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Pathology of the Kidney & Urinary Tract. RAD 240 Pathology. Radiological Sciences, Department of Health Sciences Week of November 17, 2013 Dr Shai Lecture 7. overview. Kidney structural abnormalities Diseases of the glomerulus Systemic diseases

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rad 240 pathology

Pathology of the Kidney & Urinary Tract

RAD 240 Pathology

Radiological Sciences, Department of Health Sciences

Week of November 17, 2013

Dr Shai

Lecture 7

overview
overview
  • Kidney structural abnormalities
  • Diseases of the glomerulus
  • Systemic diseases
  • Diseases of tubules, vessels, & interstitium
  • Neoplasms
  • Pathologies of renal tract
structural congenital kidney disorders
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)
congenital con t
CONGENITAL CON’T
  • B. HYPOPLASIA
    • 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’stumours in children
horseshoe kidneys
Horseshoe kidneys

Animated view

CT abdomen – horseshoe kidney

slide7

Ultra sound horseshoe kidney

Pathology specimen – horseshoe kidney

cystic kidney diseases
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
adult polycystic kidney disease apkd
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
cystic disease of renal medulla
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

glomerular diseases
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
patterns of glomerular disease
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”
aetiology of glomerular diseases
Aetiology of glomerular diseases
  • Primary (majority): disease begins in glomerululus
    • Types: proliferative*, membrnaous, glomerulosclerotic, minimal change lesions
  • Secondary: 2ndary to systemic disease (immune complex mediated, metabolic, vascular)
  • Hereditary: Alport’s Syndrome, Fabry’s disease, congenital nephortic syndrome
diagnosis symptoms
Diagnosis & Symptoms
  • Histologically
    • Glomerular response to injury
    • Percutaneous* needle biopsy
    • Immunological comple deposition investigation

Symptoms

    • Aymptomatichaematuria*
      • Haematuria without proteinaemia, continuous or intermittent, does not cause renal failure
      • Aymptomaticproteinuria*
        • 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*
slide17

Nephrotic syndrome

    • Proteinuria >3.5 g / 24 hrs, with hypoproteinaemia, oedema, hypercholesterolaemia
  • Chronic Renal failure
    • Irreversible deterioration in renal function caused by the destruction of nephronsover 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
proliferative glomerulonephritis
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
diffuse proliferative glomerulonephropathies
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
rapdily progressive glomerulonephritis
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 glomerularischaemia
focal proliferative glomerulonephritis
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: mesangialIgA disease, Goodpasteur’s syndrome
  • Secondary: systemic endocarditis, vasculitis, connective tissue disease
membranoproliferative glomerulonephritis
Membranoproliferativeglomerulonephritis
  • MPGN
  • Diffuse, global pattern of glomerulonephritis with thickening of membrane
  • Primary: idiopathic
  • Secondary: associated with SLE, endocarditis, cerebral shunts
minimal change disease
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
hereditary glomerulonephritis
Hereditaryglomerulonephritis
  • 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
chronic glomerulonephritis
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
systemic diseases
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
  • HenochSchonleinpurpura
    • Immune complex mediated systemic vasculitis
    • Affects small arteries in skin, joints, gut, kidneys
slide28

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
slide29

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
  • Polyarteritisnodosa
    • Systemic disease, inflammatory necrosis of walls of small & mediums sized arteries
    • Necrosis of medium sized arteries causes infarcts in the kidney, as fibrinoid necrosis
vascular diseases
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
malignant nephrosclerosis
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.
renal artery stenosis
Renal artery stenosis
  • Narrowing of renal arteries, from atherosclerosis or arterial fibromusculardysplasia
  • 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
neoplasms of the kidney
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.
malignant tumours of kidney
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 HippelLinday syndrome, paraneoplasticsyndomes (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
wilm s tumour
Wilm’sTumour
  • Nephroblastoma
  • Malignant embryonaltumour derived from primitive metanephros*
  • Common in childhood, peak 1 to 4 yrs age
  • 3 types identified
    • Commonest : tumoursuppresor 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
wilm s tumour1
Wilm’stumour

Macroscopical changes in Wilmstumour and CT imaging of Wilm’stumour

urinary tract obstruction
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 (egtumours 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
slide44

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
urolithiasis urinary calculi
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
slide47

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
cystitis
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)
slide50

Macroscopically: acute inflammation with oedema, erythema & ulceration of bladder mucosa

  • Microscopically: infiltration of mucosa with acute inflammatory cells
slide51

Risk factors:

    • 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*)
slide52

Examination: mid stream urine analysis

  • Treatment: anit bacterial, antibiotics, flluid therapy
  • Sequelae:
    • Resolution
    • Chronicity
    • Pyelonephritis*
bladder metaplasia
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
bladder tumours
BLADDER TUMOURS
  • TRANSITIONAL CELL CARCINOMA
    • Incidence: 1/5000 in UK, 3% of all cancer deaths
    • Males 3: 1 females, 60-70 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*
slide56

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
slide58

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
slide59
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’