Systemic Pathology - Kidney - Fatahzadeh

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  1. Anatomy of kidney
    • Cortex
    • Medulla
    • Renal pyramids - within the medulla; apices toward the cavities, the major and minor calyces.
    • Minor & major calyces
    • Columns of Bertin - cortical structure
    • Renal artery - blood with waste in
    • Renal vein - clean blood out
    • Ureter - waste out
  2. Blood Vesseles of kidney
    • Richly vascularized (cortex is receiving 90% of total renal circulation; medulla is relatively avascular)
    • Main renal artery progressively subdivides into many branches finally supplying kidney glomeruli as capillary loops.
    • Capillary loops merge.
  3. Significance of renal vessel
    • Occlusion of any branch results in the infarction of specific area it supplies.
    • Glomerular disease affecting capillary blood flow affects both cortical & medullary tubules.
    • Minor interference with blood supply may result in medullary necrosis.
  4. Glomeruli
    • An anastomosing network of capillaries lined by fenestrated endothelium invested by two layers of epithelium outside the basement membrane.
    • Visceral epithelium (podocytes) is part of intrinsic capillary wall; parietal epithelium lines Bowman’s capsule where filtrate collects.
    • Mesangial cells supporting glomerular tuft.
  5. Glomerular filtration barrier
    • • High permeability to water & small solutes
    • • Impermeable to large, negatively charged proteins
    • • Maintenaied by visceral epithelial cells
  6. Tubules
    • • The proximal tubular cells have highly developed structures - re-absorption of 2/3 of filtered solutes
    • • The proximal tubules are highly susceptible to ischemic necrosis & chemical injury
  7. Interstitium
    • • Normal cortex - compact interstitial space composed of fenestrated peritubular capillaries & cells
    • • Edema or inflammation cause abnormal expansion
    • of interstitium
  8. Kidney Functions - Urine production
    • • Maintains constancy of volume & composition of ECF
    • • Excretion of waste products of metabolism, eg. uric acid, creatinine, urea.
    • • Precise regulation of body’s concentration of salt & water
    • • Maintains acidic balance of plasma
    • Works with other systems of the body.
  9. Kidney Functions - Endocrine
    • • Renin - produced by Juxtomedullary cells, part of angiotensin system & blood pressure maintenance
    • • Erythropoeitin - Hematopoeisis
    • • 1,25-dihydroxy cholecalciferol (active Vit D) - Calcium metabolism
  10. Epidemiology of kidney disease
    • • > 8 million kidney disease in US
    • • > 360k with irreversible end stage renal disease (ESRD)
    • • 58k die from ESRD in USA each year
    • • Risk factors - old, race, male & family history
    • • In a dental practice of 2000, expect 2 with kidney disease.
    • • Cause high morbidity (low life quality) but less mortality than cancer, heart disease or stroke
    • • 20% of all females suffer from infections of urinary tract or kidney
    • • 1% of US population develop renal stones
    • • Chronic renal failure - dialysis & transplantation
  11. Diseases of the Kidney
    • • Anatomic interdependence of components
    • • Large functional reserve (one million nephrons - late diagnosis)
    • • Early signs & symptoms are crucial
    • • Each component is more vulnerable to specific forms of renal injury:
    • a) Immunologically mediated glomerular diseases
    • b) Toxic or infectious tubular & interstitial diseases
    • Medulla - ischemic necrosis
  12. Urine Analysis
    • • Proteinuria - Protein in urine; glomerular or tubular damage
    • • Hematuria - blood in urine; Extent of hematuria is diagnostic
    • • Pyuria - pus in urine; often associated with infections
    • * Should have none of above when healthy; Glomerular disease show severe proteinuria & hematuria.
    • • Organized sediments - casts
    • - Cellular casts are WBC/RBC trapped in the renal tubules
    • - Non-cellular casts are percipitated proteins
    • • Osmolarity (a measure of urinary concentration)
  13. Urine Volume
    • Normally 1.5-2.5 L per day
    • • Hyposthenuria - hypotonic urine (inability of tubules to concentrate )
    • • Oliguria - decrease in the amount of urine (400 ml per day)
    • • Anuria - lack of urine production (in fact 200 ml/d )
  14. Serum analysis for kidney disease
    • Azotemia
    • • Refers to elevation of blood urine nitrogen (BUN) & creatinine
    • • Largely related to decreased glomerular flow rate
    • • May be caused by extra-renal disorders
    • • When associated with clinical symptoms, signs & biochemical problems - uremia
    • Electrolyte imbalance – K retention (hyperkalemia), Na loss (hyponatremia), Serum Ca low (hypocalcemia); Serum Phosphate high (hyperphosphatemia).
  15. Congenital Diseases of Kidney
    • • Affects 10% of people
    • • Hereditary or acquired developmental defect during gestation
    • • Renal agenesis - failure of total formation of the kidney (bilateral is incompatible with life; unilateral hypertrophy)
    • • Renal hypoplasia - failure of complete development of the kidney (smaller, fewer renal lobes or medullary pyramid); true renal hypoplasia cases are rare; often unilateral
    • • Ectopic kidneys - development of nephrons in abnormal positions
    • • Polycystic kidney disease - a hereditary anomaly affecting both kidneys leading to progressive loss of function
  16. Adult Polycystic Disease
    • • A hereditary disorder (autosomal dominant), 1 in 500-1000
    • • multiple expanding cysts of both kidneys destroy parenchyma & cause RF (10% of all RF)
    • • A systemic disorder with cysts in other organs (1/3 have cysts in liver)
    • • Bilaterally enlarged kidneys filled with fluid
    • (weighing up to 4 kg)
    • • Flank pain / dragging sensation
    • • Remain asymptomatic until end state renal diseases occurs at about 50
    • • Faster progression in males & blacks
    • • Majority develop hypertension (75%), risk of urinary tract infection.
    • • Need renal transplantation
    • • Death due to uremia or hypertensive crisis
  17. Childhood Polycystic Disease
    • • Autosomal recessive inheritance
    • • Perinatal, neonatal, infantile & juvenile forms
    • • Bilaterally enlarged kidneys with smooth external appearance
    • • Many small cortical & medullary cysts, sponge-like appearance
    • • Nearly all cases have hepatic cysts
    • • Early death from pulmonary or renal failure
    • • If survive infancy, will develop congenital hepatic fibrosis
  18. Glomerular syndromes
    • Asymptomatic hematuria or proteinuria (subtle or mild glomerular abnormalities) - microscopic amount of blood/protein, late detection.
    • Acute nephritic syndrome
    • Nephrotic syndrome
    • Chronic renal failure (end stage kidney)
  19. Acute Nephritic syndrome
    • A glomerular syndrome
    • Acute onset of severe hematuria, mild to moderate proteinuria, oliguria / anuria & HTN (fluid retention & increased renin release from ischemic kidneys)
    • Pathogenesis: Proliferation of cells within glomeruli, WBC infiltrate, capillary wall damage & low GFR.
  20. Nephrotic Syndrome
    • A clinical complex including:
    • • Severe proteinuria ( >3.5g/d )
    • • Hypoalbuminemia ( <3g/dl in plasma )
    • • Generalized edema
    • • Hyperlipidemia (increased synthesis of liver lipoproteins, abnormal lipid transport & decreased lipid catabolism)
    • • Lipiduria (leakage of lipoproteins across glomerular capillary wall )
    • • Increased risk of infection (loss of immunoglobulins & complements)
    • • Increased risk of thrombosis (loss of anticoagulant factors)
    • In < 15 year old often due to kidney disease; In adults often due to systemic disease (SLE).
    • Pathogenesis:
    • • Glomerular capillary wall damage -> increased
    • permeability to plasma proteins -> massive proteinuria
    • • Highly selective proteinuria (albumin only)
    • • poorly selective proteinuria (globulins & albumin)
    • • Low blood albumin -> low colloid osmotic pressure, interstitial Na & water retention -> generalized edema
  21. Functional changes in RF
    • • Decreased GFR (<20-25% of normal )
    • • Decreased tubular secretion & absorption
    • • Failure to detoxify blood & ECF (azotemia)
    • • Failure to regulate volume & solutes
    • • Edema, metabolic acidosis & hypocalcemia
    • • Overt uremia in terminal stages
  22. Normal function to symptomatic CRF
    • Slow progress
    • • Diminished renal reserve (asymptomatic, GFR is 50% normal)
    • • Renal insufficiency (GFR is 20-50% normal)
    • • Renal failure (GFR • End-stage renal disease(GFR
  23. Clinical signs & symptoms of RF
    • • high BUN, Azotemia - Loss of GF function, build up of nitrogenous wastes in the blood (urea)
    • • metabolic acidosis, nausea, fatigue, hyperventilation - Accumulation of acids
    • • oliguria, anuria - Decline in urine output
    • • hyperkalemia - Retention of potassium
    • • hyponutremia - Loss of electrolytes, esp. Na
  24. Urination in Renal Failure
    • polyuria, nocturia & dehydration - Early in RF, loss of ability to concentrate urine (isosthenuria) & conserve water, massive Na loss
    • oliguria & anuria - Later at ESRD, loss of ability to dilute urine, massive salt & water overload, HTN, CHF
  25. Acute vs. Chronic Renal Failure
    • Acute:
    • • Rapid onset & often reversible after dialysis
    • • Caused by glomerular, interstitial or vascular injury & acute tubular necrosis
    • Chronic:
    • • Gradual onset, irreversible
    • • Prolonged signs & symptoms
    • • The end result of all chronic renal diseases
  26. Chronic Renal Failure
    • • More common than acute RF
    • • A major cause of death from renal disease.
    • • Oliguria, anuria, azotemia, acidosis, hyperkalemia
    • • Uremia with marked extra-renal disturbance of organs:
    • CNS - headache, mental slowness, coma
    • GIT - gastroenteritis & non-specific stomatitis
    • Skin - uremic frost
    • Heart - diffuse fibrinous pericarditis, left ventricular hypertrophy due to HTN (CHF)
    • Lung - uremic pneumonitis, Pulmonary alveolar damage
    • Liver - drug metabolism & clearance
    • Hematologic - platelet dysfunction, anemia
    • Immune - WBC dysfunction
    • • Vit D deficiency, Osteodystrophy, secondary hyperparathyroidism, metastatic calcification
  27. Glomerular Diseases of Kidney
    • Primary:
    • • kidney is the main or the only organ involved
    • • Many different types :
    • - IgA nephropathy
    • - Lipoid nephrosis ( minimal change disease )
    • - Rapidly progressive GN ( Crescentric GN )
    • - Acute diffuse proliferative glomerulonephritis (GN)
    • - Membranous GN
    • - Focal segmental GN
    • - Membranoproliferative GN
    • Secondary: Results from other diseases such as HTN, SLE, DM (diabetes mellitus)
  28. Glomerular Diseases of Kidney are Often caused by immune injury by:
    • 1- Antibodies within glomerulus reacting with intrinsic antigens or planted extrinsic antigens
    • 2- Deposition of soluble circulating antigen-antibody complexes in the glomerulus (SLE, Hep B, HIV):
    • - Subepithelial deposits
    • - Epimembraneous deposits - between podcytes
    • - Subendothelial deposits
    • - Mesangial deposits
    • Eventually the attacks breaks apart the filtration barrier.
  29. Rapidly progressive Glomerulonephritis
    • • Rapid & progressive loss of renal function & severe oliguria which results in death if not treated
    • • Also known as Crescentric GN
    • • Hematuria, proteinuria, HTN & edema
    • • Most are immune mediated
    • • Good response to steroids & cytotoxic agents but many require dialysis or transplantation
    • • Distinctive crescents formed by cellular proliferation & WBC migration of cells, collection of fibrin strands internal to bowman capsule, subepithelial deposits
    • • EM: Subepithelial humps & BM ruptures
  30. Minimal Change Disease
    • • aka lipoid nephrosis
    • • Most frequent cause of nephrotic syndrome in children
    • • Relatively benign disorder
    • • May follow a respiratory infection or routine prophylactic immunization
    • • Dramatically responsive to corticosteroid therapy
    • • Despite massive proteinuria (albumin selective), renal function remains good with no hematuria or HTN
    • • Long-term prognosis is good in both children & adults
  31. Pathogenesis of Minimal Change Disease
    • • No immune complexes present
    • • Immune dysfunction leads to circulating cytokines affecting visceral epithelial cells, proteinuria
    • • Normal glomeruli & BM
    • • Uniform & diffuse effacement of foot processes
    • of visceral epithelium, no cellular profileration
    • • Tubular cells filled with lipid due to lipid reabsorption through diseased glomeruli, hence lipoid nephrosis - Cross section through tubule shows bland, washed-out appearance
  32. IgA nephropathy
    • • aka Berger disease
    • • The most common glomerular disease.
    • • Affects children & young adults
    • • Hematuria & loin pain after Upper Respiratory / GI / UT infectious exposure
    • • A frequent cause of gross / microscopic hematuria
    • • Many patients maintain renal function
    • • Abnormality in production & clearance of IgA in response to infectious agents
    • • Deposition of circulating IgA immune complexes in
    • mesangium, Mesangial proliferation & matrix increase
    • (Immune type gomerular injury)
  33. Urinary Tract Infections
    • • With / without symptoms
    • • if Confined to bladder (cystitis)
    • • if Spread to kidney (pyelonephritis)
    • • More common in Female (shorter urethra; lack of prostatic fluid with antibacterial action, urethral trauma during intercourse, hormonal effect on binding bacteria to urethral mucosa ) & older Male (prostatic hyertrophy, frequent instrumentation)
    • • Risk factors: instrumentation, pregnancy, urinary obstruction, DM, immunosuppression, vesicoureteral reflux.
  34. Pyelonephritis
    • One of the most common kidney diseases
    • 85% by gram negative bacilli (normal inhabitants of GIT)
    • - colonization of distal urethra, access to bladder by catheterization
    • - Bladder dysfunction or outflow obstruction causes incomplete emptying, then bacteria multiply in bladder
    • - Incompetence of vesicoureteral valve, bacteria ascend from ureter into pelvis
    • - Few cases due to hematogenous spread of infection from distant foci during septicemia or infective endocarditis, & seeding of kidney (more common in cases of ureter obstruction, in immunosuppressed & debilitated)
  35. Acute Pyelonephritis
    • • Sudden onset with pain at costovertebral angle, fever, malaise, dysuria
    • • Frequency & urgency of urination
    • • Tubular necrosis, interstitial suppurartive inflammation (kidneys are swollen with superficial abcesses)
    • • Diagnosis: Quantitative urine culture
    • • Pyuria & bacteriuria
    • • Antibiotic therapy…recovery but scarred
    • • Recurrent / chronic disease if predisposing factors remain
  36. Chronic Pyelonephritis
    • • An important cause of ESRD
    • • Clinically silent or manifested with Back pain, fever, pyuria, bacteriuria & HTN
    • • Organisms are very difficult to demonstrate
    • • kidneys are SHRUNKEN & irregularly scarred
    • • Dilated tubules with thyroidization in cortex,
    • cortico-medullary fibrosis /scarring, blunted
    • calyx & chronic interstitial inflammation
  37. Urinary tract obstructions
    • • Intrinsic to urinary tract or Extrinsic compressing on structures
    • • May be sudden or insidious; partial or complete; unilateral or bilateral; at any level of UT
    • • Unilateral, complete or partial obstruction often
    • silent as other kidney can maintain RF
    • • Partial bilateral obstruction - unable to concentrate urine, polyuria & nocturia
    • • Complete bilateral obstruction - anuria, oliguria, incompatible with survival
    • • Obstruction below bladder - bladder distention
    • • Increases risk of infection / stone formation
    • • Acute obstruction may cause pain due to distention of collecting system or renal capsule
    • • Unrelieved obstruction almost always leads to enlarged kidneys, interstitial inflammation & permanent cortical & medullary atrophy
  38. Etiology of urinary tract obstructions
    • • Congenital anomalies (strictures, stenosis)
    • • Urinary calculi (intrinsic)
    • • Benign prostatic hypertrophy
    • • Tumors (extrinsic)
    • • Inflammation (prostatitis, uretritis,…)
    • • Normal pregnancy (extrinsic )
    • • Functional disorders (spinal cord damage)
    • • Uterine prolapse
  39. Urinary tract obstructions
    • • Even with complete obstruction, GFR initially persists due to back diffusion of filtrate into renal interstitium - renal atrophy & compression of medullary renal vasculature
    • • Hydronephrosis: Dilation of renal pelvis & calyces associated with progressive atrophy of the kidney due to outflow obstruction of urine
    • Bilateral if obstruction below ureters / bladder
    • Unilateral if above ureters / bladder
  40. Renal Calculi
    • • A common occurrence; M>F
    • • 80% Unilateral
    • • Most stones arise in the kidney
    • • Different types (Ca oxalate, uric acid, cystine, etc.)
    • • High urinary concentration of stone’s constituents exceeding urinary solubility
    • • Formation influenced by urinary pH, volume, bacteria & inhibitors of crystal formation
    • • Smaller stones go through ureters - colic pain, gross hematuria & increased risk of infection; larger stones often asymptomatic
    • • Often diagnosed radiologically
  41. Renal Cell carcinoma
    • • Most common malignant renal tumor (85% in adults)
    • • Often in older people; M>F
    • • Tobacco is most prominent risk factor (2x)
    • • Classic signs: costovertebral pain, palpable mass &
    • hematuria; only in 10% of patients. Majority will present with nonspecific systemic symptoms such as fever & malaise, weight loss once kidney mass is large; late detection.
    • • Arise from kidney tubular epithelium
    • • Metastasis to lungs (50%) & bone (33%)
    • • Five year survival rate of 45 to 70% if no metastasis
    • • Treated by nephrectomy
  42. Oral manifestations of kidney disease
    • • Pallor oral mucosa - Erythropoietin associated
    • • Metallic taste & urine-like mouth odor - uremia
    • • Uremic stomatitis - uremia
    • • Uremic frost (also on the skin) - uremia
    • • Enlarged salivary glands, xerostomia, but fewer caries - uremia
    • • Spontaneous gingival bleeding, Poor WBC function - uremia
    • • Tooth mobility & malocclusion with no periodontal disease - vit D difficiency, RF.
    • • Enamel hypoplasia - Ca -> kidney
    • • Tooth erosions due to persistent vomiting - uremia, metabolic acidosis
    • • Bone changes (Renal osteodystrophy)

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Author:
neopho
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326052
Filename:
Systemic Pathology - Kidney - Fatahzadeh
Updated:
2016-11-27 15:45:20
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SystemicPathology
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SystemicPathology
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Systemic Pathology - Kidney - Fatahzadeh
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