LAPORAN KAJIAN KASUS

PENYAKIT UROGENITAL
“RENAL DYSPLASIA” PADA ANJING

Oleh
Tifany Beby Sonia B
2009612032
KELOMPOK 18A

LABORATORIUM ILMU PENYAKIT DALAM

PENDIDIKAN PROFESI DOKTER HEWAN
FAKULTAS KEDOKTERAN HEWAN
UNIVERSITAS UDAYANA
2021
 PENDAHULUAN
Renal Dysplasia adalah penyebab umum gagal ginjal pada anjing muda. Renal
dysplasia didefinisikan sebagai disorganisasi dalam perkembangan parenkim ginjal, dengan
diferensiasi yang bersifat abnormal. Pada semua spesies hewan domestik, Renal Dysplasia
dapat bersifat herediter atau dapatan. Hewan yang terkena menunjukkan tanda-tanda klinis
penyakit ginjal kronis awal, biasanya antara 3 bulan sampai 3 tahun. Perubahan tersebut
meliputi duktus metanefrik persisten yang dikelilingi oleh mesenkim primitif, glomerulus dan
tubulus janin, serta jaringan fibrosa interstisial yang abnormal (Cruz et al., 2019). Anjing ras
Shih Tzu, Lhasa Apso, Golden Retriever, Alaskan Malamute, dan Chow Chow secara genetik
lebih rentan terhadap penyakit ini (Polzin et al., 2008; Cruz et al., 2019).

REKAM MEDIK
Anamnesa dan Signalment
Kasus pertama diambil dari case report Cruz et al pada tahun 2019, pada seekor
anjing ras Maltese, berjenis kelamin jantan, dan berusia 1 tahun. Pasien datang setelah
direferensikan oleh klinik lain dengan keluhan polyuria dan polydipsia selama 3 hari,
muntah, diare berdarah, berat badan berkurang, apathy dan anorexia.
Kasus kedua diambil dari case report yang diterbitkan oleh Canadian Veterinary
Journal pada tahun 2011 oleh Kim et al pada seekor anjing ras Mongrel, usia 1 tahun,
berjenis kelamin betina, dengan keluhan anorexia dan muntah dalam 4 hari sebelumnya.
Tidak ada riwayat konsumsi obat atau tertelan racun oleh pasien. Pasien sudah mendapatkan
vaksinasi terkini. Client juga mengeluhkan, hewan menjadi lebih lemah dan kecil
dibandingkan hewan peliharaan yang lain. Pasien menunjukkan gejala polydipsia, polyuria
dan muntah secara intermiten sejak lahir.
Kasus ketiga diambil dari case report Ohara et al, pada anjing ras Shih Tzu, berumur
5 bulan, berjenis kelamin jantan dengan keluhan polyuria dan polydipsia sejak berumur 2
bulan, serta muntah dan lemas selama beberapa hari.

Pemeriksaan Klinis
Hasil pemeriksaan klinis kasus pertama yaitu, BCS pasien adalah 3 dari 9, halitosis,
suhu tubuh 37.5 C, dan mukosa hipokromik.
Pemeriksaan klinis pada kasus kedua, menunjukkan hewan mengalami dehidrasi
hebat (8% - 10%), membran mukosa pucat, CRT yg lama, dan halitosis. Pasien kurus dan
abdomen tegang pada saat dipalpasi.
Dilakukan pemeriksaan klinis hewan kasus ketiga, dengan hasil hewan mengalami
dehidrasi dan lemas.

Pemeriksaan Penunjang
Kasus 1:
Berdasarkan pemeriksaan klinis dan anamnesa, dicurigai bahwa terjadi neprophaty.
Pemeriksaan dilanjutkan dengan melakukan CBC, serum biochemistry, urinalisis dan USG
pada seluruh bagian abdomen.
CBC menunjukkan hematokrit 18%, hemoglobin 7,2 g/dL, kadar eritrosit di bawah
nilai normal (2,56 juta/mm³), serta nilai retikulosit 5.000/μL, menunjukkan anemia
hipokromik, normositik, dan generatif. Tes biokimia menunjukkan peningkatan kadar ureum
(530 mg/dL) dan kreatinin (10,2 mg/dL), hiperproteinemia (7,9 mg/dL) karena
hiperglobulinemia (4,7 g/dL), dan sedikit peningkatan alanin aminotransferase (100 U/L).
Ringkasan urin menunjukkan kepadatan urin yang rendah (1005), proteinuria (300
mg/dL) dan pH 7,0. Sedimen menyajikan sel skuamosa dan ginjal, >5 sel darah merah per
bidang dan >3 leukosit per bidang.
Pemeriksaan ultrasonografi menunjukkan bahwa ginjal secara bilateral berkurang
ukurannya (lebih menonjol di ginjal kiri), serta hilangnya definisi kortiko-meduler, dengan
formasi kistik dengan ukuran berbeda pada permukaan ginjal dan area hyperechoic di
parenkim ginjal. Perubahan ini konsisten dengan nefropati kronis bilateral.

Kasus 2:
Pemeriksaan penunjang dilakukan dengan melakukan pemeriksaan CBC dengan hasil
leukopenia (5400 sel/mL; rentang referensi (RR): 6000 hingga 17.000 sel/mL), dan anemia
normositik, normokromik, anemia nonregenerative (hematokrit (Hct), 27,5%; RR: 35%
hingga 55%). Pemeriksaan biokimia menunjukkan konsentrasi tinggi BUN (.200 71,4
mmol/L; RR: 2,9 hingga 11,1 mmol/L) dan kreatinin (892 mmol/L; RR: 70,7 hingga 141,4
mmol/L), hiperglikemia ringan (7,2 mmol/L; RR: 3,9 hingga 6,5 mmol/L), hiperkalsemia (3,6
mmol/L; RR: 1,9 hingga 2,8 mmol/L), dan hiperfosfatemia (2,13 mmol/L; RR: 0,68 hingga
2,03 mmol/L). Analisis urin yang dikumpulkan dengan cystocentesis mengungkapkan berat
jenis 1,021, pH 7,0, proteinuria (1+), dan glukosuria (1+). Tidak ada kelainan signifikan yang
terdeteksi pada pemeriksaan sedimen urin dan kultur urin tidak dilakukan
Radiografi perut mengungkapkan detail perut yang buruk karena kondisi tubuh anjing
yang kurus kering. Ultrasonografi perut mengungkapkan ginjal kecil dengan hilangnya
arsitektur normal dan perbedaan kortikomedullary yang buruk secara bilateral. Ginjal kanan
memiliki 3 kista anechoic besar dan peningkatan akustik distal yang kuat. Beberapa struktur
bulat berbatas tegas, berdinding tipis, dengan berbagai ukuran yang mengandung cairan
anechoic terdeteksi di ginjal kanan; lesi kistik di ginjal kiri tidak terdefinisi dengan baik
karena bayangan akustik umum yang kuat yang disebabkan oleh hiperekogenesitas kortikal
(Gambar 1).
 Gambar 1. Sonografi ginjal kiri (A dan B) dan kanan (C dan
D). Ginjal kecil, dengan hilangnya arsitektur normal karena lesi kistik
dan bayangan akustik distal. Anechoic, multipel, berbatas tegas,
berdinding tipis, struktur bulat dengan berbagai ukuran terdeteksi di
ginjal kanan.

Kasus 3:
Pemeriksaan penunjang dilakukan pada hewan kasus ketiga. Pemeriksaan radiografi
dilakukan dengan hasil tidak terdeteksinya ginjal hewan.

Diagnosa dan Prognosa

Berdasarkan laporan pada ketiga jurnal, diagnosa dilakukan dengan cara melihat hasil
pemeriksaan klinis hewan dengan diagnosa penunjang. Meskipun ultrasonografi membantu
dalam diagnosis penyakit ginjal displastik multikistik, diagnosis diperkuat dari: analisis
histologis (Kim et al., 2011). Prognosis displasia ginjal pada anjing umumnya buruk.
Kebanyakan pasien meninggal dalam beberapa hari setelah terapi suportif atau dilakukan
euthanasia (Ohara et al., 2001).

Treatment dan Pengobatan

Kasus 1:
Pada kasus pertama, sebagai bagian dari perawatan, transfusi darah diminta, namun
tidak diizinkan oleh pemiliknya. Untuk mengatasi anemia, suplemen vitamin berbahan dasar
asam folat dan zat besi (Metacell Pet®) dosis 1 mL/10 kg per oral setiap 24 jam. Pengobatan
suportif dengan ranitidin hidroklorida dalam dosis 1 mL/kg, subkutan, setiap 8 jam,
metoklopramid (Plasil®) dalam dosis 0,5 mg/kg, setiap 8 jam melalui rute intramuskular dan
omeprazole (Gaviz®) pada dosis 1 mg/kg, secara oral setiap 24 jam, diresepkan untuk
muntah. Pasien menjalani terapi cairan parenteral (NaCl 0,9%) dengan perkiraan dosis 40
mL/kg/hari selama tiga hari. Selain itu, pengobatan suportif diresepkan dengan suplemen
vitamin hiperkalori (Nutralife intensiv®) takaran setiap 24 jam, Renadog® 2 takaran kecil
setiap 24 jam. Setelah 3 hari, pemeriksaan ureum (325 mg/dL) dan kreatinin (5,25 mg/dL)
diulang, yang menunjukkan perbaikan signifikan, dengan perburukan klinis kondisi pasien.
Satu minggu setelah memulai pengobatan, pasien kembali ke klinik dengan keluhan kejang,
yang diobati dengan diazepam (1 mg/kg IV), tetapi tidak berhasil, yang berpuncak pada
kematian. Setelah otorisasi pemilik, nekropsi dilakukan.

Kasus 2:
Pengobatan dengan diet rendah protein (Resep Diet Canine k/d, kaleng; Hill's Pet
Products, Topeka, USA), ranitidine HCl (Ranis; Skynewpham, Siheung, Korea), 2 mg/kg
berat badan (BB), BID, PO, dan gel aluminium hidroksida kering (Amphojel; Ildong,
Ansung, Korea), dimulai 50 mg/kg BB, BID, PO. Terapi cairan awal dengan NaCl 0,9%
diberikan melalui kateter sefalik dengan kecepatan 20 mL/jam dengan pengumpulan urin
melalui kateter urin. Kecepatan infus diubah menjadi 15 mL/jam setelah 3 jam terapi cairan
awal. Anjing itu di-eutanasia setelah 2 hari dirawat di rumah sakit karena prognosis yang
buruk dan tanda-tanda klinis yang memburuk.

Kasus 3:
Pada kasus ketiga, pasien diberikan terapi cairan dan obat glukokortikoid untuk gagal
ginjal kronis. Terlepas dari terapi simptomatik yang diberikan untuk gagal ginjal kronis,
hewan mati sehari setelah diberikan pengobatan.

Pembahasan
Penyakit ginjal pada anjing seringkali tidak terlihat sampai ginjal mulai gagal. Pemilik
cenderung melewatkan tanda peningkatan minum dan buang air kecil, kecuali mereka
menyadari hal tersebut dapat berakibat pada kecenderungan berkembangnya penyakit ginjal.
Renal Dysplasia adalah penyakit ginjal anjing yang berpotensi fatal, sangat sulit dikenali
karena anjing yang terkena mungkin tidak pernah menunjukkan tanda-tanda khas, sementara
gejala yang timbul mungkin tampak normal selama bertahun-tahun sebelum tanda-tanda yang
lebih serius tampak. Sementara itu, anjing pembawa dapat mewariskan mutasi genetik kepada
keturunannya, meskipun pada anjing pembawa tersebut tidak menunjukkan gejala yang
berarti. Perkembangbiakan hewan-hewan ini dengan demikian menyebarkan penyakit ke
seluruh breed (Raval et al., 2014).
Displasia ginjal adalah perkembangan yang tidak teratur dari parenkim ginjal karena
diferensiasi bersifat anomali. Jika perkembangan normal dari collecting duct system
("morfogenesis percabangan ginjal") terganggu, maka displasia ginjal dapat terjadi. Pada
embriogenesis normal, perkembangan metanefros dimulai sebagai evaginasi dari duktus
mesonefrik yang tumbuh menjadi massa sel mesenkim (blastema metanefros). Perkembangan
ginjal dan ureter yang normal tergantung pada interaksi tunas ureter dan blastema metanefrik.
Displasia ginjal adalah gangguan perkembangan yang disebabkan oleh interaksi yang tidak
tepat antara tunas ureter dan blastema metanefrik. Ini dapat berupa keturunan atau akibat dari
infeksi neonatal seperti virus panleukopenia kucing, virus diare virus sapi, atau infeksi virus
herpes anjing.
Tanda-tanda klinis displasia ginjal termasuk anoreksia, lesu, penurunan berat badan,
poliuria, polidipsia, dan muntah. Rentang umur hidup hewan tergantung pada tingkat
keparahan cacat saat lahir. Hewan dengan cacat sedang sampai berat mungkin tidak memiliki
gejala sampai fungsi ginjal berkurang 70-75%. Gangguan ini bisa memakan waktu bertahun-
tahun untuk berkembang. Dalam sebagian besar kasus displasia ginjal anjing yang
dipublikasikan, ginjalnya lebih kecil dari biasanya (Picut dan Lewis, 1987). Pada
pemeriksaan nekropsi ginjal hewan yang mengalami Renal Dysplasia tampak pucat,
hipotrofik dengan konsistensi keras, permukaan kapsul tidak teratur yang mengandung kista
kortikal multipel dengan ukuran berbeda, dan proporsi kortiko-meduler yang berubah (Cruz
et al., 2019; Kim et al., 2011).
 DAFTAR PUSTAKA

Cruz, T.N.D.A.O., Silva, J.T., Silva, F.L., Carlos, R.S.A. 2019. Renal Dysplasia in a Maltese
Dog. Acta Scientiae Veterinarie 2019. 57(Sippl1); 410: 1-5

Kim, J., Choi, H., Lee, Y., Jung, J., Y, S., Lee, H., Lee, H., 2011. Case report Multicystic
Dyplastic Kidney Disease in a Dog. Canadian Veterinary Journal 2011; 52:645-649

Ohara, K., Kobayashi, Y., Tsuchiya, N., Furuoka, H., Matsui, T. 2001. Renal Dysplasia in a
Shih Tzu Dog in Japan. The Journal of Veterinary Science 63(10): 1127-1130

Raval, S.H., Joshi, D.V., Patel, B.J., Patel, J.G., Karantim A.M., Panchbuddhe, B.N. 2014.
Renal Dysplasia in Labrador Male Dog: A Case Report. Indian Journal Veterinary
Pathology 39(1): 87-89

Picut, C.A., and Lewis, R.M. 1987. Microscopic Features of Canine Renal Dysplasia.
Veterinary Pathology 24: 156-163
 Acta Scientiae Veterinariae, 2019. 47(Suppl 1): 410.

CASE REPORT ISSN 1679-9216

Pub. 410

Renal Dysplasia in a Maltese Dog

Thais Nascimento de Andrade Oliveira Cruz1, Juneo Freitas Silva2, Fabiana Lessa Silva3,
& Renata Santiago Alberto Carlos3

ABSTRACT
Background: Renal dysplasia (RD) is a common cause of renal failure in young dogs. It is defined as a disorganization in
renal parenchymal development, with abnormal differentiation. In all domestic animal species, RD may be hereditary or
acquired. The affected animals show clinical signs of early chronic kidney disease, usually between 3 months to 3 years
of age. The alterations include persistent metanephric ducts surrounded by primitive mesenchyme, glomeruli and fetal
tubules, and abnormal interstitial fibrous tissue. We aimed to report the case of a 1-year-old canine with renal dysplasia.
Case: A 1-year-old male Maltese dog experiencing polyuria, polydipsia, recurrent episodic vomiting, bloody diarrhea,
weight loss, apathy, and anorexia was referred to a private clinic in the municipality of Itabuna-Bahia. Physical exami-
nation revealed hypochromic mucosa, dehydration estimated at 8%, rectal temperature of 37.5ºC, halitosis, and a body
score of 3 out of 9. Laboratory abnormalities included hematocrit of 18%, with hypochromic normocytic aregenerative
anemia, azotemia (urea - 530 mg/dL, creatinine - 10.5 mg/dL), hyperglobulinemia (4.7 g/dL), low urinary density (1005),
proteinuria (300 mg/dL), and urinary pH - 7.0. Ultrasonography revealed bilateral small kidneys with loss of cortico-
medullary definition, cystic formations of different sizes on the renal surface, and hyperechoic areas in the parenchyma;
these alterations were suggestive of bilateral chronic nephropathy. Considering the clinical, hematological, biochemical, and
ultrasonographic presentation associated with the age of the patient, renal dysplasia was suspected. The patient’s clinical
condition progressed to loss of consciousness and convulsions, followed by death. Necropsy revealed pale, hypotrophic
kidneys with firm consistency, irregular capsular surface containing multiple cortical cysts of different sizes, and altered
cortico-medullar proportion.. Kidney fragments were sent to the Laboratory of Histopathology of the State University of
Santa Cruz. Histopathological analysis revealed a marked alteration of renal architecture with glomeruli and immature
tubules (adenomatous aspect), persistent primitive mesenchyme, and remnants of the metanephric ducts, as well as tubular
dilatation associated with marked interstitial fibrosis, discrete lymphohistiocytic interstitial nephritis, and multifocal areas
of mineralization.
Discussion: The clinical changes observed in the present case occurred as a consequence of chronic kidney failure caused
by RD and included anorexia, apathy, vomiting, bloody diarrhea, polyuria, polydipsia, and dehydration. These alterations
were also found in other reported cases. The macroscopic findings were similar to those described in the literature and are
characteristic of chronic kidney disease: small, firm, pale-colored kidneys. Microscopic changes of renal dysplasia include
persistent metanephric ducts surrounded by primitive mesenchyme, glomeruli and fetal tubules, and abnormal interstitial
fibrous tissue. In the histopathological renal evaluation in the present report, morphological alterations compatible with
the described alterations in the literature were observed, thus allowing the diagnosis of renal dysplasia. Renal dysplasia
can affect young dogs of different breeds, causing clinical manifestations of chronic kidney disease. In view of this, this
disease should be included as a differential diagnosis in patients under 3 years old who present signs of chronic nephropathy.
Keywords: dog, juvenile kidney disease, renal insufficiency.

DOI: 10.22456/1679-9216.93264
Received: 8 April 2019 Accepted: 15 July 2019 Published: 11 August 2019
1
PhD student at the Graduate School of Animal Science (PPGCA), Department of Biological Sciences & Department of Agrarian and Environmental
2 3

Sciences, Veterinary Medicine Course, State University of Santa Cruz (UESC), Ilhéus, BA, Brazil. CORRESPONDENCE: R.S.A. CARLOS [rsacarlos@
uesc.br - Tel: +55 (73) 98818-4025.] Rua Lauro Farani de Freitas n. 101, ap. 704. CEP 45.652-160 Ilheus, BA, Brazil.

1
T.N.A.O. Cruz, J.F. Silva, F.L. Silva & R.S.A. Carlos. 2019. Renal Dysplasia in a Maltese Dog.
INTRODUCTION
Chronic renal failure (CRF) is a clinical
syndrome and an important cause of morbidity and
mortality in dogs and cats [2,13]. Regardless of the
etiology, during the evolution of a chronic renal dise-
ase, glomerular, tubular, and interstitial involvement of
the glomerulus occurs, resulting in morphofunctional
changes and consequent reduction in the glomerular
filtration rate (GFR) [13]. It is characterized by a decre-
ased ability to concentrate urine, clinically manifested
by polyuria, and by the difficulty to maintain water
and electrolyte homeostasis [2]. When CRF occurs in
young dogs, it is usually associated with juvenile or
familial nephropathies [4,7], which include disorders
such as agenesis, renal dysplasia and hypoplasia,
primary cystic disease, tubulo-interstitial diseases,
glomerulopathies, and tubular dysfunction [7].
Renal dysplasia (RD) is a common cause of
renal failure in young dogs. It is defined as disorganiza-
tion in renal parenchymal development with abnormal
differentiation [7,10]. In all species, RD may have a
hereditary or acquired cause [5]. Dogs of the Shih Tzu,
Lhasa Apso, Golden Retriever, Alaskan Malamute, and
Chow Chow breeds are genetically more susceptible
to this disease [10]. Affected animals present with
clinical manifestations of early chronic kidney disease,
usually between 3 months to 3 years of age [5,11].
Dysplastic kidneys present characteristics of chronic
nephropathy with morphological alterations divided
into three groups: primary dysplastic lesions, compen-
satory alterations, and degenerative and inflammatory
lesions [13]. This article reports the case of a 1-year-old
Maltese dog with renal dysplasia who developed CRF.
CASE
A 1-year-old male Maltese dog was referred
to a private clinic in the municipality of Itabuna-BA,
with complaints of polyuria and polydipsia for 3 days,
episodes of recurrent vomiting, bloody diarrhea, weight
loss, apathy, and anorexia. Physical examination showed
hypochromic mucosa, marked dehydration, temperature
of 37.5ºC, halitosis, and a body score 3 out of 9 [9].
Considering the clinical examination and the
anamnesis, a suspicion of nephropathy was estab-
lished, and investigations including Complete Blood
Count (CBC), serum biochemistry, urinalysis, and
ultrasonographic examination of the total abdomen
were conducted.
2
Acta Scientiae Veterinariae. 47(Suppl 1): 410.
CBC revealed hematocrit of 18%, hemoglobin
of 7.2 g/dL, erythrocyte level below normal values
(2.56 million/mm³), as well as reticulocyte values of
5,000/μL, evidencing hypochromic, normocytic, and
aregenerative anemia. Biochemical tests demonstrated
elevation of urea (530 mg/dL) and creatinine (10,2
mg/dL) levels, hyperproteinemia (7,9 mg/dL) due to
hyperglobulinemia (4,7 g/dL), and a slight increase of
alanine aminotransferase (100 U/L).
Urine summary revealed low urinary density
(1005), proteinuria (300 mg/dL) and pH 7.0. The sedi-
ment presented squamous and renal cells, >5 red blood
cells per field and >3 leukocytes per field.
The ultrasonographic examination showed
that the kidneys were bilaterally reduced in size (more
pronounced in the left kidney), as well as loss of the
cortico-medullary definition, with cystic formations
of different sizes on the renal surface and hyperechoic
areas in the renal parenchyma. These changes were
consistent with bilateral chronic nephropathy.
Considering the clinical, hematological, bio-
chemical, and ultrasonographic presentation associ-
ated with the age of the patient, renal dysplasia was
suspected.
As part of the treatment, a blood transfusion
was requested, which was not authorized by the owner.
In order to treat the anemia, a vitamin supplement
based on folic acid and iron (Metacell Pet®)1 in the dose
of 1 mL/10 kg orally every 24 h. Supportive treatment
with ranitidine hydrochloride in the dose of 1 mL/kg,
subcutaneously, every 8 h, metoclopramide (Plasil®)2
in the dose of 0.5 mg/kg, every 8 h by intramuscular
route and omeprazole (Gaviz®)3 in the dose of 1 mg/
kg, orally every 24 h, was prescribed for vomiting. The
patient underwent parenteral fluid therapy (NaCl 0.9%)
at an estimated dose of 40 mL/kg/day for three days.
In addition, supportive treatment was prescribed with
hypercaloric vitamin supplement (Nutralife intensiv®)4
2 measures every 24 h, Renadog®5 2 small measures
every 24 h. After 3 days, investigations for urea (325
mg/dL) and creatinine (5.25 mg/dL) were repeated,
which showed a significant improvement, with clini-
cal worsening of the patient’s condition. One week
after begining of treatment, the patient returned to the
clinic with convulsive episodes, which were treated
with diazepam (1 mg/kg IV)3, but without success,
culminating with death. After authorization of the
owner, necropsy was performed.
T.N.A.O. Cruz, J.F. Silva, F.L. Silva & R.S.A. Carlos. 2019. Renal Dysplasia in a Maltese Dog.
At necropsy, the kidneys were very pale, hy-
potrophic, with a firm consistency, and an irregular
capsular surface containing multiple cystic spaces of
different sizes in the renal cortex (Figure 1). A reduced
cortico-medullary relation was observed on the cut
surface (Figure 1). In addition to renal changes, areas
of ulceration were observed in the stomach and small
intestine. Kidney fragments were sent to the Labo-
ratory of Histopathology of the State University of
Santa Cruz. Microscopic analysis revealed a marked
alteration of the renal architecture with glomeruli and
immature tubules (adenomatous aspect), persistent
primitive mesenchyme and remnants of metaneph-
ric ducts, as well as tubular dilation associated with
marked interstitial fibrosis, discrete lymphohistiocytic
interstitial nephritis, and multifocal areas of mineral-
ization (Figure 3).
Figure 1. Macroscopic view of the cut surface of the dysplastic kidney of
a 1-year-old Maltese dog. Note the reduced kidney size, white color, and
altered cortico-medullary relationship (black arrow).
Figure 2. Histological section of the dysplastic kidney (100×). Note the
remaining mesonephric ducts (black arrow).
3
Acta Scientiae Veterinariae. 47(Suppl 1): 410.
DISCUSSION
The clinical changes observed in the subject
of the present report occurred as a consequence of
chronic kidney failure caused by RD and included
anorexia, apathy, vomiting, bloody diarrhea, polyuria,
polydipsia, and dehydration. These alterations have
also been reported in cases reported by other authors
[6,13,14]. Polyuria and polydipsia result from the in-
ability of the kidneys to concentrate urine even though
the animal is dehydrated, due to loss of hypertonicity
of the medullary interstitium and high filtrate flow in
the remaining nephrons [7]. Anorexia and vomiting
are the result of stimulation of the chemoreceptor
zone by uremic toxins, gastritis that develops due to
direct injury by uremic toxins, and by increased gastrin
concentrations, causing excessive production of gastric
acid and production of ammonia from urea [2].
The aregenerative anemia presented by the
patient was mainly due to the reduction in erythropoi-
etin production. This is perhaps the most significant
hematologic finding described in the literature [8].
Increased urea and creatinine serum concentrations
confirmed renal failure, a terminal condition of pa-
tients with RD that has also been described by other
authors [8]. In cases of aregenerative anemia second-
ary to CRF, the most effective therapy is with human
erythropoietin; however, the medication is not easily
Figure 3. Histological cut of the dysplastic kidney (400×). The fetal
glomeruli (black arrow) and dilated renal tubules (green arrow) are visible.
T.N.A.O. Cruz, J.F. Silva, F.L. Silva & R.S.A. Carlos. 2019. Renal Dysplasia in a Maltese Dog.
accessible in the region. The treatment instituted to
control anemia was included the use of multivitamins
based on folic acid, and ferrous sulfate. Some animals
may present improvement of anemia with only vitamin
supplementation [12].
The animal was administered fluid therapy
aimed at the correction of dehydration and consequent
improvement of renal perfusion. Polyuria, vomiting,
and diarrhea contribute to dehydration, reduction
of renal perfusion, and worsening of renal function.
Therefore, fluid therapy with crystalloids (Ringer’s
lactate or 0.9% NaCl) is indicated [7]. Gastrointesti-
nal disorders contribute to anorexia and weight loss
[7]. The treatment performed in this case to control
gastrointestinal complications is in accordance with
the literature, which recommends the administra-
tion of drugs such as ranitidine hydrochloride and
omeprazole [12]. Omeprazole specifically inhibits
the H+/K+-ATPase enzyme in the parietal cells of the
stomach, whereas ranitidine has histamine antagonistic
action, reducing acid secretion in the stomach [12].
Metoclopramide has an antiemetic action, in addition
to increasing the tone and strength of gastric contrac-
tions and relaxing the pyloric, duodenal, and jejunal
sphincters, resulting in accelerating gastric emptying
and intestinal transit [12].
Ultrasound abnormalities of renal dysplasia
may exhibit a variety of characteristics depending
on the degree of organ involvement by inflammatory
processes and fibrosis, which occurs as a consequence
of dysplasia [1]. However, the alterations found in this
case corroborate with those cited in the literature, which
include irregular edges, loss of corticomedullary pro-
portion and delimitation, and presence of cysts that are
identified ultrasonographically as areas of defined and
regular limits, presenting anechoic content within them.
The macroscopic findings were similar to those
described in the literature [12] and are characteristic
of chronic renal disease, mainly due to the second-
ary fibrosis process, resulting in small, firm, and
REFERENCES
1 Babicsak V.R., Zardo K.M., SSantos D.R., Bellota A.F., Oliveira H.S., Mamprim M.J., Machado V.M.V. & Vulcano
L.C. 2012. Contribuição da ultrassonografia para o diagnóstico da displasia renal em cães. Veterinária e Zootecnia.
19(2): 181-185.
2 Guimarães L.L.B., Reis M.O., Hesse K.L., Boabaid F.M., Pavarini S.P., Sonne L. & Driemeier D. 2014. Achados
patológicos em caninos com displasia renal no Sul do Brasil. Pesquisa Veterinária Brasileira. 34(12): 1227-1230.
4
Acta Scientiae Veterinariae. 47(Suppl 1): 410.
pale-colored kidneys. Reports of dysplastic kidneys
with presence of cysts have also been reported by other
authors [12,14]. These cysts may be multiple and of
varying sizes, from 0.1 to 5 cm in diameter, and may
be distributed on the subcapsular and cut surface [12].
At cut surface, attention is drawn to cortical-medullary
alteration and dilation of the pelvis, similar to descrip-
tions in the literature [12]. The differential diagnosis
for this type of macroscopic presentation would be the
terminal kidney that occurs in older dogs [3].
Microscopic alterations in dysplastic kidneys
are classified as: primary lesions characterized by the
presence of immature or fetal glomeruli, mesangial
tissue and persistent metanephric duct, atypical tubular
epithelium, or dysontogenetic metaplasia; compensa-
tory alterations evidenced by metaplasia or glomerular
and tubular hypertrophy; and inflammatory or degen-
erative lesions represented by nephritis/pyelonephritis,
interstitial fibrosis, dystrophic mineralization, cystic
glomerular atrophy, and glomerular lipidosis [6,14].
In the histopathological evaluation of the kidney of
this report, morphological alterations observed were
compatible with the three types of alterations described
in the literature, allowing for a conclusive diagnosis
of renal dysplasia.
Renal dysplasia can affect young dogs of
different breeds, causing clinical manifestations of
chronic kidney disease. In view of this, this disease
should be included as a differential diagnosis in pa-
tients under the age of 3 years who present with signs
of chronic nephropathy.
MANUFACTURERS
1
Ouro Fino Saúde Animal Ltda. Osasco, SP, Brazil.
2
Sanofi, São Paulo, SP, Brazil.
3
Agener União Saúde Animal Ltda. São Paulo, SP, Brazil.
4
Vetnil Ltda, Louveira, SP, Brazil.
5
Bioctal Comércio de Produtos Veterinários Ltda, Valinhos, SP,
Brazil.
Declaration of interest. The authors report no conflicts of
interest. The authors alone are responsible for the content and
writing of the paper.
T.N.A.O. Cruz, J.F. Silva, F.L. Silva & R.S.A. Carlos. 2019. Renal Dysplasia in a Maltese Dog.
Acta Scientiae Veterinariae. 47(Suppl 1): 410.

3 Hunning P.S., Aguiar J., Lacerda L.A., Sonne L., Oliveira E.C. & Haas G.F. 2009. Displasia renal em um cão.
Acta Scientiae Veterinariae. 37(1): 73-77.
4 Laflamme D.P. 2006. Understanding and managing obesity in dogs and cats. Veterinary Clinics Small Animal Practice.
36(6): 1283-1295.
5 Lees G.E. 1996. Congenital Renal Diseases. Veterinary Clinics of North America: Small Animal Practice. 26(6):
1379-1399.
6 Lima S.R., Silva L.A., Dias G.B.G., Lopes L.L., Cruz, R.A.S., Sonne L., Pescador C.A. & Colodel E.M. 2017.
Displasia renal em cães: estudo retrospectivo (2008-2013). Acta Scientiae Veterinariae. 45(Suppl. 1): 184
7 Lustoza M.D. & Kogika M.M. 2003. Tratamento da Insuficiência renal crônica em cães e gatos. Revista Brasileira
de Medicina Veterinária- Pequenos Animais e Animais de Estimação. 1(1): 62-69.
8 Notomi M.K., Kohika M.M., Ikesaki, J.YY.H., Monteiro P.R.G. & Marquesi M.L. 2006. Estudo retrospectivo de
casos de insuficiência renal crônica em cães no período de 1999 a 2002. Brazilian Journal of Veterinary Research and
Animal Science. 43(Suppl.): 12-22.
9 Ohara K., Kobayashi Y., Tsuchiya N., Furuoka H. & Matsui T. 2001. Renal dysplasia in a Shih Tzu dog in Japan.
Journal of Veterinary Medical Science. 63(10): 1127-1130.
10 Polzin D.J., Osborne C.A., Jacob F. & Ross S. 2008. Insuficiência renal crônica, In: Ettinger S.J. & Feldman E.C.
(Eds). Tratado de Medicina Interna Veterinária: Doenças do Cão e do Gato. 5.ed. Rio de Janeiro: Guanabara Koogan,
pp.1721-1751.
11 Picut C.A. & Lewis R.M. 1987. Microscopic features of canine renal dysplasia. Veterinary Pathology. 24(2): 156-163.
12 Rubin S.I. 1997. Chronic renal failure and its management and nephrolithiasis. Veterinary Clinics of North America:
Small Animal Practice. 27(6): 1331–1354.
13 Volkweis F.S., Almeida A.M.S., Wong L., Mulinari F. & Santos Júnior H.L. 2012. Displasia renal em cão da raça
Rotweiller. Arquivo Brasileiro de Medicina Veterinária e Zootecnia. 64(6): 1511-1514.
14 Whiteley M.H. 2014. Allelic variation in the canine Cox-2 promoter causes hypermethylation of the canine Cox-2
promoter in clinical cases of renal dysplasia. Clinical Epigenetics. 6(1): 7.

CR410
http://seer.ufrgs.br/ActaScientiaeVeterinariae

5
Case Report  Rapport de cas

Multicystic dysplastic kidney disease in a dog

Jaehoon Kim, Hojung Choi, Youngwon Lee, Jiyoul Jung, Seongchan Yeon, Hyojong Lee, Heechun Lee

Abstract — A 1-year-old female mongrel dog was evaluated for anorexia and vomiting of 4 days duration.
Abdominal ultrasonographic findings revealed small kidneys with multiple anechoic cysts. The dog was euthanized
due to poor prognosis. A full necropsy was performed, and the histopathologic findings were consistent with
multicystic dysplastic kidney disease.

Résumé — Maladie rénale dysplasique multikystique chez un chien. Une chienne bâtarde âgée de 1 an a été
évaluée pour anorexie et des vomissements d’une durée de 4 jours. Des échographies abdominales ont permis de
révéler la présence de petits reins avec des kystes anéchoïques multiples. La chienne a été euthanasiée en raison
d’un pronostic sombre. Une nécropsie complète a été réalisée et les constatations histopathologiques étaient
conformes à une maladie rénale dysplasique multikystique.
(Traduit par Isabelle Vallières)
Can Vet J 2011;52:645–649

A 1-year-old, 2.5-kg, female mongrel dog was admitted to

the Gyeongsang National University Veterinary Teaching
Hospital with a presenting complaint of anorexia and vomiting
for the previous 4 d. Vaccinations were up-to-date and there was
no history of drug or toxicant ingestion. The owner reported
that the dog was weaker and smaller than its littermates. The
dog had been polydipsic and polyuric and had vomited inter-
mittently since birth.
Case description
Physical examination revealed severe dehydration (8% to 10%),
pale mucous membranes, prolonged capillary refill time, and
halitosis. The dog was emaciated and the abdomen was tense
on palpation.
A complete blood (cell) count revealed leukopenia
[5400 cells/mL; reference range (RR): 6000 to 17 000 cells/mL],
and moderate normocytic, normochromic, non-regenerative ane-
mia [hematocrit (Hct), 27.5%; RR: 35% to 55%]. A biochemical
profile revealed high concentrations of BUN (. 200 71.4 mmol/L;
RR: 2.9 to 11.1 mmol/L) and creatinine (892 mmol/L; RR: 70.7
College of Veterinary Medicine, Jeju National University, Jeju
690-756, Korea (Kim, Jung); College of Veterinary Medicine,
Chungnam National University, Daejeon 305-764, Korea (Choi,
Youngwon Lee); Research Institute of Life Sciences, College of
Veterinary Medicine, Gyeongsang National University, Jinju
660-701, Korea (Yeon, Hyojong Lee, Heechun Lee).
Address all correspondence to Dr. Heechun Lee; e-mail:
lhc@gnu.ac.kr
The first two authors contributed equally to this work.
Use of this article is limited to a single copy for personal study.
Anyone interested in obtaining reprints should contact the
CVMA office (hbroughton@cvma-acmv.org) for additional
copies or permission to use this material elsewhere.
to 141.4 mmol/L), mild hyperglycemia (7.2 mmol/L; RR:  3.9
to 6.5  mmol/L), hypercalcemia (3.6 mmol/L; RR: 1.9 to
2.8 mmol/L), and hyperphosphatemia (2.13 mmol/L; RR: 0.68 to
2.03 mmol/L). Analysis of urine collected by cystocentesis revealed
a specific gravity of 1.021, a pH of 7.0, proteinuria (11), and
glucosuria (11). No significant abnormalities were detected on
examination of the urine sediment and culture of the urine was
not performed.
Abdominal radiographs revealed poor abdominal detail
because of the dog’s emaciated body condition. Abdominal
ultrasound revealed small kidneys with a loss of normal archi-
tecture and a poor corticomedullary distinction bilaterally. The
right kidney had 3 large anechoic cysts and strong distal acoustic
enhancement. Multiple sharply demarcated, thin-walled, round
structures of various sizes containing anechoic fluid were detected
in the right kidney; the cystic lesions in the left kidney were not
as well-defined because of strong generalized acoustic shadow-
ing caused by cortical hyperechogenecity (Figure 1). Treatment
with a low protein diet (Prescription Diet Canine k/d, canned;
Hill’s Pet Products, Topeka, USA), ranitidine HCl (Ranis;
Skynewpham, Siheung, Korea), 2 mg/kg body weight (BW),
BID, PO, and dried aluminum hydroxide gel (Amphojel; Ildong,
Ansung, Korea), 50 mg/kg BW, BID, PO was initiated. Initial
fluid therapy with 0.9% NaCl was given via a cephalic catheter at
20 mL/h with urine collection by a urinary catheter. The infusion
rate was changed to 15 mL/h after 3 h of the initial fluid therapy.
The dog was euthanized after 2 d of hospitalization because of
a poor prognosis and worsening clinical signs.
A full necropsy was performed. Both kidneys were pale tan
and smaller than normal; each had an irregular capsular sur-
face. The right kidney measured approximately 4 3 3 3 3 cm
and had 5 large cysts ranging from 1 to 2 cm in diameter and
numerous small cysts. The left kidney measured approximately
3 3 2 3 2 cm and had 5 to 6 large cysts approximately 0.5 to
1  cm in diameter. On the cut surface, the cortico-medullary

CVJ / VOL 52 / JUNE 2011 645

R A P P O R T D E CA S

Figure 1.  Sonographs of the left (A and B) and right (C and D) kidney. The kidneys are small, with loss of normal
architecture due to cystic lesions and distal acoustic shadowing. Anechoic, multiple, sharply demarcated, thin-walled,
round structures of various sizes were detected in the right kidney.

junction of both kidneys was obscure (Figure 2). Various sized
cysts filled with clear fluid were present in subcapsular areas of
the cortex. There were no similar lesions in any other visceral
organs.
Histopathological samples of kidney, lung, heart, liver, spleen,
small intestine, stomach, pancreas, bladder, adrenal gland,
trachea, uterus, and ovary were examined after staining with
hematoxylin and eosin (H&E). Selected sections of kidney were
stained with alcian blue (pH 2.5), Masson’s trichrome, periodic
acid-Schiff (PAS), and von Kossa stains.
Microscopic examination of the subcapsular area of the kid-
neys revealed multiple, variable-sized cysts that were lined with
single squamous epithelium (Figure 3A). Most cysts appeared
empty, and some were surrounded by a fibrotic capsule. Some
enlarged cysts in the cortex mimicked dilated Bowman’s capsules
and were lined by a single cell layer of flattened epithelium.
Multifocal dysplastic lesions were found throughout the cor-
tex and medulla of both kidneys (Figure 3A). In dysplastic
areas, immature glomeruli or tubules were distributed from
the subcapsular area to the corticomedullary junction of both
kidneys (Figure 3B), and associated with interstitial fibrosis
and proliferative arterioles. In the medulla, irregularly shaped
immature tubules, similar to metanephric ducts, were embedded
in persistent mesenchyme (Figure 3C). These immature tubules
were lined by pseudostratified, tall columnar epithelial cells. The
persistent mesenchyme consisted of proliferated small spindle
cells and stellate cells with myxomatous stroma, which was
weakly stained with alcian blue but not with Masson’s trichrome.
Adenomatoid proliferation of cuboidal epithelium was also pres-
ent in the dilated collecting ducts of the medulla (Figure 3D).

646 CVJ / VOL 52 / JUNE 2011


Figure 2.  Left (A) and right kidney (B). Both kidneys were a pale tan with an irregular capsular surface and
were smaller than normal. On the cut surface, the cortico-medullary junction of both kidneys was obscured.
Various sized cysts were present in subcapsular areas.
In both kidneys, varying degrees of degenerative and inflam-
matory lesions were noted. Interstitial fibrosis was present within
the segmental cortical zones of immature nephrons. Cystic
glomerular atrophy was also present in the areas of interstitial
fibrosis. Severe mineralization positively stained with von Kossa
and epithelial necrosis were present in most of the cortical renal
tubules. Mild to moderate multifocal chronic pyelonephritis
lesions containing lymphocytes, plasma cells, and macrophages
were found in the renal pelvis and medulla (Figure 3C). Mild
multifocal mineralization was found in the alveolar walls of the
lung, and diffuse hemosiderosis was seen in the spleen; there
were no other abnormalities.
Discussion
Multicystic dysplastic kidney disease, a type of renal dyspla-
sia  (1), is also referred to as renal dysgenesis, or multicystic
kidney disease (2). Renal dysplasia has been described in several
canine breeds, including Shih Tzu (3), border terrier (4), golden
retriever (5,6), standard poodle (7), boxer (8), Finnish harrier
(8), Rhodesian ridgeback (9), and Dutch kooiker (10). To the
authors’ knowledge, this is the first reported case of chronic
renal failure associated with renal dysplasia in a mongrel dog.
The causes of renal dysplasia in humans include genetic
defects, lower urinary tract obstruction, and teratogens/drugs
(11); the cause of renal dysplasia in dogs is unknown (4,8–10).
In humans, the interaction between these causes leads to renal
dysplasia and results in abnormal collecting duct development
and branching, and the loss of potentially functional nephrons,
as well as the formation of aberrant structures, such as cysts
(11). In human renal dysplasia, cysts are considered coincidental
CVJ / VOL 52 / JUNE 2011
CA S E R E P O R T
findings. In canine renal dysplasia, cysts may be considered sec-
ondary degenerative changes, not a primary lesion of dysplasia
(12). It was once thought that cyst formation was a consequence
of tubular obstruction (13). Similarly, it was presumed that cys-
tic changes in nephrons were attributed to progressive interstitial
fibrosis in 1 study of dogs with renal dysplasia (12). Considering
that interstitial fibrosis was present within the segmental cortical
zones of immature nephrons and cystic glomerular atrophy was
also present in the areas of interstitial fibrosis, as in this case,
fibrosis seemed to cause formation of the cysts. Certain genes
have been associated with the formation of renal cysts. In mice,
deficiency of Bcl-2 contributes to cystic formation of the kidneys
(13). In humans, mutation of TCF-1 and Pax-2 leads to cystic
dysplastic kidneys (11). The possibility that genetic factors may
have contributed to the disease or that the interstitial fibrosis
secondary to chronic pyelonephritis may have led to the cyst
formation cannot be ruled out.
The clinical signs in this case were those expected in dogs
with advanced renal failure and included vomiting, anorexia,
polyuria, polydipsia, and weight loss. Two clinical types of the
renal dysplasia have been reported in Shih Tzu dogs (14). A
severe type of renal dysplasia was seen in young dogs presenting
with only a short history of clinical signs and with laboratory
tests that reveal severe abnormalities suggesting renal disease.
These dogs usually died within a few days or were euthanized
(14). As indicated by a short history of clinical signs (4 days),
severe hematological abnormalities, and poor prognosis in this
case, it is considered to be a severe type of renal dysplasia.
The laboratory findings were those expected in dogs with
advanced renal failure: azotemia, low urine specific gravity,
647
R A P P O R T D E CA S

Figure 3.  Microscopic appearance of the kidney. (A, right kidney) — There are large bands of fibrous connective
tissue with irregular dilated cysts, and atrophic glomeruli within cystic Bowman’s capsules. Note the large cyst (*) in
the subcapsular area, lined by flattened epithelium (insert, arrows). H&E, Bar = 200 mm. (B, right kidney) — Note the
immature glomeruli (arrows), tubules (arrow head), and proliferative arteriole (open arrow) in the dysplastic area. H&E,
Bar = 100 mm. (C, right kidney) — Primitive metanephric ducts lined by pseudostratified columnar epithelium (arrows)
are embedded in loose mesenchyme. Note large cysts and mild inflammation. H&E, Bar = 200 mm. (D, left kidney) —
Adenomatoid proliferation (arrows) of cuboidal epithelium in two dilated collecting ducts. H&E, Bar = 50 mm.

hyperphosphatemia, and nonregenerative anemia. Usually hypo-
calcemia is observed more frequently in dogs with chronic renal
failure (15), but hypercalcemia is present in young dogs with
chronic renal failure (15,16). Although a cause of hypercalcemia
was not identified, in our opinion hypercalcemia was associated
with the young age. As for the hyperphosphatemia, increased
plasma phosphate probably bonded with free ionized calcium,
producing soft tissue calcification and reducing the ionized
calcium concentration. Such a relationship between calcium and
phosphate has been reported previously (17). Mineralization of
the basement membrane of the Bowman’s capsules and renal
tubules is frequently observed in dysplastic kidneys in dogs
(3,10,12). Moderate to severe mineralization in renal tubules
and alveolar walls in this case may be related to hypercalcemia.
The ultrasonographic features of renal dysplasia in dogs are
poorly documented (5,6,8,9,18). Small, irregular hyperechoic
kidneys with a poor corticomedullary distinction are described
(5,6,9,18). In this case, the level of renal medullar echogenicity
and the degree of abnormality could not be determined because
of cystic lesions and the distal acoustic shadowing. The latter
might have been caused by renal mineralization, which was
confirmed histopathologically.
On ultrasonography, identification of renal cysts should dis-
tinguish multicystic dysplastic kidney from polycystic kidney
disease. With polycystic disease, the kidneys are usually larger
than normal and concurrent cystic lesions may be present in
other organs such as the liver and pancreas (12,19,20). In con-
trast, multicystic dysplastic kidneys are usually smaller than nor-
mal, and cystic lesions are only found within the kidneys (12).
Although ultrasonography helps in the diagnosis of multi-
cysic dysplastic kidney disease, definitive diagnosis comes from
histological analysis (5). Histopathologic findings in this dog
were consistent with the criteria for renal dysplasia, and there-
fore multicystic dysplastic kidney disease was diagnosed. Five
primary features of dysplasia in dogs are fetal/immature glo­
meruli and/or tubules (asynchronous differentiation of nephrons),
persistent mesenchyma, persistent metanephric ducts, atypical
or adenomatoid tubular epithelium which lining the collecting
ducts, and dysontogenic metaplasia (5,8–10,12,21). Associated
with and often obscuring the primary lesions of renal dysplasia,

648 CVJ / VOL 52 / JUNE 2011

various degrees of compensatory, degenerative, and inflamma-  
tory lesions are observed in the affected kidneys (12). In both
 
kidneys in the present case, there were immature glomeruli,
primitive mesenchyme and metanephric ducts, and adenomatoid  
proliferation of tubular epithelium in the dilated collecting ducts.
 
Gross lesions of renal dysplasia are similar and often indistin-
3. Ohara K, Kobayashi Y, Tsuchiya N, Furuoka H, Matsui T. Renal dys-
plasia in a Shih Tzu dog in Japan. J Vet Med Sci 2001;63:1127–1130.
4. Clark TP, Panciera R. Calcium phosphate urolithiasis and renal dysplasia
in a young dog. J Am Vet Med Assoc 1992;200:1509–1511.
5. Miyamoto T, Wakizaka S, Matsuyama S, et al. A control of a golden
retriever with renal dysplasia. J Vet Med Sci 1997;59:939–942.
6. de Morais HS, DiBartola SP, Chew DJ. Juvenile renal disease in golden
retrievers: 12 cases (1984–1994). J Am Vet Med Assoc 1996;209:

guishable from end stage lesions in old dogs (10,12). Reduced
numbers of normal nephrons are responsible for increased
intrarenal vascular resistance, which eventually leads to chronic
renal disease and hypertension (11,22). Renal dysplasia has
been reported as a cause of chronic renal failure in juveniles
and young adult dogs (8–10,23). It has been suggested that
dysplastic kidneys may be susceptible to pyelonephritis (12,23).
Renal tubular degeneration and dystrophic mineralization can
also elicit inflammatory response in some cases of dysplastic kid-
neys (12). Although many secondary lesions are found in renal
dysplasia, adenomatoid epithelium within tubules is a unique
feature of renal dysplasia. The chronic pyelonephritis observed
in this case is likely secondary, as adenomatoid proliferation
of cuboidal epithelium was identified in the dilated collecting
ducts of the medulla.
Treatment of dogs with renal dysplasia is usually supportive.
One report suggested that clinical signs improved after initiation
of supportive therapy and protein restricted diets in a dog with
renal dysplasia (5). However, the prognosis of renal dysplasia
in dogs is generally poor; most patients either die within a few
days of supportive therapy or euthanasia is performed (3,6,9).
Although similar treatment was performed as indicated in a
previous report (5), there was no clinical improvement. In order
to correct dehydration, the infusion of initial fluid therapy was
done at a rapid rate. Erythropoietin (EPO) was scheduled to
be prescribed as progress was carefully observed. However, due
to the poor prognosis, euthanasia was performed without the
EPO treatment. We did not include antibiotics as part of our
treatment because pyelonephritis was not diagnosed. The treat-
ment would have yielded a better prognosis, in our opinion, if
pyelocentesis or fine-needle aspiration of the renal cysts was
performed to evaluate the presence of urinary tract infection. CVJ
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Ultrasonographic findings of renal dysplasia in cocker spaniels: Eight
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CVJ / VOL 52 / JUNE 2011 649

NOTE Pathology

Renal Dysplasia in a Shih Tzu Dog in Japan

Kiminari OHARA1), Yoshiyasu KOBAYASHI2)*, Noriko TSUCHIYA2), Hidefumi FURUOKA2) and Takane MATSUI2)
1)
Ohara Animal Hospital, 13–32 Yamadahira, Kawada, Shinshiro, Aichi 441–1346 and 2)Department of Veterinary Pathology, Obihiro
University of Agriculture and Veterinary Medicine, Obihiro 080–8555, Japan

(Received 19 March 2001/Accepted 12 July 2001)

ABSTRACT. A 5-month-old, male, Shih Tzu dog manifesting polyuria and polydipsia since 2-month-old was presented to our hospital with
additional clinical complaints of vomiting and depression during recent a few days. Despite the symptomatic therapy for chronic renal
failure, he died on the day after medication. Macroscopically, both kidneys were small in size with rough surface. Microscopical exam-
ination revealed bilateral renal fibrosis with dysplastic changes consisting of immature glomeruli and tubules, and foci of adenomatoid
proliferation of tubular epithelium. In addition, incomplete lobulation of medulla with pelvic structures was also noticed in the right kid-
ney. From these findings, the present case was diagnosed as renal dysplasia in Shih Tzu dog which was documented in the literatures.
KEY WORDS: canine, renal dysplasia, Shih Tzu.
J. Vet. Med. Sci. 63(10): 1127–1130, 2001

Chronic renal failure or renal fibrosis occurs most fre- lary ratio was markedly reduced. The right kidney was
quently in adult or aging domestic animals, particularly in larger than the left one with relatively preserved area (Fig.
dogs and cats, and may have a number of causes [1]. One of 1). The cortico-medullary junction of the right kidney was
the most common clinical sings observed in this chronic irregular. There were no significant lesions in other abdom-
renal disease state is dysfunction to concentrate urine, inal organs including ureter and urinary bladder.
resulting in polyuria, dehydration and polydipsia [1]. Hypo- Both kidneys were fixed in the 10% buffered formalin
plastic anemia also occurs as the result of failure to synthe- and embedded in paraffin wax by a routine procedure. Par-
size and secrete erythropoietin in the kidney [1]. affin sections were stained with hematoxylin and eosin
The development of severe bilateral renal fibrosis has (HE), Masson’s trichrome, and periodic acid-methenamine-
also been reported in young dogs of several breeds and des- silver impregnation.
ignated as progressive juvenile nephropathy, canine renal Histopathological examination revealed bilateral severe
dysplasia or familial renal disease [1–4, 6–8]. There are var- renal fibrosis, particularly in the medulla (Fig. 2). The cor-
ious degrees of compensatory, degenerative and inflamma- tex was very thin with fibrosis and contained some hyper-
tory changes in the lesion. Renal dysplasia of Golden trophic glomeruli and urinary tubules. Cystic dilation of
Retriever dog has been reported in Japan [5]. However, Bowman’s capsular space and some sclerotic glomeruli
there is no report describing renal dysplasia in Shih Tzu were also noted in the cortex. Mineralization of basement
dogs in Japan. This paper deals with the clinical and patho- membranes of the Bowman’s capsules and urinary tubules
logical characteristics of renal dysplasia in a Shih Tzu dog.
A 5-month-old, male, Shih Tzu dog weighing 4.0 kg
manifesting polyuria and polydipsia since 2-month-old was
presented to our hospital with additional clinical complaints
of vomiting and depression during recent a few days. Phys-
ical examination revealed severe depression and dehydra-
tion. The kidneys were not detected in abdominal
radiographs. Clinical pathology revealed hypoplastic ane-
mia (PCV: 24 %), azotemia (blood urea nitrogen: 224.0 mg/
dl), increased creatinine (12.0 mg/dl), and hyperkalemia
(6.7 mmol/l). The animal received fluid therapy and gluco-
corticoid therapy. Despite these symptomatic therapy for
chronic renal failure, the animal died on the day after medi-
cation.
With request by the owner, partial necropsy restricted to
the abdominal cavity was performed. Macroscopically,
both kidneys were firm and small in size with rough surface
(Fig. 1). On cut surface of the kidneys, the cortico-medul-
Fig. 1. Both kidneys are small in size with rough surface. The
* CORRESPONDENCE TO: KOBAYASHI, Y., Department of Veterinary right kidney (R) is larger than the left one (L) with relatively
Pathology, Obihiro University of Agriculture and Veterinary preserved area (arrowheads).
Medicine, Obihiro 080–8555, Japan.
1128 K. OHARA ET AL.

Fig. 2. Left kidney. Severe renal fibrosis, especially in the medulla. Masson’s trichrome stain. × 44.
Fig. 3. Left kidney. A immature glomerulus with mineralization of the basement membrane of the Bowman’s capsule. Masson’s
trichrome stain. × 396.
Fig. 4. Left kidney. Adenomatoid proliferation of cuboidal epithelium in a dilated collecting duct. Masson's trichrome stain. × 139.

were frequently observed. In the medulla, there was slight
inflammatory cell infiltration, including neutrophils. In
addition, there were some immature glomeruli (Fig. 3) and
primitive tubules lined by hyperchromatic epithelium in the
cortex. Proliferation of arterioles was also seen in the inter-
stitium of the cortex. In the medulla, adenomatoid prolifer-
ation of cuboidal epithelium in the dilated lumina of
collecting ducts was also noted (Fig. 4). Persistent mesen-
chyma, which does not stained blue with Masson’s
trichrome, was not apparent.
In addition to these changes, incomplete lobulation of
medulla with pelvic structures was also noticed in the right
kidney (Fig. 5). Furthermore, some urinary tubules in deep
cortex of the right kidney were irregular in shape and
showed increased cellularity of the epithelial lining (Fig. 6).
The hypercellular area was composed of stratified epithelial
cells with low nucleus/cytoplasm ratio. The margin
between severely atrophied and relatively preserved areas in
the right kidney was also clearly demonstrated in histo-
pathological examination, and the relatively preserved area
showed compensatory hypertrophy of glomeruli and urinary
tubules with widespread mineralization (Fig. 7).
Renal dysplasia is defined as disorganized development
of renal parenchyma due to abnormal differentiation [4]. In
dogs, the lesions associated with dysplasia include fetal/
immature glomeruli and/or tubules, persistent mesenchyma,
persistent metanephric ducts, adenomatoid tubular epithe-
lium which lined collecting duct, or dysontogenic metapla-
sia [7]. Associated with and often obscuring the primary
lesions of renal dysplasia, various degrees of compensatory,
degenerative and inflammatory lesions are observed in the
affected kidneys [7]. In both kidneys of the present case,
there were immature glomeruli and tubules, and adenoma-
toid proliferation of tubular epithelium in the collecting
ducts. Thus the present case was pathologically diagnosed
as bilateral renal dysplasia with severe fibrosis.
 RENAL DYSPLASIA IN A SHIH TZU DOG 1129

Fig. 5. Right kidney. Marked renal fibrosis with incomplete lobulation of medulla. The medullary structures are separated by renal pel-
vis (arrows) and connective tissue. HE. × 22.
Fig. 6. Right kidney. A urinary tubule with irregular shape. Note the increased cellularity of the epithelial lining. The hypercellular area
is composed of stratified epithelial cells with low nucleus/cytoplasm ratio. HE. × 198.
Fig. 7. Right kidney. Margin between severely fibrosed (right) and relatively preserved (left) areas is clearly demonstrated. Relatively
preserved area shows compensatory hypertrophy of glomeruli and urinary tubules with widespread mineralization. HE. × 18.

In addition, incomplete lobulation of medullary structure
and urinary tubules with increased cellularity of the epithe-
lial lining were noticed in the right kidney of the present
case. The former lesion might reflect a disorganized devel-
opment of renal parenchyma. However, the significance of
the latter proliferative change remains unclear.
In Shih Tzu dogs, renal dysplasia has been reported in the
literatures as progressive nephropathy, progressive juvenile
nephropathy, or familial nephropathy with autosomal reces-
sive inheritance [1, 2, 4, 6]. It has been reported that there
are two different clinical manifestations in progressive juve-
nile nephropathy of Shih Tzu dog [2]. One type is seen in
young dogs presenting with only a short history of depres-
sion, polydipsia and vomiting and the affected dogs die after
a short clinical course. The other type is found to be in good
health condition, but blood analysis and urine examination
indicate the signs of renal disease. These dogs can live for
several years with gradually developing azotemia and ane-
mia. The clinical features of the present case were con-
curred with those of previous one.
Unfortunately, we could not discuss the familial history.
However, clinical and pathological similarities among the
progressive nephropathy in Shih Tzu dog and the present
case may indicate the possibility of the prevalence of this
disease in Japan.
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