JPC SYSTEMIC PATHOLOGY
URINARY SYSTEM
January 2018
U-M15

Signalment (AFIP #1518769):  New Zealand Black (NZB) mouse

HISTORY:  None

HISTOPATHOLOGIC DESCRIPTION:  M15a:  Kidney: Glomerular tufts diffusely and globally exhibit the following changes:  mild to moderate thickening of mesangial matrix and basement membranes by eosinophilic amorphous material (matrix), moderate hypercellularity, and hypertrophic visceral epithelial cells/podocytes.  Focally, glomeruli exhibit one or more of the following changes:  occasional karyorrhectic debris in place of mesangial and/or endothelial cells (lytic necrosis), multifocal adherence of tufts to Bowman’s capsule (synechia), mild thickening of Bowman’s capsule, hypertrophied parietal epithelial cells, and ectatic urinary spaces.  Multifocally, tubules are ectatic and occasionally contain proteinaceous eosinophilic material (proteinosis), sloughed epithelial cells (cellular casts) and/or mineral.  Tubular epithelial cells are often attenuated, and/or contain yellow-brown pigment, or many eosinophilic globules within the cytoplasm.  Plasma cells and lymphocytes are present multifocally in scattered small aggregates within the interstitium frequently around vessels.  The kidney surface is diffusely irregular and pitted. 

M15b:  Kidney (PAS):  The mesangium and basement membranes of glomerular capillaries, Bowman’s capsules, and occasional tubules are mildly thickened by PAS-positive material.

MORPHOLOGIC DIAGNOSIS:  Kidney:  Glomerulonephritis, membranoproliferative, chronic, diffuse, global, moderate, with glomerulosclerosis, and lymphoplasmacytic interstitial nephritis, NZB mouse, rodent.

Signalment (AFIP #1771042):  8-year-old mixed breed terrier

HISTORY:  Polyuria/polydipsia, lethargy and ascites.  Significant clinical laboratory data include: BUN-145; creatinine-4.5; total protein-3.6; albumin-1.1; calcium-7.2; urinary protein 3+; urine specific gravity-1.018; no significant sediment in urine.  No reference intervals are provided. 

HISTOPATHOLOGIC DESCRIPTION:  M15c:  Kidney:  Diffusely within the cortex, the glomeruli exhibit one or more of the following changes: diffusely and globally, the glomerular basement membrane (GBM) is thickened by a densely eosinophilic homogenous material (membranous change); glomerular tufts are occasionally enlarged with increased numbers of hypertrophic visceral epithelial cells; dilated uriniferous spaces; rare, small periglomerular interstitial aggregates of plasma cells and lymphocytes.  Renal tubular epithelium exhibit one or more of the following changes: mild tubular degeneration (swollen and vacuolated cytoplasm); necrosis (hypereosinophilic cytoplasm with nuclear pyknosis, karyorrhexis, or karyolysis); rare regeneration (basophilic cytoplasm with vesiculate nuclei, mitotic figures, piling up of epithelium);  intraluminal eosinophilic homogenous material (proteinaceous fluid) occasionally admixed with sloughed cellular and karyorrhectic debris (cellular casts); and tubular epithelial and luminal yellow-brown globular pigment (hemosiderin or lipofuscin)  

M15d:  Kidney (PAMS - silver):  Glomerular basement changes, including spikes and holes, associated with membranous glomerulonephropathy and best visualized with silver stain are subtle and inconsistent in this section 

M15e:  Kidney (Masson):  Diffusely there are regularly spaced red nodules along the abluminal surface of capillary walls (immune deposits)

MORPHOLOGIC DIAGNOSIS:  Kidney:  Glomerulonephritis, membranous, diffuse, global, moderate, with tubular degeneration and protein casts, terrier mix, canine.

ETIOLOGIC DIAGNOSIS: Immune-mediated glomerulonephritis (presumed, demonstration of immune complexes or complement required for definitive diagnosis)

CAUSE: Immune-mediated

GENERAL DISCUSSION:

PATHOGENESIS:

TYPICAL CLINICAL FINDINGS:

TYPICAL GROSS FINDINGS:

TYPICAL LIGHT MICROSCOPIC FINDINGS:

ULTRASTRUCTUAL FINDINGS:

ADDITIONAL DIAGNOSTIC TESTS: 

contours of the GBM

DIFFERENTIAL DIAGNOSIS:

COMPARATIVE PATHOLOGY:

REFERENCES:

  1. Aresu L, Benali S, Ferro S. et al. Light and electron microscopic analysis of consecutive renal biopsy specimens from Leishmania-seropositive dogs. Vet Pathol. 2012; 50(5):  753-760.
  2. Barthold SW, Griffey SM, Percy DH. Mouse. In: Barthold SW, Griffey SM, Percy DH eds. Pathology of Laboratory Rodents and Rabbits. 4th ed. Ames, IA: John Wiley & Sons, Inc. 2016:102.
  3. Breshears MA, Confer AW. The urinary system. In: Zachry JF, ed. Pathologic Basis of Veterinary Disease. 6th ed. St Louis, MO: Elsevier; 2012017:644-650.
  4. Cianciolo RE, Brown CA, Morh FC et al. Consensus statement: Pathololgic evaluation of canine renal biopsies:  methods for identifying features that differentiate immune-mediated glomerulonephritides from other categories of glomerular diseases.  J Vet Intern Med. 2013; 27:S10-18.
  5. Cianciolo RE, Mohr FC. Urinary system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 2. 6th ed. St. Louis, MO: Elsevier; 2016:401-418
  6. Cianciolo RE, Mohr FC, Aresu L et al. World small animal veterinary renal pathology initiative:  classification of glomerular disease in dogs.  Vet Pathol. 2016; 53(1):  113-135.
  7. Isobe K, Adachi K, Hayashi S: Spontaneous Glomerular and Tubulointerstitial lesions in Common Marmosets (Callithrix jacchus). Vet Pathol. 2012; 49(5):839-845.
  8. Gonzales-Viera O, Ruoppolo V, Marigo J et al. Renal lesions in cetaceans from Brazil. J Comp Path.  2015; 152(4): 345-354.
  9. Vezzali E, Manno RA, Slaerno D. Spontaneous Glomerulonephritis in Gottingen Minipigs. Tox Pathol. 2011;39:700-705


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