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RAD 240 Pathology Pathology of the Kidney & Urinary Tract
Radiological Sciences, Department of Health Sciences Week of November 17, 2013 Dr Shai Lecture 7
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overview Kidney structural abnormalities Diseases of the glomerulus
Systemic diseases Diseases of tubules, vessels, & interstitium Neoplasms Pathologies of renal tract
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Renal anatomy
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Structural – congenital kidney disorders
1. AGENESIS of the kidney UNILATERAL in 1/1000 births Solitary kidney undergoes hypertrophy Susceptible to infections Males 2:1 females, left kidney usually absent BILATERAL in 1/3000 births, part of Potter’s syndrome Abnormal face, urinary tract and nervous system Oligohydramnios* in pregnancy as kidneys not present to contribute amniotic fluid (absence of fetal urine) Not compatible with post natal life (DEATH)
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CONGENITAL CON’T B. HYPOPLASIA C. ECTOPIC KIDNEYS D. HORSESHOE KIDNEY
Kidneys fail to reach normal adult size (congenitally or from shrinkage), often a result of early life chronic infection C. ECTOPIC KIDNEYS 1 or 2 kidneys in abnormal position (usually pelvis) D. HORSESHOE KIDNEY Poles of kidneys are fused, usually inferiorly, to form a large U-shaped (horseshoe) kidney 1/500 people, asymptomatic as collecting systems are normal 2 to 8 times more likely to develop Wilm’s tumours in children
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Horseshoe kidneys Animated view CT abdomen – horseshoe kidney
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Ultra sound horseshoe kidney
Pathology specimen – horseshoe kidney
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Cystic Kidney Diseases
Includes: Hereditary, developmental and acquired disorders Important: 1. appropriate patient management to delay onset of renal failure 2. Appropriate genetic counseling to relatives at risk
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Adult Polycystic Kidney Disease (APKD)
Hereditary (Autosomal Dominant, 50% are new mutations) Linked to alpha globin cluster on chromosome 16 Both kidneys replaced by cysts, develop over years Incidence: 1/250 live births Associated with berry aneurysms (cerebral), liver cysts, pancreas, lung In stillborns* or neonates with enlarged kidneys (15 times normal size) with radiating cystic pattern (SUNBURST PATTERN) Prognosis*: usually die within 2 months of life
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Cystic disease of renal medulla
Medullary sponge kidney (tubular ectasia) Multiple cysts develop in renal papillae Incidence: 1/20,000 Renal function not impaired, but calculi (renal stones) develop and predispose* individual to renal colic & infection CT - KIDNEY
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GLOMERULUS ANATOMY & HISTOLOGY
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Glomerular Diseases Typically caused by structural abnormalities
4 significant components may be damaged: i) endothelial cells lining the capillary Ii) glomerular basement membrane (BM) Iii) mesangium: supporting mesentery to the capillary comprised of mesangial cells (phagocytic cells) & associated matric Epithelial cells or podoctyes, coat outer layer of BM
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Patterns of glomerular disease
Most diseases affect different glomeruli to varying degrees Global: affecting entire glomerulus uniformly Segmental: affecting one glomerular segment, sparing others Diffuse: affecting all glomeruli in both kidneys Focal: affecting proportion of glomeruli, sparing others Eg. “diffuse global” or “ focal segmental”
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Aetiology of glomerular diseases
Primary (majority): disease begins in glomerululus Types: proliferative*, membrnaous, glomerulosclerotic, minimal change lesions Secondary: 2nd ary to systemic disease (immune complex mediated, metabolic, vascular) Hereditary: Alport’s Syndrome, Fabry’s disease, congenital nephortic syndrome
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Diagnosis & Symptoms Histologically Glomerular response to injury
Percutaneous* needle biopsy Immunological comple deposition investigation Symptoms Aymptomatic haematuria* Haematuria without proteinaemia, continuous or intermittent, does not cause renal failure Aymptomatic proteinuria* Proteinuria >0.3 g / 24 hours, without haematuria, continuous, orthostatic (postural), or transient Acute Nephritic syndrome Sudden haematuria, proteinuria, hypertension Loin pain, headache, orbital oedema*
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Nephrotic syndrome Chronic Renal failure
Proteinuria >3.5 g / 24 hrs, with hypoproteinaemia, oedema, hypercholesterolaemia Chronic Renal failure Irreversible deterioration in renal function caused by the destruction of nephrons over time Impairment of excretory, metabolic, endocrine functions of kidney Management: excretory function may be replaced by dialysis, metabolic and endcrine functions need transplant to re initiate
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Proliferative glomerulonephritis
Group of disorders characterized by histological degrees of proliferation in mesangial & epithelial cells in glomerulus Types Diffuse proliferative Rapidly progressive Focal proliferative Membranoproliferative * these are patterns of reactions, not diagnoses
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Diffuse proliferative glomerulonephropathies
Diffuse, global, acute inflammation From deposition of immune complexes in glomeruli Stimulated by infection Aetiology: post streptococcal infection , or less frequently viruses, protozoas and other bacterial infection
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Rapdily progressive glomerulonephritis
CRESCENTIC GLOMERULONEPHRITIS (RPGN) From severe glomerular injury characterized by formation of cellular crescent shaped masses within Bowman’s space Often post streptococcal Crescent shaped masses are composed of epithelial cells & macrophages, causing glomerular ischaemia
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Focal proliferative glomerulonephritis
Acute inflammation within cellular proliferation in a few glomeruli (focal), affecting one segment (segmental) Better known as focal segmental proliferative glomerulonephritis Primary: mesangial IgA disease, Goodpasteur’s syndrome Secondary: systemic endocarditis, vasculitis, connective tissue disease
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Membranoproliferative glomerulonephritis
MPGN Diffuse, global pattern of glomerulonephritis with thickening of membrane Primary: idiopathic Secondary: associated with SLE, endocarditis, cerebral shunts
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Minimal change disease
LIPOID NEPHROSIS No significant abnormality can be detected by light microscopy* Children, under age 6 years, males more than females Aetiology: unknown Pathogenesis: thought to be immunological Morphological features: on electron microscopy* diagnostic loss of epithelial foot processes, tubules show accumulation of lipid in cells Prognosis: good, no permanent renal damage
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Minimal change disease – electron microscopy
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Hereditary glomerulonephritis
1. Alport’s Syndrome Clinical triad: deafness, glomerulonephritis, ocular lesions X linked inherited*, mutatin of COLIValpha5 gene Clinical features: glomerulonephritis (microscopic haematuria & proteinuria in childhood, later nephrotic syndrome), ocular disease & deafness to high pitched sounds 2. Fabry’s syndrome Rare, X linked recessive syndrome Glycosphingolipid metabolism, resulting in painful extermities, red hyperkeratotic papules on skin*, proteinura, renal failure Congenital Nephrotic Syndrome: rare, mesangial proliferation or glomerulosclerosis
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Chronic Glomerulonephritis
Chronic renal failure with small contracted kidneys, and all glomeruli are hyalinized (end stage kidneys) Macroscopically: affected kidneys are small, granularity of external surface, scarring from nephron hyalinization Microscopically: hyalinization of glomeruli
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Systemic diseases Systemic lupus erythematosus
Renal involvement causes diffuse or focal glomerular disease Basis of glomerular damage is immune complex deposition in basement membrane, BM thickens Henoch Schonlein purpura Immune complex mediated systemic vasculitis Affects small arteries in skin, joints, gut, kidneys
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Bacterial Endocarditis
Renal lesions in infective endocarditis from immune complexes or embolism infarction of heart valve vegetations Diabetic Glomerulosclerosis Diabetic glomerular damage causes increased permeability of capillaries in the BM, leading to proteinuris and nephrotic syndrome Pathogenesis: not fully understood, involves deficiency in proteoglycans, glomerular hypertrophy, BM thickening, mesangial cell hypertrophy Histologically 1) capillary wall thickening – mild proteinuria 2) diffuse glomerulosclerosis 3) nodular glomerulosclerosis
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Wegener’s Granulomatosis
Amyloidosis Amyloid, an extra cellular fibrillar protein* is deposited in tissues, including kidney Amyloid fibrils deposited in BM, and mesangium Proteinuria & nephrotic syndrome & chronic renal failure Wegener’s Granulomatosis Immune complex, systemic, necrotizing vasculitis, affecting nose, respiratory and renal tracts Polyarteritis nodosa Systemic disease, inflammatory necrosis of walls of small & mediums sized arteries Necrosis of medium sized arteries causes infarcts in the kidney, as fibrinoid necrosis
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Vascular Diseases Benign Nephrosclerosis
Hyaline arteriosclerosis of the kidney, associated with benign hypertension* It is an important complication of long term benign hypertension, chronic renal failure being the most important outcome It is the commonest nephropathy, found in about 75% of autopsies over the age of 60 years Long standing hypertension cuases reduced blood flow to glomeruli, caused by vascular changes, branches of renal artery thicken with hypertrophy of muscular media, results in ischaemia with scarring. Afferent arterioloes undergo hyalinization (arteriosclerosis) Clinically: increase blood urea & reduction in creatinine clearance Prognosis: <5% die from renal failure, death from congestive heart failure associated with renal failure
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nephrosclerosis
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Malignant nephrosclerosis
Renal disease associated with malignant hypertension Pathogenesis: in accelerated hypertension, the rise in blood pressure is rapid, large muscular vessels undergo fibroplastic proliferation, BUT NO MUSCULAR HYPERTROPHY Afferent arterioles undergo necrosis, and necrosis of glomerular capillary network. 90% of cases untreated cause death.
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Renal artery stenosis Narrowing of renal arteries, from atherosclerosis or arterial fibromuscular dysplasia Outcomes Chronic ischaemia of affected kidney Renovascular hypertension Inadequate perfusion of kidney caused by renal artery stenosis leads to hypertension, and abnormal activation of the renin-angiotensin system
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Neoplasms of the kidney
Benign tumours Cortical adenoma: epithelial tumours of renal tubular epithelium Macroscopically: discreet nodules < 20mm diameter in cortex Microscopically: well differentiated large clear cells Renal hamartoma: commonest benign tumour of kidney, made of spindle cells Macroscopically: firm white nodules in medulla, 3-10mm size Microscopically: spindle cells Angiomyolipoma: hamartoma* composed of smooth muscle, blood vessels, and fate.
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Renal hamartoma
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Malignant tumours of kidney
Renal cell carcinoma Adenocarcinoma made of renal tubular epithelium, in adults 3% of all carcinomas, 90% of primary malignant renal tumours Males 3:1 females Associated with tobacco use, and patients with von Hippel Linday syndrome, paraneoplastic syndomes (hypercalcaemia, hypertension, polycythaemia)* Macroscopically: tumours in upper pole of kidney, rounded masses, yellow surface with areas of haemorrhage & necrosis Microscopically: clear of granular cell types (referring to cytoplasm of cells) Symptoms: haematuria, loin pain, loin mass Prognosis: 70% chance 10 year survival
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Renal cell carcinoma imaging
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Wilm’s Tumour Nephroblastoma
Malignant embryonal tumour derived from primitive metanephros* Common in childhood, peak 1 to 4 yrs age 3 types identified Commonest : tumour suppresor gene WT1 located on chromosome 11 Macroscopically: large rounded masses of solid, fleshy white lesions with necrosis. Tumour is aggressive, rapidly growing, extends beyond capsules into mesentery Microscopically: composed of up to 4 elements {primitive blastematous tissue, immature glomerular structures, epithelial tubes, stroma of spindle cells) Presents with abdominal mass, treat with chemo and radio therapy
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Wilm’s tumour Macroscopical changes in Wilms tumour and CT imaging of Wilm’s tumour
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Urinary tract obstruction
Obstruction of urine drainage from kidney at ANY level within urinary tract Intrinsic lesions: within ureteric wall or lumen (eg urinary calculus*, necrotic debris*, fibrosis after trauma or infection) Extrinsic lesions: from external pressue (eg tumours of rectum or bladder, pregnancy, retroperitoneal fibrosis) Locations Renal pelvis: calculi, tumours Pelviureteric junction: strictures, calculi, ext compression Ureter: calculi, ext compression (pregnancy, fibrosis, tumour) Bladder neck: tumour, calculi Urethra: porstatic hyperplasia or carcinoma, stricture
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Pathogenesis: obstruction at any point causes increased presure, superior to blockage, with dilatation of renal pelvis and calyces (hydronephrosis) Obstruction ate pelviureteric junction > hydronephrosis @ ureter> hydro ureter with subsequent hydronephrosis @ bladder neck> bladder distension with hypertrophy of bladder muscle > hydroureter and hydronephrosis Hydronephrosis effects: Fluid entering the collecting ducts cannot empty into renal pelvis, and intra renal resorption of fluid occurs If the obstruction is removed at this stage: normal renal function resumes
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Urolithiasis (urinary calculi)
Formation of stones in the urinary tract (U/S) 1-5% population in UK, usually after 30 years age, males> females Can form anywhere in urinary tract, usually in renal pelvis Composition of stones Calcium oxalate (80%) Triple phosphates (15%) magnesium ammonium phosphate stones Uric acid (5%) Calculi in cystinuria and oxalosis Aetiology: acquired (urinary tract obstruction, persistent urinary tract infections, reduced urine volume from dehydration; or inherited 1ary metabolic disorders, cystinuria, etc
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If calcium deposition occurs, nephrocalcinosis Symptoms:
Mechanism of stone formation involves excess solute in urine (primary increase in metabolite or stasis) or due to reduced solubility of solute in urine (persistently low pH) Calculi vary in size, from sand like particles to large staghorn stones which fit the whole renal pelvis and branch into calyces If calcium deposition occurs, nephrocalcinosis Symptoms: Renal colic* with nausesa & vomitting caused by passage of small stones along ureter Dull ache in loins Strangury* desire to pass something that will not pass (stones in bladder) Recurrent urinary tract infections (UTI) Management: rest, analgesia, warmth, fluid intake to pass small stones <5mm, or ureteroscopy or lithotripsy
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Urinary calculi imaging
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CYSTITIS Inflammation of bladder
Extremely common, mostly women because of shorter urethra (less traveling distance for bacteria) Aetiology Infection or irritants (radiation) Bacterial (E Coli, proteus, strep faecalis, staphylococcus) Viral (adenovirus), fungal (candida), parasites (schistosoma)
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Macroscopically: acute inflammation with oedema, erythema & ulceration of bladder mucosa
Microscopically: infiltration of mucosa with acute inflammatory cells
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Risk factors: Routes of infection
Urinary retention (due to obstruction, bladder paralysis, calculi, foreign bodies/diverticuli, uterine prolapse) Infection of adjacent structures (prastatitis, urethritis, colon disease) Diabetes mellitus Pregnancy Trauama (catherization) Routes of infection Ascending (commonest) urethra then bladder infection (catheterization) Descending from kidney (eg renal tuberculosis) Direct spread or hameatogenous, or lymphatic Clinical features: pyrexia*, pain in rt iliac fossa*, loin and supra pubic pain, micturition disorders (frequency, urgency, dysuria*, haematuria, incontinence*)
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Examination: mid stream urine analysis
Treatment: anit bacterial, antibiotics, flluid therapy Sequelae: Resolution Chronicity Pyelonephritis*
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Bladder metaplasia GLANDULAR METAPLASIA (CYSTITIS GLANDULARIS)
Small, rounded urothelial cells under urothelial surface (Brunn’s nests) Develop central lumen surrounded by cuboidal cells ADENOMATOUS METAPLASIA Benign, metaplsia or urothelium to cuboidal epithelium SQUAMOUS METAPLASIA Keratinizing or non keratinizing
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BLADDER TUMOURS TRANSITIONAL CELL CARCINOMA
Incidence: 1/5000 in UK, 3% of all cancer deaths Males 3: 1 females, years Aetiology Chemical: eposure to environmental agents (cigarette smoking, aniline dyes, rubber industry) Leucoplakia: keratinizing metaplsia, white plaques and calculi Bladder diverticuli* Most occur at base of trigone*
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Transitional cell CT and histology
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MORPHOLOGY Papillary (commonest) warty masses, projecting into lumen with little invasion of bladder wall Solid: tumours grow directly into bladder wall, often ulcerated Mixed papillary and solid Flat in situ carcinoma: reddened mucosa GRADING TCC grades I-III I: well differentiated, no invasion II: moderately well differentiated, papillary ,atypical cells III: poorly differentaited, pleomorphic* cells, invasive
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Bladder cancer staging
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TNM Tumour-node-metastasis Staging T1: tumour confined to mucosa or submucosa T2: superficial muscle involved T3: deep muscle involved T4: invasion beyond the bladder Spread: local to pelvic structures, lymph or haematogenous Treatment: stage dependeant, diathermy +- radiotheapy, cystectomy or palliative* radiotherapy Prognosis: depends on histoogical type
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Try… Search online and app based radiology slides and identify both normal and abnormal structures 2ND MID TERM EXAMINATION: COVER CARDIOVASCULAR, RESPIRATORY, URINARY, GASTROINTESTINAL PATHOLGIES MULTIPLE CHOICE AND SHORT ANSWERS REVIEW CLASS BEFORE THE EXAM: please start studying, so you can optimize the review time, good luck’
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