د.شهباء

• Urinary System


  • Kidney
  • Ureter
  • Urinary Bladder
  • Urethra
• Function of Urinary Tract

  • Regulate blood volume and composition
  • Regulate pH
  • Produce hormone (Renin, Erythropoietin and Prostaglandin)
  • Excrete waste
  • Metabolic activity (Vitamin D requires hydroxylation in liver and again by kidney to produce 1,25 dihydroxy calciferol)
• General Urinary Diseases


  • Developmental Abnormalities
  • Glomerular Diseases
  • Acute Tubular Necrosis (Nephrosis)
  • Interstitial (Tubulointerstitial) Nephritis
  • Pyelonephritis
  • Urolithiasis
  • Ureteritis
  • Cystitis
• Aplasia


  Absence of one or both kidneys, absence of one kidney is observed in animals with compensatory hypertrophy of another kidney

  
• Hypoplasia


  The size of kidneys remains small which don't grow properly due to defect in autosomal gene

  
• Causes of Renal Hypoplasia

  • Renal fibrosis, resulting from renal disease developing at an early age
  • Dysplasia
  • Progressive juvenile nephropathy

  
• Renal dysplasia


  An abnormality of altered structural organization resulting from abnormal differentiation and the presence of structures not normally present in nephrogenesis

  
• Microscopically features of dysplasia

  • Differentiation of nephrons inappropriate for the age of the animal
  • Persistence of primitive mesenchyme such that the interstitial connective tissue
  • The presence of cartilaginous and or osseous tissue
• Renal cyst


  Spherical, thine walled, variable sized distention's principally of the cortical or medullary renal tubules and are filled with clear, watery fluid

  
• Types of renal cysts

  • Type-1-cyst: result from dilatation and hyperplasia of collected renal tubule, the kidney appear spongiform
  • Type-2-cyst: this cyst develops from renal tubules and Bowman's capsule with glomeruli, this condition is bilateral and causes enlargement of kidney due to clear or blood mixed fluid containing cysts

  
• Mechanisms of renal cyst

  • Obstraction of nephrons can cause increased normal pressure and secondary dilation
  • Modification of extracellular matrix and cell-matrix result in weakened tubular basement membrane lead to dilation of tubular
  • Focal tubular epithelium hyperplasia with production new basement membrane increased tubular secretion and increased intra tubular pressure cause dilation of tubulars
  • Dedifferentiation of the tubular epithelium and abnormal cell arrangement lead to reduced tubular absorption and increased intra tubular pressure and dilation of tubular

  
• Fused Kidney (horseshoe kidney)


  The kidneys from both sides are connected and fused at posterior portion mostly observed at doge. This fusion results in the appearance of one large kidney with two ureters

  
• Ectopic Kidney


  Misplaced from their normal sub lumber location because abnormal migration during development. Ectopic location often include the pelvic cavity or inguinal position. Ectopic kidney are usually structurally and functionally normal, malposition of the ureter predisposes them to obstruction, with result in secondary hydronephrosis

  
• Suppurative glomerulitis (embolic nephritis)


  Result from bacteremia, in which bacteria lodge in random glomeruli and capillaries and cause the formation of micro abscesses throughout the renal cortex

  
• Causative agents of suppurative glomerulitis

  • Actinobacillus suis in pigs
  • Actinobacillus equuli in foals
  • Corynebacterium pseudotuberculosis in sheep and goat
• Microscopic features of suppurative glomerulitis

  • Sever infiltration of neutrophils
  • Glomerular and interstitial hemorrhage
  • Persistence bacterial colonies
  • In chronic stage there was infiltration of lymphocyte, plasma cells, macrophage and fibroblast
• Immune-Mediated Glomerulonephritis


  Deposition of antibody-antigen complex with glomeruli, more common occur in dog and cats
• Causative agents of immune-mediated glomerulonephritis

  • Specific viral infections as: feline leukemia virus, feline infectious peritonitis virus
  • Chronic bacterial infection as: pyometra or pyoderma
  • Chronic parasitism as: dirofilariasis
• Microscopic types of immune-mediated glomerulonephritis

  • Proliferative glomerulonephritis: increased cellularity resulting from proliferation of endothelial, mesangial, and/or epithelial cells and leukocytes
  • Membranous glomerulonephritis: thickened glomerular capillary basement membrane result from subepithelial immunoglobulin deposition
  • Membrano-proliferative glomerulonephritis: combination of the previous two type
• Glomerulosclerosis


  In chronic glomerulonephritis, severely affected glomeruli shrink and become hyalinized because of an increase in both fibrous connective tissue and mesangial matrix and a loss of glomerular capillaries
• Factors associated with and accelerate glomerulosclerosis

  • Unrestricted protein in the diet
  • Increased glomerular capillary pressure in functional glomeruli
  • Cytokines
  • Platelet-derived growth factor
• Sequelae of factors accelerating glomerulosclerosis

  • Alter cellular components of the functional glomerular tufts
  • Cause hypertension and trans glomerular hyperfiltration with resultant damage to endothelium
  • Activate mesangial cells to proliferate
  • Increase mesangial matrix production
  • Accelerate visceral epithelial cell loss
• Acute Tubular Necrosis (Nephrosis)


  Degeneration and necrosis of tubular epithelium without producing inflammatory reaction as a result of toxic injury or ischemia in kidney, characterized by sloughing and necrosis of tubular epithelial cells clinically characterized by oligouria, uremia and anuria

  
• Causative agents of Acute Tubular Necrosis

  • Non-Toxic Nephrosis (Hypotension, hypoxia and infraction)
  • Toxic Nephrosis: Heavy metals, fungal toxin, Mycotoxins as Ochratoxin, Drugs as Gentamicin
• Microscopic features of Acute Tubular Necrosis

  • Vacuolation in tubular epithelium
  • Coagulative necrosis
  • Sloughing of tubular epithelium
• Interstitial (Tubulointerstitial) Nephritis


  Inflammation of kidney characterized by degeneration and necrosis of tubular epithelium, edema and infiltration of inflammatory cells in interstitial tissue
• Multifocal Interstitial Nephritis


  A common, in young calves, "white spotted kidney" is presumed to represent residual lesions of a neonatal E. coli sepsis, also seen in malignant catarrhal fever, porcine circovirus infection, porcine leptospirosis

  
• Microscopic features of Multifocal Interstitial Nephritis

  • Aggregates of lymphocytes as foci and plasma cells within the interstitial
  • In severe cases, interstitial inflammation progresses to fibrosis and tubular atrophy
• Diffuse Interstitial Nephritis


  Caused by Leptospira interrogans in dogs
• Pyelonephritis


  Inflammation of the renal pelvis and renal parenchyma; characterized by congestion with suppurative inflammation and fibrosis

  
• Causative agents of Pyelonephritis

  • Cattle: Corynebacterium renale
  • Pigs: Eubacterium suis
  • Dogs, cats: mostly members of the rectal flora (E. coli, Proteus species, Enterobacter species, Pseudomonas aeruginosa)
• Gross features of Pyelonephritis

  • Congestion, hemorrhage
  • Abscess formation in renal cortex, renal pelvis and ureters
  • Pyuria
  • Enlargement of kidneys

  
• Microscopic features of Pyelonephritis

  • Acute: necrosis and exfoliation of tubular epithelium with neutrophils and bacteria in the tubular luminal, Necrosis of collecting ducts with sloughing of cellular debris in lumen
  • Chronic: infiltration of lymphocytes and plasma cells in interstitial tissue of kidney, white bands of scar tissue extending from cortex to medulla, interstitial fibrosis, loss of tubules
• Urolithiasis


  Formation of stony precipitates anywhere in urinary passage including kidneys, ureter, urinary bladder or urethra
• Causative factors of Urolithiasis

  • Calculus precursors material in urine in quantities sufficient to be precipitated
  • Metabolic defects
  • Hereditary defects
  • Vitamin A deficiency
  • Hyperparathyroidism
  • Abnormally high levels of substances in the diet (silicic acid, phosphate, estrogens, magnesium, oxalate)
  • Bacterial infection
• Gross features of Urolithiasis

  • Obstructed Distension of ureters, urethra and urinary bladder
  • Distension portion of any parts of urinary system
  • Presence of calculi (variable in size and shape and composition) in kidney, ureter, bladder or Urethra
• Microscopic features of Urolithiasis

  • Degeneration and necrosis of tubular epithelium
  • Presence of crystals in lumen of tubules
  • Hemorrhage
  • Proliferation of fibrous tissue
• Ureteritis


  Inflammation of ureter characterized by enlargement, thickening of ureter result from accumulation of urates, or calculi, hydronephrosis and pyelonephritis
• Gross features of Ureteritis

  • Present Calculi which lead to ureter obstruction
  • Urate deposition as white to yellowish materials
• Microscopic features of Ureteritis

  • Acute: infiltration of polynuclear inflammatory cells and congestions
  • Chronic: infiltration of mononuclear cells with fibrosis