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(2)

THE PATHOLOGY OF KIDNEY DISEASES IN SHEEP

A t,hesis presented in partial fulfilment

(3Cf/o)

of the

requirements for the degree of l\laster of Philosophy in VP.tcrinary Pathology at T·1assey University.

Pavlos G-eorgiou Toum.azos

1981

(3)

ACKNOWLEDGEMENTS

I would like cordially to thank Dr A.C. Johnstone, my supervisor, for his contj.nuous and untiring guida�1ee, advice, encouragemei:t and

assistance throughout this study. Special thanl�s are also clue to

1-Tr

G. V.

Petersen for his advice and assistan

c

e in tbe statistical analysis of data and for his arrangements for visits at Longburn freezing >·rorks. JI'Ia.ny thanks ar·e expressed to the veterinary and meat inspection st<;.ff

of the 1:-or-thvlick' s freez�_ng works at Longburn, for t:heir co:Llaboration duT.Lng . :·llection period.

Professor B.\if. MankteloH, Dr M.R. Alley and Dr R.D. Jcl.J.y gELJe

helpf1}.1 advice during tbe w-.ci ting and preparation of this thRsis.

I am grateful for te chnical assistance provided by I.Jrs P .I·:. Slack and her "team" for the preparation of tissues for histopathological examination; Hr T.G. Law and tne staff of the };assey University }':cintc;:y for the preparation of the photographs and 1·qJrod.u.ction of the figures

present e d in this thesis.

I also extend my sincere st gra t:•.. /3 to many other friends frcg this and other De partments of the Ji'ncu.lty of Yeteri:nary Science who v:erc always keenly receptive to my enquiries and requests and have directly or indirectly helped me in my work.

I would like to sincerely thank my wife Vaso for typing tl:is thesl.s and the p.::l.tience, understanding and sacrifices :Jade by her and our

children Hiranda and Nestoras du:ring preparation of the manusc:cipt.

This investi,:':ation -vms partly supported by a Commor.vreal th Scholal·ship.

I am most gratefull to the administrators of this Grant, especially the secretary Miss D.L. Anderson .

(4)

iii

ABSTRACT

Renal diseases in sheep form a di verse spectrum of pathology and an extensive literature revievr of spontaneously occurring and e':per

i

­

men

ta

lly induced diseases of the 3hecp

�Kidney is

presented in Chapter l of this thes

i

s

to

pr

o

v

i

de a c

o

mpa ris

o

n vri th

the l

esions found

in

a survey

of

kidneys jn slaughter-house �illed s

h

eep

. The p resentation of results of this survey form the major part of this thesis and

provide

s

information on

th

ese diseases relative

to large populations of

sheep

uhich

is only sparsely repor

t

ed elsevrhere. The abnormal kidneys under study were obtained from 444- of

13,988

sheep sl

a

ughtered over a

consecutive five day per

i

od

at the

Borth-v;ick'

s

freez

ing

\lOrks,

Longburr1

in January

1980.

The prevalence

of

rena

l

disease

vras 3 .18 :per cen� and

no

significant variation ( p ( 0. 05) in the prevalence of lesions ";as

found beh1eE:n the various lines, chains and daily totals of sheep ex&11ined.

From t

hese sheep a

t otal

of

830 dise11sed

k

i

dneys l•rere founrl

ancl

these

vrere categorized into seven groups according to the major

pathologic&.l

le

si

on in each. In

s ome kidneys

addi b onB-1 m

i

nor lesions vrere present, making a total of 1212 macroscopic le

si

ons identified.

White spots and strealr...s conG

t

i tuted the major

gross p8.thological

finding in

188

kidneys; pale, red and

brovm discolourati on in 174,

120 and

179

respectively; scars in 107; cysts in 37 and nodules in 25 kidneys.

Abscesses, neoplasms and focal space occupying lesions of uncertain aetiology 1.vere included under the category of nodule.

Pieces of tissue selected from

181 kidneys

to represent the vario·LtS lesions seen at gross examination were examined histologically. These were identified, recorded and graded according to the anatomical location, pattern of distribution, tissue changes and degree of severity.

The main histopathological feature of the white spotted kidneys vras

(5)

chronic, mainly multifocal inflammation of the cortical interstitium.

Similar

but

radially disposed inflammatory lesions with marked fibrosis occurred in the

scarred kidneys . The

pattern of these lesions suggested a haematogenous di::;tribution of a

p

athog

en

in the spotted kidney.s vJhile the scarred kidneys were

probably

the result of ascending inflammation or infarctive processes.

Kidneys vli

th pale

discoloura tion showed mild to

moderately

severe

nephrosis

of the cortical

epithelial cells� while kidneys vli

th

brovm

discolouration shovred corticotubular

intracyt oplasmic

and intralumenal ha

emosi

derin

deposition .

In some

kidneys

haemosiderosis wa::: restricted to areas of scarring. Red discoloured kidneys

shm·red

patchy

or

d

iffuse

congestion.

Cystic lesions were either

para s i tic or

the

result of urinary

retention

caused by blockage of tubules .

In the

latter,

tha block�ge ,._,.as either congenital or associated with chronic inflammation.

With the exception of

nephrosis

and conges-tion all the

lesions were chronic

in nature and for most of

them

a definitive aetiological

diagnosis vras not established. In fact, in only those lesions containing

Echinoc o c cus

granulosus hy

dat

id

c ys t s

could such

a

diagnosis

be

made.

Additional studies are indicated for the provision of further information on

(

a

)

the prevalence of renal diseases in different

gevgraphical locations,

( b)

variation of disease types from area to area and

(

c

)

the causes of the lesions identified from this type of

investigation.

(6)

TABLE OF CONTENTS

ACKNOWLEDGEMENTS ABSTRACT

LIST OF ILLUSTRATIONS CHAPI'ER l:

CHAPTER 2:

Review o f the literatur e Introduction

( I ) ( II )

Diseases of the glomerulus

l. Spontaneous glomerulonephropathies 2. Experimental autoinrnune

glomeruloneph:ri tis' Diseases of renal tubules l. Inflammatory

2. Degenerative

( III ) ( IV ) ( v ) ( VI )

Diseases of the renal pelvis Renal Neoplasms

Renal Cysts Urolithiasi::::

A survey of diseased sheep kidneys Introduction

Materials and Ne thods Results

Gross Pathology l. Abnormal shape

2.

Increased size 3 . Reduced 8ize

4 . Discolouration

5 . Spots and streaks

6 .

Scars

7. Cysts 8. Nodules Histopathology

l. Discolouration

2.

Spots and strealm

3 . Scars

4. Cysts 5 . Nodules Discussion Conclusion BIBLIOGHAPHY

APPENDICES

V

Page ii iii vi l

l

2

7

10

10

15

24

25

25

27

30

30

30

31

34

37

37 37

37

38

38

38

39

40

41

42

45

47

49

5 2

60

62

72

(7)

Figure 2.1 Figure 2.2 Figure 2.3

Figure 2 .4

Figure 2.5

Figure 2 .6

Figure 2 . 7 Figure 2.8 Figure 2.9a

Figure 2.9b

LIST OF ILLUSTRATIONS

Foll ovling rJage

Histogram showing the distribution in weight of 8)0

l.i

< dneys collected from

444 sheep

1·ri

th renal l e sio ns .

Hi s t ogra m shovTing the gr oss pathol ogical featu r

es

of 12 12 lesions recorded in 830 diseased k id neys .

Misshapen kidney (No. 234).

a) Capsular surface s hmving dumbbell s ha pe

caused by

s evere s carring in .central area.

Le ss extensive s carr ing is pre sen t over the capsular surface of the poles.

b ) The cut surface of the same k id n ey

shovring the s car:J:'ed tissue extending from capsule to pelvis.

Pale shrunken kidney ( No. 30·t)

The

red uction in size is due to d

i

f

fu

s

e

scarring of

the

renal

parenchyma.

The incised surface of t his kidney

is shovm

in figure 2 .14 .

Pale Slwllen kidney (N o . 99). N o

t

e the pallor of

the

outer c ortex c on t rasting with the c ong e s te d c orticowodullary region.

Pa t ch :y red disc olourat i on of kidneys ( No. 5 ) due t o

c

onge sti o n. The change is less severe and. res tri c ted t o t1w right pol e in the k i d n

ey

on the righ t .

Diffuse red discolov.ra cion of a kidney ( No. 25 4) due to c ongest i on.

Diffuse dark brovm discolouration of a kidney ( No. 201) due to haemosiderosis.

Dark brown discolouration of kidneys ( No.l33 ) distributed in scarred and depressed areas of renal cortex. The pale raised areas are the remaining functional kidney tissue.

Cut section of kidneys showing radial brown streaking of scar tissue extending

from capsular surface to medulla.

34 34

37

37

37

37

Yl

37

38

38

(8)

Figure 2.10

Figure 2.11

Figure 2.12

Figure 2.13 Figure 2 .14-

Figure 2.15

Figure 2.16

a) Severe diffuse spotting of subcapsular cortical tissue ( kidney No. 119 ) .

b) The same kidney on cut section showing ill-defined, white streaks extending

radially into iriller cortical parenchyma.

a) llioderEt.tely severe

vrhi

te spott ing of the subcapsular c orti cal tissue ( kidney No.2)

b) The cut section of t h e same kidney showing ill-defined v1hi t e streaks vrhich are most prominent in the outer c ortical pa re n ch

ym

a .

a ) M ul t i p le , slightly d epr

es

s e d ill­

defined s cars in the s

u

bcap su la r tissue ( kidney No . 4).

b) Cut section of the sa m e kidney showing poorly defined linear vrhi te hands of scar

tis3ue in the cortex.

Extensive scarring of the su bca ps u la r

tissue (kidney No. 130).

Cut sect i on of a smal l scarred kidney ( no. 304) shovring diffuse fibr osis

affecting

all

areas

of

the kidney. Note the d i st o rte d renal papilla . The

capsular surface of trLis ki dney is shovm in figure 2.4.

Congeni tal cysts.

a) Capsular surface showing numerous well

d

e fined c ortical depre ssions

overl r ing the cystic parench:yma ( J:..idney No.55 ) .

b) Cut secti on of the same kidney shovring four well defined c ortical cysts.

Hydatid cysts in kidney ( No. 198) . a) Cyst of Echino c

o

cc

u

s grnulosus in parahilar cortical tissue.

b) The cut section shov;ing the mul tilo­

culated cyst.

vii Following page

38

38

)8

38

38

39

39

Figure 2. 17 Renal abscessation ( No. 59 ) .

a

) The cortical surface of a ki��ey containing an organized abscess in the left pole. Note the deformity caused by depressed, scarred tissue in paracentral areas.

b) Cut section of the same kidne�r showing the o r�a niz ing abscess ( large

arrovr

) and

scars \ small arrow) extending from the

cortex to the pelvis.

33
(9)

Following page Figure 2.18

Figure

2.19

Figure

2.20

Renal abscessation

(

No.

200) .

a)

The kidney conLa:i.ns an en

c

aps

u

l

a

te

d

caseous abscess bnlging from the capsular surface.

b)

The

cut section of the

sam8 kidney.

Renal

carcinoma (Ho. 237) .

a

)

Dist

o

t

i

o

n of the left pole of

t h

e

kidney by

a renal co.J:cinoma.

b) Cut sectior-1 of

the kidney shmving

the

sl

i

gh

t

l

y

encaps-..11a·�ccl

lobulated

tumour with extensive areas

of

necrosis and

h

ae

mo

rrhage

.

Renal lymphoma

(lTo. 236).

a

)

Distortion of a kidney by a lymphoma

occupyin& the l(�f L

polar >;tnd

hilar zones.

b)

The

incised

surf:>.ce sho1·1ing

additional

focal twnour mnssec in

the

cortical

tissue.

Figure 2. 21 Nodule of

undctcr:r;.Lr_ed cause

(

k

i

dn

e

y

No.

12 ) .

Figure

2.22

Figur�

2 . 23

a

)

A fi

b

r

o

us

no:iclle elei.Tated slightly

above the cap::;ular surface.

b)

Note

t

he

concentric lamination

of

the l

esi

on upon sectionJ.ng.

Chronic parasitic noJule (kidl1cy No. 20).

a)

Appearance on capsular

surface .

b

)

On incision

the.� uell defined

cortical

nodule

was hard and

contained gritty mate rial.

Hassive renal infarct

(

no.

kidney on left

is swo

l

len, haemorrhagic and necrotic.

thrombus is

p1·esent in the

The right kidney is normal.

2 49). 'rhe diffusely

An o

r

gan

i

z

i n

g renal vein.

l<'igure

2.24.

Neph

r

osis

.

Moderately severe �ca

t t

ere

d d

e

g

e

ne

ra

t

ive changes in epithelial cells of proximal convoluted

t u

b

u

le

s . Note

pyknotic

nuclei and cell loss. The

d

il

at

e

d

39

39

39

40

40

40

tubules

contain hyaline

g

ran

u

lar casts. HE

x 320 41 Fi.gure 2.25

Ne

p

hros

i

s

.

Lesions

a

r

e similar but less

severe than those

in

figure 2 .24.

HE

x 400 41 Figure 2.26 Haem osiderosis.

"ifuole

mount" section of

kidney stained by Perls' method for iron showing extensive cortical accumulation

of

r�emosiderin ( x 7). 42

Figure 2 .27 Haemosiderosis. Extensive deposition of haemosiderin in

cytoplasm of

epithelial cells of proximal convoluted tubules ( arrovm).

Granular casts are present in the tubular

lumena.

HE

x 320 42

(10)

Figure

2.28

Figure

2.30

Figure

2.31

Figure

2 . 32

Figure

2.33

Figure

2.34

Figure

2 . 35

Figure

2 . 36

ix

Follmring page

Haemosiderosis. Haemosiderin deposition in inflamed and scarred tissue of a kidney. HE x

50

Detail of inset in figure

2.28

sho-,ring haemosiclerin granules in epith8lial cells of tubules

(

broad arrow

)

and interstitial inflammatory reaction

(

narrow arrovm

)

.

HE X

150

Kidney vii th spots and streaks. Focal mainly lymp

h

ocytic infiltration of renal cortical interstitium. HE x

125

Kidney vri th spots and streak

s

. Interstitial infiltration by lymphocytes and plasma cells.

Note the degenerative change in epithelial cells of tubules and formation of proteina­

ceous casts 1·1i thin lumena. HE x

320

Glomerulus within an area of c·hronic inflammation in a "spotted" kidney. Note the proliferation of cells in glomerular tufts, the obliteration of glomerular capillari es and �rinary space and fibrosis of Bomn.:ln 1 s capsule. The entire field has been infiltrated by plasma cells and

phagocytes. HE x

32 0

Scarred kidney. Small linear zone of fibrosis v!i th l

y

mphocyte and plasma cell infiltr ation in the outer cortex. HEx

125

Scarred J:r.idney. An extensive iveclgeshaped cortical scar associated 'lri th marked tubular and glomerular atrophy

.

HE x

50

Renal papilla

(

on left

)

and pelvis

(

on

right

)

of a kidney vli th extensive radial scarring. Note the reduced numbers of tubules, several containing casts

(

broad

arrows

)

and others with calcification of basement membrane and epithelial cells

(

narrovT arrows

)

. The interstitial tissue of the papilla is fibrotic and lightly infiltrated by lymphocytes. The pelvic epithelium is slightly hyperplastic and shows mild infiltration of subepithelial tissue by lymphocytes. HE

x 50

Renal papilla

(

on left

)

and pelvis

(

on

right

)

of a severely scarred kidney showing extensive replacement of tubules by

fibrosis. Remaining tubules are atrophied.

There i s extensive fibrosis of the renal pelvis. HE x

125

42

42

45

45

4-5

45

4'7

47

47

(11)

Figure 2.37 Degeneration of pelvic and papillary epithelia associated with fibrosis,

lymphocytic and plasmacytic infiltrations.

HE X 320 47

Figure 2.38 Renal cortex of a scarred kidney showing tubular atrophy, dilatation of tubules 1vi th accumulation of highly eosino:philic material in lumena ( thyroidiza tion

)

,

interstitial fibrosis and infiltration by lymphocytes and plasma cells. T1v0

atrophied glomeruli are present

(

narrow

arrmvs

)

. HE x 125 4 7

Figure 2.39 Glomeruli in area of inflamm�tion and s carring sho-vring gradation in the severity of basement membrane thickening due to membranous deposition. Note the segmental

lesion in one glomerulus (arrow). PAS x 125 47

Figure 2.40 Glomerulus in an area of chronic inflamma­

tion shmving severe sclerosis of Bo1:nnan' s capsule

1vi

th collagenous adhesion

(

arroi·r

)

to the adjacent glorneru.lar tuft. HE x 320 4

7

Figure 2.4-l Renal cyst

(c)

associated -vrith qhronic inflammatory exudate of lymphocytes and plasma cells in adjacent renal tiDsue.

HE X 320 47

Figure 2.42 Renal cyst

(c)

vrith no inflammatory changes

in the adjacent renal parenchyma. HE x 125 48 Figure 2.43 Echinococcus granulosu: cyst shm·Iing

laminated cuticle

(Le)

adjacent to the

collagenous tissue in the second layer of the cyst

(cc).

HEx320

Figure 2.44 Carcinoma. Acinar and tubuloacinar

arrangement of neoplastic cells supported by a slight reticu�ar stroma. The cells are polyhedral to ovoid vri th abundant,

slightly vacuolated, eosinophilic cytoplasm.

48

RE X 320 49

Figure 2.45 Carcinoma.

A

more densely, cellular area of tumour to that shovrn in figure 2.44 showing greater cellular pleomorphlsm.

HE X 320 49

Figure 2.46 Carcinoma showing dystrophic calcification

(

v1hi te arrow

)

and a band of fibrous tissue representative of that dividing the tumour

into lobules. HE x 320 49

(12)

xi

Foll owing page Figure 2 .47 Rene.l a denoma . The tumou:r i s well

encapsulated and the neoplastic cells are arranged in acinar, tubular and

papillary f ormations.

HE x 125

49

Figure 2. 4 8 Na l igPant l�'Tllphoma. Monotonous regularity of lymphoid cells with round,ov0id or indented pachychromatic nucle i and inapparent

nucle oli .

llli x 500 50

Figure 2.49 Focal granuloma in renal c ortex, probably of parasitic origin, shoHing central are a of case ous ne crosis and eosinophilic

debris (N). Surrounding this material are

several polykaryons ( arr ovis ) . The adjacent

tis sue is heavily infiltrated by lymphocytes,

plasma cells, p h ag o cyt e s

and

occasional

e osinophils.

HE x 320 50

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