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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
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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.
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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.
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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.
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Glomerular filtration barrier
- • High permeability to water & small solutes
- • Impermeable to large, negatively charged proteins
- • Maintenaied by visceral epithelial cells
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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
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Interstitium
- • Normal cortex - compact interstitial space composed of fenestrated peritubular capillaries & cells
- • Edema or inflammation cause abnormal expansion
- of interstitium
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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.
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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
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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
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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
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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)
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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 )
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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).
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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
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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
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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
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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)
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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.
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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
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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
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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
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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
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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
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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
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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
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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)
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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.
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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
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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
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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
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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)
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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.
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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)
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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
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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
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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
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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
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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
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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
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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
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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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