconstriction in suppurative areas. Shows abscesses
• DMSA scintigraphy: when available, extremely sensitive, results in two hours. Inexpensive. The imaging technique of choice in children
• Gallium scan: rarely indicated nowadays
Ultrasound diagnosis of pyelonephritis
Pyélonéphrite vue en échographieUltrasound diagnosis of pyelonephritis
Abscess
Bilateral pyelonephritisHypodense radiating appearance of presuppurative areas
CT scan
Large nodular hypodense "nephronia" from medulla to cortex Note the perirenal edema *
*
CT scan
Juxta cortical hypodense area
in a swollen, edematous
kidney
CT CT scanscan
Left sided pyelonephritis. Large edematous kidney with twohypodense, ischemic areas
Cortical scars two months later
Further progression to chronic interstitial nephritis
Abscess
Pseudo-renal cancer: febrile, painless renal abscess in a malnourishedchronic alcoholic patient Note calcifying pancreatitis
Pseudorenal cancer: febrile, painless renal abscess in a malnourishedchronic alcoholic patient Note calcifying pancreatitis
Gallium scan beforetreatment
Gallium scan aftertreatment
****
*** ***RL
Clinically right sided PN. In fact, bilateral on scintigraphy
99mTc-DMSA scintigraphy
Scintigraphy
CT scan
Pyelonephritis in pregnancy
• Frequent• Heralded by asymptomatic bacteriuria• Occurring in a physiological state of
immunodepression• Difficult imaging (dilatation of the urinary tract is
physiological)• Dangerous: risk of contractions and premature
labor
Patterson & al
Kidney Int
45:571, 1994
Patterson & al
Kidney Int
45:571, 1994
VUR
The most commoncause ofpyelonephritis in children
Risk of renal growtharrest, cortical scars, chronicpyelonephritis
Best diagnostic procedure:
DMSA scintigraphy
Compound papillae
Diabetics
• Male + Obese + Poor glycemic control• Bladder autonomic neuropathy + Glycosuria +
Neutrophil phagocytic impairment• May be painless• Leads to hyperosmolarity and acidocetosis• Abscess formation and papillary necrosis• Rescue nephrectomy may be the last recourse
Necrosis and abscess formation
Papillary necrosis
Papilla recovered in the urine
Acute pyelonephritis
Young woman
No urologic disease
No compromisedbackground
"Simple" pyelonephritis
Apparentlybenign
Ten dayambulatory Rx
Apparentlysevere
Hospitalization
Male
Elderly
Diabetic
Pregnant
Child
Antibiotic treatmentNot advisable before sensitivity tests
• Ampicillin• Cotrimoxazole
Recommended first line regimen
70 % of community acquiredenterobacteriaceae are now resistant
Aminoglycoside 4 days
Fluoroquinolone 10 days
Pregnancy3rd generation β lactamin
Children
Aminoglycoside + 3rd generation β lactamin
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