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1170

Renal

Malakoplakia

Robert

A. Clark,1

and

George

Mark

M.

Weiss,2

David

Renal

Malakoplakia

is an unusual

chronic

to the urinary involvement

in only 1 3 cases [1 -7]. of renal malakoplakia,

inflammatory

tract is rare

process

collecting and has

We describe which have

Anticoagulants

system. been ne-

with

renal

fluids

and

dl and hospital

the radiographic not been empha-

well

In

tubular

she tract

dl;

had

serum

bacter

been

infection. creatinine

diversus,

raphy

from

neys

and

this

with

On

woman, was admitted to Cincinnati General been found at home unconscious. Three years

after having

urinary

hospitalized

with

chronic

At that

blood

urea

1 .6 mg/dl.

The

urine

was

with

oral

admission,

was

10

mg/dl.

(24

x

1 09/L);

organisms

were

cultured

sepsis

with

for

improvement

visualized

on

enlarged

kidneys

and

years

earlier

(fig. was

revealed

Percutaneous granulomatous the

walls

cells which

to granular

findings

with

24,000

the

urine

had

time

was

and

showed

lymphocytic

pyelonephritis

(fig.

Concomitantly, to normal

of

doing

sterile time

a scant

chronic

returned

patient

at this

with

with

at 30 mg/ at the

remained

of malakoplakia.

kidneys

mg/dl

biopsy

fibrosis

compatible

showed

excluded since

The

medullary renal

were

demonstrated

complete

renal

vein

but

urog-

size.

unogram

was

(fig.

not visualized

(fig. 26). Selective

vein

3

stretched, branches

thrombosis

(fig.

arteries,

with

characteristic

malakoplakia

[1

,

arterioles,

5]. There

inclusion

nidus

of

December

and

renal

2C).

was

no evidence

1979

invaded

(fig.

inclusion iron stains

bodies

Michaelis-Guttman

process

venules

3A).

(fig. bodies

The

bodies (fig. 3B).

demonstrated

mineralization

for

Received January 1 7, 1 979; accepted ‘ Department of Radiology, University requests to R. A. Clark. .. Department of Pathology, University

AJR 133:1170-1173,

The

intracytoplasmic von Kossa and

of these a central

cytoplasm.

large

3C). and

These renal

may

after revision of Cincinnati

August Medical

1 5, 1979. Center, Cincinnati

of Cincinnati

Medical

Center,

Cincinnati

1 70 $00.00

cases,

urinary levels

therefore

of this

with

ture

of the lesion.

The

infiltrate

[4,

have

5],

but

not

been

have mentioned enthis finding. Enlargerenal

pyelography obstruction

arteniographic

involving

as-

vein

throm-

showed bilatover a 3 year

appearance of the calyces on demonstrated the infiltrative

ing of the interlobar and explained by the histologic tory

were

Blood urea were elevated.

disease

or without

retrograde without

period. In addition, the left retrograde pyelogram

majority

with the entity is more frequent.

features

bosis. Urography and eral renal enlargement

[5].

the

tract infection. when reported

has been reported without obstruction

occur

of an inflamPAS-positive bodies [1],

for malakoplakia reported

radiographic

encasement

arcuate arteries demonstration

the outer

parts

and

the na-

prun-

in this case of the inflamma-

of the arterial

wall

is

(fig.

3). Selective

renal

thrombosis is

most

with often

venography several

by the

Hospital,

234

General

Hospital,

Cincinnati,

© American

Roentgen

of

Renal various

renal

inflammatory

Goodman

Ray Society

St., OH

45267.

Cincinnati,

vein

vein

thrombosis

renal

disorders,

process [8-10]. In this case the be due to venous encasement

dense

General

demonstrated

collaterals.

a complication

rather than a primary vein thrombosis may occlusion

of amyloidosis.

0361-803X/79/1336-1

inflammatory lesion that rarely The lesion is a yellowish-

described. Most of the case reports larged kidneys and our case confirms ment

obstruc-

the

pathognomonic previously with E. coli and creatinine

The

not

parenchyma

demonstrated

pruned

with

were

is an unusual renal parenchyma.

Obstruction renal failure

was

antibiotics

are

Of the sociated nitrogen

coli She

ultrasound renal

size

arteniography

PAS-positive positive with

microscopy are

in kidney

was

kidneys

pyelography

eosinophilic

of interlobar

lysosomes

Renal

mg/dl;

renal biopsy demonstrated a destructive, pseudoinflammatory infiltrate of histiocytic cells with abun-

contained stained

Electron

the

The renal

interstitial

no evidence

showed

which

kid1 A).

300

urine.

and The

of the

Retrograde

Citro-

Escherichia

and

uremia.

no neovasculanity.

collaterals

count

22%.

transfusions,

infiltration

arteries

venography

foamy

and

to 2.8 follow-up,

Repeat

of continued

stabiized

brown plaque with a characteristic histology matory histiocytic infiltrate. The cells contain inclusion bodies, termed Michaelis-Guttman

Urog(fig.

was

blood

urognam.

solid

1 B). Renal

and venous

dant

blood

the

and

grew

material

cell

was

continued

an increase

intenlobar

There

stable.

infiltrate,

Malakoplakia involves the

43 mg/

normal-sized

nitrogen

blood

both

excretory with

confirmed

encased 2A).

fluid, but

the

white

hematocnit from

hydronephrosis.

without tion

The

urea

was

culture

of contrast

blood

disease

sulfonamides.

demonstrated

concentration

cells/mm

clinical

treated

admission

creatinine

treated

renal nitrogen

she

renal

current

time,

was earlier

impaired

the

6 months

regimen

nitrogen

decreased

anticoagulation. was

was

urea

Discussion

T. A. , a 65-year-old earlier

After

atrophy There

to the treatment

blood

creatinine

long-term

function

3D).

Report

Hospital

serum

inflammatory

malakoplakia.

The

discharge. on

renal

added

were

antibiotics.

the

raphy

Case

Thrombosis

P. Colley,1

sized previously, and add a new case to the literature. addition, this is the first report of renal vein thrombosis associated

Vein

Wyatt1

generally confined Renal parenchymal ported findings

A.

with

renal and

infiltrate.

OH

45267.

Address

reprint

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AJR:133,

Fig.

December

1 -A,

Renal

Urogram

enlargement

unogram.

Bladder

from

without was

The pathogenesis most all cases have oles [1 1

demonstration of ,

1 2].

first

admission.

obstruction,

normal

Fig. 2.-A, Selective anteniovenous shunting. identified (curved arrow). penirenal collateral veins

The

CASE

1979

Kidneys

but with

of normal

stretched.

size:

infiltrated

night,

left renal anteniognam, B, Selective left renal

nephnitis ten entity graphic

diagnosis

Poor

nephrognam.

(curved

arrows)

,

filled.

of renal malakoplakia Gram-negative urinary of bacteria

within

the

is unknown. Altract infections. phagocytic

an impairment of malakoplakia

diagnosis

should

should

include

and xanthogranulomatous particularly may have presentations.

left,

1 1 .0 cm.

kidney.

Right

(B)

1 1 .5 cm; left,

and

left

(C) retrograde

14.0 cm.

Kidneys

pyelognams did not visualize

arterial phase. Stretched, smoothly encased, pruned intenloban and arcuate arteries without arteniognam, venous phase. Renal vein incompletely seen (open arrow); several perirenal selective left renal venogram. Complete renal vein occlusion by thrombus (small arrows) Catheter in renal artery, used to deliver arterial epinephnine, ovenlies renal vein.

vacu-

of phagocytosis with various do-

be

suspected

enlargement of the kidneys occurs with urinary tract tion, particularly if obstruction has been excluded. differential

cm;

Right

3 years later. on excretory

at cystoscopy.

histiocytes implies The association

radiographic

1 0.5

calyces.

bilitating diseases such as sarcoidosis, tuberculosis, diabetes mellitus, and liver disease suggests an underlying immunologic defect as a prerequisite for the disease [7]. The

1 1 71

REPORTS

Renal

acute

bacterial

pyelonephnitis. similar clinical

biopsy

should

be

for

the

man

definitive

inclusion

absent

in

diagnosis, since the typical Michaelis-Guttbodies, pathognomonic for malakoplakia,

the

pyelonephnitis It is difficult thrombosis appearances.

(fig. 4). to determine in this

case

From

the

when infecThe

the radiographic tive infiltrative

pyelo-

performed

and bosiS

of

the

to the

contribution

histology

result

are

of and

of the

renal

vein

angiographic

limited

needle

bi-

case and the gross and microscopic reported cases, it is conceivable that

of the kidney also

or

xanthogranulomatous

unographic

findings are solely nature of malakoplakia.

congestion could

cells

inflammatory

opsy specimen in this pathology of the other

The atand radio-

neovasculanity

venous collaterals with capsular and

the result of the destrucHowever, the edema

secondary

in similar

to renal

radiographic

vein

throm-

abnormalities

[13].

Therefore,

since

the

radiogaphic

findings

of renal

malak-

CASE

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1172

-----

-

. ‘-

.

.

:.

,

.‘ .

.

‘

,

1

p.

...

AJR:133,

,

-

LL

.:O...

REPORTS

.

,

-

1979

capsule

(BC).

1.!

.

,$

T

-

.

December

;.;.,

,

,

,

. .

.

,

.

I-,

:

;L

I

I

.

,‘ .,

, ,

I

a_ Fig.

of arteriolar

of Michaelis-Gutman

cortex

A,

malakoplakia.

and infiltration Renal

D Replacement

-

3.-Renal

body.

with atrophic

Cortex

wall (ART) Large

tubules

with

(PAS,

intracytoplasmic

separated

dense

histiocytic

x 1 60). B, Numerous

infiltrate.

Michaelis-Gutman

phagolysozome

by a fibrotic

interstitium

has

central

containing

and

destruction

of tubules

(T),

disruption

of Bowman’s

x

(arrows) (PAS, 400). C, Ultrastructure nidus of mineralization (x 26, 657). D, Renal biopsy after 6 months of therapy. scant chronic inflammatory infiltrate (Jones, x 100). inclusion

bodies

oplakia

with

within

or

histiocytes

without

renal

vein

may

thrombosis

and since the clinical, laboratory, of renal vein thrombosis are

and urographic variable, renal

should

of renal

be

performed

in cases

addition of anticoagulants may be necessary if renal

to the funciton

the complication

vein

of renal

overlap,

indications venography

malakoplakia.

The

usual therapy of antibiotics is to be preserved despite

thrombosis

[8].

REFERENCES 1

.

Michelis

z 2.

K/in

Fig.

Dense

4.-Example inflammatory

of xanthogranulomatous infiltrate in renal

pyelonephnitis for comparison. medulla consists of histiocytes with (H & E, x 1 00). Inset: Note absence of Michaelis-

abundant foamy cytoplasm Gutman bodies (H & E, x400).

Bennett

C: Ueber

47:208-21

McDonald kidneys.

3.

L, Guttmann Med

S,

Sewell

J Pathol

WH:

5.

Lambird

PA,

WT:

Malakoplakia 1 8:306-31

Bacteriol

Malakoplakia

cases. J Urol 70:84-90, 4. Ravel A: Megaloystic related to malakoplakia. Yardley

in Blasentumoren.

einschleusse

5, 1902

of the

of

the

bladder

and

8, 1913

urinary

tract:

report

of three

1953

interstitial

nephnitis:

Am

Pathol

JH:

J C/in

Urinary

tract

an entity probably 47: 781 -789, 1967 malakoplakia: report of

AJR:133,

6.

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7.

8.

9.

December

1979

CASE

a fatal case with ultrastructral observations of Michaelis-Guttman bodies. Johns Hopkins Med J 1 26: 1 -1 3, 1970 Bowers JH, Cathey WJ: Malakoplakia of the kidney with renal failure. Am J C/in Pathol 55:765-769, 1971 Cadnapaphornchai P, Rosenberg BT, Taher 5, Pnosnitz EH, McDonald FD: Renal parenchymal malakoplakia: an unusual cause of renal failure. N EngI J Med 299: 1 1 10-1 1 1 3, 1978 Clark RA, Wyatt GM, Colley DP: Renal vein thrombosis: An underdiagnosed complication of multiple renal abnormalities. Radiology 132:43-50, July 1979 Llach F, Anieff Al, Massry SG: Renal vein thrombosis and nephrotic syndrome. Ann Intern Med 83:8-1 4, 1975

1173

REPORTS

1 0.

Llach

F,

Koffler

A,

Finck

E:

On

the

incidence

of

renal

vein

thrombosis in the Nephrotic syndrome. Arch Intern Med 137: 333-336, 1977 1 1 . McClurg FB, D’Agostino AN, Martin JH: Ultrastructural demonstration of intracellular bacteria in three cases of malakoplakia of the bladder. Am J C/in Pathol 60:780-788, 1973 1 2. Abdon NI, NaPombejara C, Sagawa A: Malakoplakia: evidence for monocyte lysosomal abnormality correctable by cholinergic agonist in vitro and in vivo. N EngI J Med 297:1413-1419, 1977 1 3.

Mulhern

C, Anger

vein thrombosis.

P, Miller AJR

W,

Chait

125:291-299,

A: The

1975

specificity

of renal