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 there’s 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 doesn’t 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

necrosis, however, eventually destroy

*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

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

complete obstruction,

particularly when it is high

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.

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

and pelvis, reflecting the role of

ascending infection and vesicoureteral

- 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 function—in particular of

concentrating ability—gives rise to polyuria

and nocturia.

- Radiographic studies show asymmetrically

contracted kidneys with characteristic

coarse scars and blunting and deformity of

the calyceal system.

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).