Urinary System Pathology PDF

Renal failure Acute renal failure (ARF) Chronic renal failure (CRF)  Acute glomerular or Tubulo-interstitial injury  End result of many chronic renal diseases  oliguria or anuria  Polyuria (Usually irreversible)  Azotemia...

Renal failure Acute renal failure (ARF) Chronic renal failure (CRF)  Acute glomerular or Tubulo-interstitial injury  End result of many chronic renal diseases  oliguria or anuria  Polyuria (Usually irreversible)  Azotemia  Uremia Azotemia Uremia blood urea and creatinine blood urea and creatinine Without clinical manifestations of renal disease. Clinical syndrome & extra-renal lesions (often) 1- Prerenal azotemia: Renal hypoperfusion (heart failure, shock, or hemorrhage) 2- Renal azotemia: 3- Postrenal azotemia: Urinary obstruction.  Clinical Pathology  Anemia  Hypoproteinemia:  Metabolic acidosis:  Due to loss of erythropoietin  Edema Due to loss of Bicarbonate  Azotemia  BUN and creatinine  Hypocalcemia (via three mechanisms) 1- Retention of phosphate 2- Metabolic acidosis > decreased serum calcium 3-Decreased renal 1-α-hydroxylase activity  Hypocalcemia > Parathyroid gland hyperplasia > increased parathyroid hormone (PTH) > bone resorption > fibrous osteodystrophy and pathologic fractures  CLINICAL FINDINGS  Polyuria  Neurologic abnormalities (Uremic encephalopathy)  metabolic acidosis  hypocalcemia  Gastrointestinal signs  ULCERS caused by: Bacteria 1- Urea Ammonia 2- Damage to endothelial cells  Vomiting  Hypertension  Pulmonary edema  GROSS FINDINGS  Kidneys:  Small, firm, with irregular surface (usually bilateral)  Capsule: Difficult to remove from the cortex because of adhesions  Cut surface: Thinned cortex   Gastrointestinal tract Stomach: “uremic gastritis” Ulcerations Marked mineralization Red-black blood Oral Cavity Foul-smelling odor in oral cavity Ulcers (especially at ventral surface of the tongue)  Widespread soft tissue mineralization Lungs: “pumice stone” beneath the parietal pleura, “ladder like” Endocardial mineralization  Parathyroid glands  hyperplasia  Bone: Fibrous osteodystrophy (Rubbery Jaw) (especially bones of the head) Congenital anomalies  Agenesis  Bilateral agenesis is inconsistent with postnatal life  Renal hypoplasia  Unilateral contralateral hypertrophy is expected Renal dysplasia  Polycystic kidney GROSS FINDINGS:  Kidneys are large, pale  contain numerous 1-5 mm diameter cysts contain watery liquid material  “Swiss cheese” appearance on cut surface  Horseshoe kidney  fusion of the cranial or caudal poles of the kidneys  Kidneys function normally.  renal hemorrhages Petechial hemorrhages occur beneath the capsule: 1) Classical swine fever (hog cholera) 2) African swine fever 3) Porcine salmonellosis 4) Porcine erysipelas (hemorrhages tend to be larger and more irregular in size and shape) 5) Porcine circovirus-2  renal infarction  Local Ischemic necrosis.  Occlusion of the renal artery or of one of its branches )End-artery)  In cats indicator of underlying hypertrophic cardiomyopathy and distal aortic thromboembolism  Wedge of tissue is swollen & congested  Dehemoglobinization 24 hours later  2-3 days infarcted area then becomes white  Progressively replaced by fibrous tissue ( healed) pale gray-white scars, wedge shaped, and depressed renal medullary necrosis  Analgesic Nephropathy Nonsteroidal Anti-inflammatory Drugs (NSAIDs) (Aspirin, Phenylbutazone, Flunixin, Ibuprofen) Inhibit Cyclooxygenase Decreased Production Of PGE2 Loss of its Vasodilatory Effect On Arterioles Of Juxtamedullary Nephrons Papillary Necrosis (Renal Crest Necrosis) hydronephrosis  Dilation of the renal pelvis & progressive atrophy renal parenchyma kidney Cause: urinary obstruction (incomplete)  Calculi  Prostatic enlargement in the dog  Cystitis  Compression of the ureters  Bilateral obstruction results in early death from uremia Early: Progressive dilation of the pelvis and calyces advanced cases: the kidney is transformed into a thin-walled sac  Sequel:  If the obstruction is removed within about 1 week, renal function returns.  After about 3 weeks of complete obstruction, irreversible renal damage.  Unilateral hydronephrosis, the contralateral kidney can compensate if it is normal.  Urinary stasis predisposes to infection ( pyelonephritis)  amyloidosis  Deposition of amyloid (an amorphous, hyaline substance)  interfere with normal tissue function + pressure atrophy of adjacent cells  GROSS FINDINGS:  Enlarged  Firm  Pale gray to yellowish orange  Waxy organs  Kidney has finely stippled appearance with fine yellow spots representing glomeruli  Iodine: Glomeruli stain red-brown with iodine solution and turn purple when subsequently exposed to acetic acid/vinegar  MICROSCOPIC FINDINGS: glomerular tufts are expanded by variable amounts of amorphous, finely fibrillar to waxy, lightly eosinophilic material (amyloid)  Acellular, pale eosinophilic, homogenous, extracellular material  Congo red staining of amyloid “apple green” birefringence  nephritis Inflammation of renal parenchyma  CLASSIFICATION OF Nephritis According to route of infection 1- Ascending (uriniferous) 2- Descending (hematogenous)  Suppurative Tubulo-intersitial Non-suppurative According to histologic distribution Proliferative Glomerulonephritis Membranous Membranoproliferative  glomerulonephritis (gn) Classified based on histologic appearance as:  Membranous: Thickening of capillaries of basement membrane  Proliferative: Increased cellularity due to proliferation of endothelial, mesangial cells and/or epithelial cells.  Membranoproliferative (mesangiocapillary): both membranous and Membranoproliferative proliferative changes Membranous Proliferative Most cases of GN are immune-mediated: 1. Antibodies binding antigens in the glomerulus (exogenous) 2. Deposition of circulating immune complexes in glomeruli 3. Formation of antibodies against the glomerular basement membrane Antigen-antibody complexes complement components (C3a, C5a) attract neutrophils & releasing chemokines and oxidants that damage cellular constituents  TYPICAL CLINICAL FINDINGS  Proteinuria: hallmark sign  Nephrotic syndrome: proteinuria, hypoalbuminemia; generalized edema; hypercholesterolemia  GROSS FINDINGS  Bilateral distribution  Early: pale, edematous large kidney , bulge on cut surface  Later: shrunken with granular pitted surface