Veterinary Urinary Pathology

Front 1

STEREOTYPIC APPEARANCE OF CHRONIC NEPHRITIS

Back 1

- "End Stage" Kidney disease
- Diffuse fibrosis
- Nodularity
- Loss of corticomedullary junction
Ex) Geriatric cat with small kidneys in chronic renal failure
- This pattern not specific for etiology

Front 2

DUE TO CENTRAL ROLE IN HEMOSTASIS

Back 2

- Most systemic diseases may affect renal function

Front 3

GLOMERULAR NEPHRITIS - 3 WAYS TO CLASSIFY

Back 3

- Morphologic Changes
- Etiology
- Duration and stage of injury

Front 4

CLINICAL HALLMARK OF GLOMERULAR DISEASE

Back 4

- Proteinuria in the face of a quiet urine sediment

- Type of glomerular disease may not impact treatment of the patient except in a few cases

Front 5

IMPORTANT POINTS IN GLOMERULAR DISEASE IN SMALL ANIMALS

Back 5

- Majority likely induced by deposition of Ag/Abd complexes - GN - and subsequent inflammation
- In some species there is famialial glomerular disease (amyloidosis, collagen defects leading to glomerular dysfunction)
- If a patient presents with GN, important to look for underlying Ag stimulation, but often times there is no underlying inflammatory response or neoplasia

Front 6

MOST CASES OF GN ARE SLOWLY PROGRESSIVE : EXCEPTIONS TO THIS?

Back 6

- Lyme nephritis
- Acute septicemia
- DIC

Front 7

2 MAIN HISTOPATHOLOGIC TYPES OF GLOMERULONEPHRITIS

Back 7

- Membranous
- Membranoproliferative

Front 8

MEMBRANOUS GN

Back 8

Basement membrane zone and/or mesangium are altered

- In cats, associated with nephrotic syndrome

Front 9

MEMBRANOPROLIFERATIVE GN

Back 9

Membranous and a cellular proliferation (mesengial cells, macrophages)

Front 10

RENAL AMYLOID IN BRIEF

Back 10

Amyloid is a protein folding disease, not a specific protein.
- Deposition idiopathic
- Marked proteinuria
- In familial form - amyloid can be glomerular or interstitial

Front 11

ACUTE RENAL FAILURE AND TUBULAR DISEASE

Back 11

- Tubular dz is one of the main causes of ARF
- Tubular necrosis one of the main manifestations - oliguria/anuria
- Obstruction of lumen by cellular casts, decreased GFR (increased tubular pressure), filtrate backflow into interstitium leading to edema

Front 12

MECHANISMS OF TUBULAR EPITHELIUM NECROSIS

Back 12

- Ischemia
- Direct Toxic Damage
- Pressure (obstruction) or inflammation
- Some fx deficits may not have morphologic changes detectable: In acute tubular nephritis - slight renal enlargement and edema
- Repair dependent on BM zone integrity, 1 wk to regen, 2-3wk to total recovery

Front 13

NEPHROTOXIC AGENTS

Back 13

- Certain antibiotics
- Antifungals
- Ethylene glycol metabolites, metabolic acidosis, pulmonary edema/tachycardia...
- Lily toxicosis
- Grape/raisan toxicosis
- Heavy Metals
- Pigmentary nephrosis (hemoglobin, myoglobin)

Front 14

TUBULO-INTERSTITIAL DISEASE

Back 14

- Histopathologic dz pattern strongly assc with INFECTIOUS AGENTS.
- Inflammation targets tubules and interstitium
- Clinical presentation varies greatly