private study only. The thesis may not be reproduced elsewhere without
the permission of the Author.
THE PATHOLOGY OF KIDNEY DISEASES IN SHEEP
A t,hesis presented in partial fulfilment
(3Cf/o)
of therequirements for the degree of l\laster of Philosophy in VP.tcrinary Pathology at T·1assey University.
Pavlos G-eorgiou Toum.azos
1981
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<;.ffof 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 .
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 thesi
sto
pro
vi
de a co
mpa riso
n vri ththe l
esions foundin
a surveyof
kidneys jn slaughter-house �illed sh
eep. The p resentation of results of this survey form the major part of this thesis and
provide
s
information onth
ese diseases relativeto large populations of
sheep
uhich
is only sparsely report
ed elsevrhere. The abnormal kidneys under study were obtained from 444- of13,988
sheep sla
ughtered over aconsecutive five day per
i
odat the
Borth-v;ick's
freezing
\lOrks,Longburr1
in January
1980.
The prevalenceof
renal
diseasevras 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 at otal
of830 dise11sed
ki
dneys l•rere founrlancl
thesevrere categorized into seven groups according to the major
pathologic&.l
le
si
on in each. Ins ome kidneys
addi b onB-1 mi
nor lesions vrere present, making a total of 1212 macroscopic lesi
ons identified.White spots and strealr...s conG
t
i tuted the majorgross p8.thological
finding in
188
kidneys; pale, red andbrovm discolourati on in 174,
120 and179
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
chronic, mainly multifocal inflammation of the cortical interstitium.
Similar
but
radially disposed inflammatory lesions with marked fibrosis occurred in thescarred kidneys . The
pattern of these lesions suggested a haematogenous di::;tribution of ap
athogen
in the spotted kidney.s vJhile the scarred kidneys wereprobably
the result of ascending inflammation or infarctive processes.Kidneys vli
th pale
discoloura tion showed mild tomoderately
severenephrosis
of the corticalepithelial cells� while kidneys vli
thbrovm
discolouration shovred corticotubular
intracyt oplasmic
and intralumenal haemosi
derindeposition .
In somekidneys
haemosiderosis wa::: restricted to areas of scarring. Red discoloured kidneysshm·red
patchyor
diffuse
congestion.
Cystic lesions were either
para s i tic or
theresult of urinary
retention
caused by blockage of tubules .
In thelatter,
tha block�ge ,._,.as either congenital or associated with chronic inflammation.With the exception of
nephrosis
and conges-tion all thelesions were chronic
in nature and for most ofthem
a definitive aetiologicaldiagnosis vras not established. In fact, in only those lesions containing
Echinoc o c cus
granulosus hydat
idc ys t s
could sucha
diagnosisbe
made.Additional studies are indicated for the provision of further information on
(
a)
the prevalence of renal diseases in differentgevgraphical locations,
( b)
variation of disease types from area to area and(
c)
the causes of the lesions identified from this type ofinvestigation.
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
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·rith renal l e sio ns .
Hi s t ogra m shovTing the gr oss pathol ogical featu r
esof 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
if
fus
escarring of
therenal
parenchyma.The incised surface of t his kidney
is shovmin figure 2 .14 .
Pale Slwllen kidney (N o . 99). N o
te the pallor of
theouter 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
conge 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
eyon 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
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
vrhite 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
yma .
a ) M ul t i p le , slightly d epr
ess e d ill
defined s cars in the s
ubcap 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
allareas
ofthe 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
de 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
occ
us 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.
33Following page Figure 2.18
Figure
2.19
Figure
2.20
Renal abscessation
(
No.200) .
a)
The kidney conLa:i.ns an enc
apsu
la
ted
caseous abscess bnlging from the capsular surface.
b)
Thecut section of the
sam8 kidney.Renal
carcinoma (Ho. 237) .
a
)
Disto
�t
io
n of the left pole oft h
ekidney by
a renal co.J:cinoma.b) Cut sectior-1 of
the kidney shmvingthe
sl
i
ght
ly
encaps-..11a·�ccllobulated
tumour with extensive areasof
necrosis andh
aemo
rrhage.
Renal lymphoma
(lTo. 236).
a
)
Distortion of a kidney by a lymphomaoccupyin& the l(�f L
polar >;tnd
hilar zones.b)
Theincised
surf:>.ce sho1·1ingadditional
focal twnour mnssec in
the
corticaltissue.
Figure 2. 21 Nodule of
undctcr:r;.Lr_ed cause(
ki
dne
yNo.
12 ) .
Figure
2.22
Figur�
2 . 23
a
)
A fib
ro
usno:iclle elei.Tated slightly
above the cap::;ular surface.
b)
Notet
heconcentric lamination
ofthe l
esion upon sectionJ.ng.
Chronic parasitic noJule (kidl1cy No. 20).
a)
Appearance on capsularsurface .
b
)
On incisionthe.� uell defined
corticalnodule
was hard andcontained gritty mate rial.
Hassive renal infarct
(
no.kidney on left
is swol
len, haemorrhagic and necrotic.thrombus is
p1·esent in the
The right kidney is normal.
2 49). 'rhe diffusely
An o
r
gani
zi n
g renal vein.l<'igure
2.24.
Nephr
osis.
Moderately severe �cat t
ered d
eg
ene
rat
ive changes in epithelial cells of proximal convolutedt u
bu
les . Note
pyknotic
nuclei and cell loss. Thed
ilat
ed
39
39
39
40
40
40
tubules
contain hyalineg
ranu
lar casts. HEx 320 41 Fi.gure 2.25
Nep
hrosi
s.
Lesionsa
re similar but less
severe than those
infigure 2 .24.
HEx 400 41 Figure 2.26 Haem osiderosis.
"ifuolemount" 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 ofepithelial cells of proximal convoluted tubules ( arrovm).
Granular casts are present in the tubular
lumena.
HEx 320 42
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 x125
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. HEx125
Scarred J:r.idney. An extensive iveclgeshaped cortical scar associated 'lri th marked tubular and glomerular atrophy
.
HE x50
Renal papilla
(
on left)
and pelvis(
onright
)
of a kidney vli th extensive radial scarring. Note the reduced numbers of tubules, several containing casts(
broadarrows
)
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. HEx 50
Renal papilla
(
on left)
and pelvis(
onright
)
of a severely scarred kidney showing extensive replacement of tubules byfibrosis. 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
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
(
narrowarrmvs
)
. HE x 125 4 7Figure 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 changesin the adjacent renal parenchyma. HE x 125 48 Figure 2.43 Echinococcus granulosu: cyst shm·Iing
laminated cuticle
(Le)
adjacent to thecollagenous tissue in the second layer of the cyst
(cc).
HEx320Figure 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 tumourinto lobules. HE x 320 49
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 12549
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 50Figure 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
andoccasional
e osinophils.
HE x 320 50