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ACUTE & CHRONIC PYELONEPHRITIS

DEF: Pyelonephritis is a renal disorder that affects the tubules, interstitium and the renal pelvis and it
is one of the most common diseases of the kidney.
Occurs in 2 forms 1) Acute pyelonephritis 2) Chronic Pyelonephritis



ACUTE PYELONEPHRITIS


CHRONIC PYELONEPHRITIS

ETIOLOGY
- Mainly caused by the upward spread of
bacterial infection of the lower UT
- 85% of the UTIs are caused by Gram ve
bacilli that are normally inhabitants of the
GIT
- Agents include:
* Bacteria: E coli, Proteus, Klebsiella,
Enterobacter, Strep faecalis, Staph
* Fungi
* Virus: CMV, Polyoma, Adenovirus esp in
IC pts
- Orgs can reach the UTI via 2 main routes:
1) hematogenous
2) ascending infections
PREDISPOSING FACTORS
- UT Obstruction
- Instrumentation
- VUR
- Pregnancy

CHARACTERISED BY:
- Chronic tubulointerstitial inflamm
- renal scarring involving the calyces and
pelvis
- Only analgesic nephropathy and chronic
pyelo involves the calyces
- 10-20% of ESRD
- Can be assoc w/ reflux or obstruction
Chronic pyelonephritis can be divided
into two forms: chronic reflux-associated
and chronic obstructive.
1) Reflux Nephropathy.
- the more common form of chronic
pyelonephritic scarring.
- Renal involvement in reflux nephropathy
occurs early in childhood as a result of
superimposition of a urinary infection on
congenital vesicoureteral reflux and
intrarenal reflux.
- Reflux may be unilateral or bilateral;
- Pts sex and age
- Pre-existing renal lesions
- DM
- Immunosuppression & immunodef
PATHOGEN: ASCENDING INFECTION
1) There is colonization of the distal urethra
by coliform bac
2) Orgs travel from urethra bladder
[common in due to short urethra; also
due to long term catheterization]
3) Orgs multiply in bladder- normally orgs
entering the bladder will be flushed out w/
voiding theres outflow obstruction of
bladder incomplete voiding of urine
stasis of urine orgs can multiply
UTIs are common in pts w/ BPH, tumors,
stones, neurogenic dysfn in DM, spinal
injury
4) VUR presence of an incompetent VU
valve which may be due to congenital
shortening/absence of a intravesical ureter
that doesnt compress during micturition
urine refluxes back into the ureters when
voiding
*Dx of VUR micturating
cystourethrogram
HEMATOGENOUS SPREAD
- Less common
- seeding of bacteria in the kidney can
occur in pts w/ septicemia or IE
- can occur in ureteric obstruction in
thus, the resultant renal damage may
cause scarring and atrophy of one kidney
or involve both, leading to chronic renal
insufficiency.
- Vesicoureteral reflux occasionally causes
renal damage in the absence of infection
(sterile reflux), but only when
obstruction is severe.
2) Chronic Obstructive Pyelonephritis.
- Obstruction predisposes the kidney to
infection. Recurrent infections
superimposed on diffuse or localized
obstructive lesions lead to recurrent
bouts of renal inflammation and scarring,
resulting in a picture of chronic
pyelonephritis.
- In this condition, the effects of
obstruction contribute to the
parenchymal atrophy;
- The disease can be bilateral, as with
posterior urethral valves, resulting in
renal insufficiency unless the anomaly is
corrected, or unilateral, such as occurs
with calculi and unilateral obstructive
anomalies of the ureter.
MORPHOLOGY
- The characteristic changes of chronic
pyelonephritis are seen on gross
examination.
* The kidneys usually are irregularly
scarred;
debilitated pts, pts that are receiving
immunosuppressive therapy
MORPHOLOGY:
The hallmarks of acute pyelonephritis
are patchy interstitial suppurative
inflammation, intratubular aggregates of
neutrophils, and tubular necrosis. The
suppuration may occur as discrete focal
abscesses involving one or both kidneys,
which can extend to large wedge-shaped
areas of suppuration ( Fig. 20-28 ). The
distribution of these lesions is
unpredictable and haphazard, but in
pyelonephritis associated with reflux,
damage occurs most commonly in the
lower and upper poles.
In the early stages, the neutrophilic
infiltration is limited to the interstitial
tissue. Soon, however, the reaction
involves tubules and produces a
characteristic abscess with the
destruction of the engulfed tubules ( Fig.
20-29 ). Since the tubular lumens
present a ready pathway for the
extension of the infection, large masses
of intraluminal neutrophils frequently
extend along the involved nephron into
the collecting tubules. Characteristically,
glomeruli seem to be relatively resistant
to the infection. Large areas of severe
*if bilateral, the involvement is
asymmetric. This contrasts with chronic
glomerulonephritis, in which both
kidneys are diffusely and symmetrically
scarred.
*The hallmarks of chronic pyelonephritis
are coarse, discrete, corticomedullary
scars overlying dilated, blunted, or
deformed calyces, and flattening of the
papillae
*The scars can vary from one to several
in number and may affect one or both
kidneys. Most are in the upper and lower
poles, consistent with the frequency of
reflux in these sites.
- The microscopic changes involve
predominantly tubules and interstitium.
*The tubules show atrophy in some
areas and hypertrophy or dilation in
others.
*Dilated tubules with flattened
epithelium may be filled with colloid
casts (thyroidization). *There are varying
degrees of chronic interstitial
inflammation and fibrosis in the cortex
and medulla. In the presence of active
infection there may be neutrophils in the
interstitium and pus casts in the tubules.
*Arcuate and interlobular vessels
demonstrate obliterative intimal
sclerosis in the scarred areas; and *In the
necrosis, however, eventually destroy
the glomeruli, and fungal pyelonephritis
(e.g., Candida) often affects glomeruli.
COMPLICATIONS

Papillary necrosis is seen
mainly in diabetics and in
those with urinary tract
obstruction. Papillary
necrosis is usually bilateral
but may be unilateral. One
or all of the pyramids of
the affected kidney may
be involved. On cut
section, the tips or distal
two thirds of the pyramids
have areas of gray-white
to yellow necrosis ( Fig. 20-
30 ). On microscopic
examination the necrotic
tissue shows characteristic
coagulative necrosis, with
preservation of outlines of
tubules. The leukocytic
response is limited to the
junctions between
preserved and destroyed
tissue.

Pyonephrosis is seen when
there is total or almost
presence of hypertension, hyaline
arteriosclerosis is seen in the entire
kidney.
*There is often fibrosis around the
calyceal epithelium as well as a marked
chronic inflammatory infiltrate.
*Glomeruli may appear normal except
for periglomerular fibrosis, or exhibit a
variety of changes, including ischemic
fibrous obliteration and secondary
changes related to hypertension.
* Large collection of chronic inflamm
cells seen in pt with recurrent UTIs
severity of disease depends on the
amount of remaining functional renal
parenchyma.
* Presence of lymphocytes and plasma
cells lymphocytes are common in other
chronic renal disease but presence of
plasma cells is characteristic for chronic
pyelonephritis

XANTHOGRANULOMATOUS
PYELONEPHRITIS

- This is an unusual and relatively rare
form of chronic pyelonephritis
characterized by accumulation of foamy
macrophages intermingled with plasma
cells, lymphocytes, polymorphonuclear
leukocytes, and occasional giant cells.
complete obstruction,
particularly when it is high
in the urinary tract. The
suppurative exudate is
unable to drain and thus
fills the renal pelvis,
calyces, and ureter with
pus.

Perinephric abscess is an
extension of suppurative
inflammation through the
renal capsule into the
perinephric tissue.
After the acute phase of pyelonephritis,
healing occurs. The neutrophilic infiltrate
is replaced by one that is predominantly
composed of macrophages, plasma cells,
and (later) lymphocytes. The
inflammatory foci are eventually
replaced by irregular scars that can be
seen on the cortical surface as fibrous
depressions. Such scars are
characterized microscopically by tubular
atrophy, interstitial fibrosis, and a
lymphocytic infiltrate in a characteristic
patchy, jigsaw pattern with intervening
preserved parenchyma. The
pyelonephritic scar is almost always
associated with inflammation, fibrosis,
and deformation of the underlying calyx
- Often associated with Proteus infections
and obstruction, the lesions sometimes
produce large, yellowish orange
nodules that may be grossly confused
with renal cell carcinoma.

Clinical Features.

- Chronic obstructive pyelonephritis may be
insidious in onset or present with clinical
manifestations of acute recurrent
pyelonephritis, such as back pain, fever,
frequent pyuria, and bacteriuria.
- Chronic pyelonephritis associated with
reflux may have a silent onset.
- These patients come to medical attention
relatively late in the course of their disease
because of the gradual onset of renal
insufficiency and hypertension or because
of the discovery of pyuria or bacteriuria on
routine examination.
- Reflux nephropathy is often discovered
when hypertension in children is
investigated.
- Loss of tubular functionin particular of
concentrating abilitygives rise to polyuria
and nocturia.
- Radiographic studies show asymmetrically
contracted kidneys with characteristic
coarse scars and blunting and deformity of
the calyceal system.
and pelvis, reflecting the role of
ascending infection and vesicoureteral
reflux in the pathogenesis of the disease.
END RESULT:
* Healing uncomplicated, resolves w/
antibiotics:
- Neutrophils are replaced by mononuclear
cells
- Cortical scar formation w/ inflamm &
fibrosis
- deformation of the renal pelvis

CANDIDA PYELONEPHRITIS
- Pyelonephritis caused by fungi, Candida
albicans
- Less common than bacterial infections
- Commonly spreads due to ascending
infection originating in the bladder
- MICRO:
*Transitional lining epithelium shows many
budding cells and pseudohyphae of
Candida albicans.

POLYOMA VIRUS INFECTION
- Latent infection can become reactive w/
immunosuppression
- 1-5% due to allograft failure
- Viral CPE seen in tubular epi
- Interstitial inflamm
- Significant bacteriuria may be present, but
it is often absent in the late stages.
- Although proteinuria is usually mild, some
individuals with pyelonephritic scars
develop secondary focal segmental
glomerulosclerosis with significant
proteinuria, even in the nephrotic range,
usually several years after the scarring has
occurred and often in the absence of
continued infection or persistent
vesicoureteral reflux.
- The appearance of proteinuria and focal
segmental glomerulosclerosis is a poor
prognostic sign, and patients with these
findings may proceed to chronic or end-
stage renal failure.
- The glomerulosclerosis may be attributable
to the adaptive glomerular alterations
secondary to loss of renal mass caused by
pyelonephritic scarring (renal ablation
nephropathy).