JPC SYSTEMIC PATHOLOGY
URINARY SYSTEM
December 2017
U-M11

Signalment (JPC #1565530):  Rat

HISTORY:  Tissue from an old laboratory rat

HISTOPATHOLOGIC DESCRIPTION:  Kidney:  Diffusely, all levels of the nephron are moderately to severely affected by the following changes.  There is a mild reduction in the number of glomeruli and multifocally those remaining have one or more of the following changes:  The basement membrane of Bowman’s capsule is variably thickened and hyalinized  and there is periglomerular fibrosis; the parietal epithelium of Bowman’s capsule is hypertrophied; there are multifocal adhesions of the glomerular tuft to Bowman’s capsule (synechia); the uriniferous space is dilated; there is segmental or global glomerulosclerosiswith multifocal obsolescence of glomerular tufts.  Diffusely within the cortex and medulla, tubules have one or more of the following changes:  swollen epithelium with indistinct cell borders and microvacuolated eosinophilic cytoplasm (degeneration); marked tubular ectasia with attenuation and/or loss of epithelium; abundant basophilic cytoplasm with vesiculate nuclei (regeneration) that occasionally piles up and forms irregular tubules (hyperplasia), with multifocally thickened basement membranes; or shrunken atrophic tubules with attenuated epithelium.  Ectatic tubule lumina often contain one or more of the following:  variable amounts of pale granular to brightly eosinophilic homogenous proteinaceousmaterial (proteinosis, hyaline casts), deeply basophilic granular material (mineralization), sloughed epithelial cells with cellular and karyorrhectic debris (necrosis), few degenerate neutrophils, and rare erythrocytes.  Tubular epithelia, primarily of the proximal convoluted tubule, multifocally contain variably distinct, irregularly round, intracytoplasmic 1-4um diameter eosinophilic hyaline droplets.  Diffusely, the interstitium is moderately expanded by fibrosis, edema, and multifocal infiltrates of low numbers lymphocytes and plasma cells.  Multifocally there is a small amount of light golden-brown material (hemosiderin) within the interstitium and tubules.  Multifocally, the capsular surface is irregular and undulant. 

MORPHOLOGIC DIAGNOSIS:  Kidney:  Glomerulosclerosis, segmental to global, multifocal, marked, with synechia, periglomerular fibrosis, tubular degeneration, necrosis, and regeneration, marked tubular ectasia with proteinosis, and chronic interstitial nephritis, rat, rodent.

CONDITION:  Chronic progressive nephropathy (CPN)

SYNONYMS:  Glomerulosclerosis, progressive glomerulonephrosis, “old rat nephropathy”, protein overload nephropathy, chronic renal disease, chronic nephritis, dietary nephritis, glomerulonephritis, chronic progressive glomerulonephropathy, glomerular hyalinosis, progressive renal disease, spontaneous nephrosis, others

GENERAL DISCUSSION:

PATHOGENESIS:

TYPICAL CLINICAL FINDINGS:

TYPICAL GROSS FINDINGS:

TYPICAL LIGHT MICROSCOPIC FINDINGS:

ULTRASTRUCTURAL FINDINGS: 

DIFFERENTIAL DIAGNOSIS:

Histologic:

COMPARATIVE PATHOLOGY:

REFERENCES:

  1. Barthold SW, Griffey SM, Percy DH. Pathology of Laboratory Rodents and Rabbits. 4th ed. Ames, IA: Blackwell Publishing; 2016: 102, 157-158.
  2. Benali SL, Lees GE, et. al. X-linked hereditary nephropathy in Navasota dogs: clinical pathology, morphology, and gene expression during disease progression. Vet Pathol. 2016;53(4):803-812.
  3. Delaney MA, Kinsel MJ, Treuting PM. Renal pathology in a nontraditional aging model: the naked mole rat (Heterocephalus glaber).  Vet Pathol. 2016;53(2):493-503.
  4. Hard GC, Seely JC. Recommendations for the interpretation of renal tubule proliferative lesions occurring in rat kidneys with advanced chronic progressive nephropathy (CPN).  Toxicol Pathol. 2005;33(6):641-649.
  5. Isobe K, Adachi K, Hayashi S, Ito T, Miyoshi A, Kato A, Suzuki M. Spontaneous Glomerular and Tubulointerstitial Lesions in Common Marmosets (Callithrix jacchus). Vet Pathol. 2012;49(5):839-845.
  6. King WW, Russell SP. Metabolic, traumatic, and miscellaneous disease.  In: The Laboratory Rat. 2nd ed. Burlington, MA: Elsevier Academic Press. 2006:525-529.
  7. McInnis EF. Background lesions in laboratory animals.  Edinburgh, UK: Saunders Elsevier; 2012:28.
  8. Seely JC, Brix A. Kidney- nephropathy, chronic progressive.  NTP Nonneoplastic Lesion Atlas.  National Toxicology Program U.S. Dept of Health and Human Services.
  9. Seely JC, Hard GC. Chronic progressive nephropathy (CPN) in the rat: review of pathology and relationship to renal tumorigenesis. J Toxicol Pathol.  2008;21:199-205.
  10. Terrell SP, Origgi FC, Agnew D. Glomerulonephropathy in aged captive Key Largo woodrats (Neotoma floridana smalli).  Vet Pathol. 2012;49(4):710-716.
  11. Zhang Y, Connelly KA, et. al. Sirtuin 1 activation reduces transforming growth factor-β1-induced fibrogenesis and affords organ protection in a model of progressive, experimental kidney and associated cardiac disease.  Am Jour Pathol. 2017;187(1):80-90.

 


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