Histopathology Renal Pathology Flashcards
(84 cards)
1
Q
Functions of the kidney
A
• Excretion of waste products
• Regulation of water/salt
• Maintenance of acid/base balance
Secretion of hormones
2
Q
Nephrotic syndrome – chronic
A
- Massive proteinuria (selective albumin)
- Hypoalbuminaemia
- Oedema
- Hyperlipidaemia/ - uria
3
Q
Nephritic Syndrome acute
A
- Variable proteinuria (not selective)
- Haematuria
- Mild oedema
- Oliguria
- Azotaemia
- Hypertension
4
Q
Nephrotic Syndrome: Definition
A
Damage to the filtration of the glomerulus not accompanied by inflammation or proliferative response
5
Q
Nephrotic Syndrome: Histological damage
A
Loss of foot processes
6
Q
Nephrotic Syndrome: Triad
A
Hypoproteinaemia (hypoalbuminaemia)
Oedema
Hyperlipidaemia
7
Q
Nephrotic Syndrome: Massive proteinuria
A
> 3.5 g/day
Hypoalbuminaemia
8
Q
Nephrotic Syndrome: Children
A
Minimal damage disease
9
Q
Nephrotic Syndrome: Adults
A
Systemic disease (diabetes)
10
Q
Nephrotic Syndrome: Nephrotic disease type?
A
Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulonephritis
11
Q
Nephrotic Syndrome: Minimal change disease/glomerulopathy
A
- Commonest cause of nephrotic syndrome in childhood
- No detectable immune deposit but has, nonetheless an immune basis
- Strong association with resp. infection and immunization
12
Q
Nephrotic Syndrome: Minimal change disease/ glomerulopathy histological
A
Diffuse effacement of foot processes (fused)
13
Q
Nephrotic Syndrome: Focal segmental glomerulosclerosis
A
- Primary or Secondary
- Some (focal) glomeruli show partial (segmental) hyalinization
- Unknown pathogenesis
- Poor prognosis
14
Q
Nephrotic Syndrome: Membranous glomerulonephritis
A
- Deposition of anti-glomerular basal membrane antibodies
* Thickened GBM and sub epithelial deposits/spikes
15
Q
Nephrotic Syndrome: Membranous glomerulonephritis epi
A
- Commonest causes of nephrotic syndrome in adults
* 85% idiopathic, 15% association with malignant tumours, SLE, drugs, chronic infection.
16
Q
Nephritic Syndrome: Description
A
Expression of acute glomerular injury
• Inflammation
• Vascular and epithelial damage
• Plus or minus proliferation of glomerular cells
17
Q
Nephritic Syndrome: Triad
A
- Haematuria
- Azotemia
- Oliguria
- Mild oedema (facial puffiness)
- Variable proteinuria
- Mild to moderate Hypertension
18
Q
Nephritic Syndrome: Membranoproliferative (mesangiocapillary) glomerulonephritis
A
- Diffuse mesangioproliferative glomerulonephritis
- Crescentric glomerulonephritis
- Lupus nephritis
19
Q
Nephritic Syndrome: Glomerulonephritis
A
- Primary or secondary to systemic disease
* Immunological aetiology (+++ deposition of immune complex in the glomerular/capillary wall).
20
Q
Nephritic Syndrome: Glomerulonephritis features
A
- Local deposition of circulating immune complexes
- Anti-glomerular basal membrane antibodies
- Antibodies against glomerular component
21
Q
Nephritic Syndrome: Prognosis
A
- Benign outcome in children
* Permanent compromised of renal function in adults
22
Q
Nephritic Syndrome: The Major cause of acute nephritis in childhood
A
Acute proliferative Glomerulonephritis
23
Q
Nephritic Syndrome: Acute proliferative Glomerulonephritis arises
A
Arises following a group A beta-haemolytic streptococcal infection
24
Q
Nephritic Syndrome: Acute proliferative Glomerulonephritis features
A
- Endocapillary hypercellularity with numerous neutrophils and closure of glomerular vessels
- The glomeruli are increased in size and cellularity
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Nephritic Syndrome: Glomerulonephritis – antibodies against glomerular component
* Usually presents with a combined nephritis – nephrotic picture
* Cresentic or rapidly progressing glomerulonephritis
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Nephritic Syndrome: Glomerulonephritis – antibodies against glomerular component
Increase in mesangial substance. Localized capillary wall thickenings, increased cellularity and pronounced lobulation.
27
Diseases affecting tubules and interstitium: types
Acute tubular necrosis
| Tubulointerstitial nephritis
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Acute tubular necrosis epi
Most common cause of ARF
| Reversible tubular injury
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Causes of acute tubular necrosis
Ischemia (shock)
| Toxic (Drugs)
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Prognosis Acute tubular necrosis
Most patients recover
31
Acute tubular necrosis histology
There is focal necrosis and desquamation of the cells into the tubular lumen.
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Tubulointersitial nephritis
Acute pyelonephritis
Chronic pyelonephritis: and reflux nephropathy
Drugs and toxins – analgesic nephropathy
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Urinary tract infections and Reflux nephropathy
Women, elderly
Patients with catheters or malformations
Dysuria, frequency
34
Urinary tract infections and Reflux nephropathy organisms
E. coli
| Proteus
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Acute pyelonephritis
Acute pyelonephritis in a patient presenting with fever and elevated creatinine. There is an acute inflammatory infiltrate in the interstitium and tubular lamina.
36
Chronic pyelonephritis
* The surface of the kidney is irregular/ or geographically, depressed in the scarred area with pseudo bulging of the remaining intact parenchyma.
* Chronic pyelonephritis can affect both kidneys simultaneously; however, the scarring is asymmetrical.
* The cut surface would reveal dilated, blunted or deformed calyces.
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Chronic pyelonephritis features
• Many dilated “colloid” filled tubules are present – ‘thyroidisation of the kidney’.
38
Diseases of the blood vessels:
Hypertensive kidney disease
| Benign nephrosclerosis
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Hypertensive kidney disease
Benign nephrosclerosis
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Benign nephrosclerosis
* Focal sclerosis of renal arterioles and small arteries > focal ischemia > cortical scarring.
* Some degree of nephroscleosis is present at autopsy with increased age.
* HTN and DM increased the severity of the lesion.
41
More severe
Malignant HTN and accelerated nephrosclerosis
42
Cystic Disease of the Kidney: Types
Malformative/congenital
| Acquired
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Cystic Disease of the Kidney: Malformative/congenital
Multicystic renal dysplasia (most common causes of abdominal mass in newborn)
Medullary sponge kidney
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Cystic Disease of the Kidney: Acquired
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Acquired renal cystic disease (mostly post dialysis)
Simple cysts (most common abnormality of the kidney)
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45
Cystic Disease of the Kidney:Hereditary
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Autosomal dominant (adult) polycystic kidney disease (ADPKD)
Autosomal recessive (infantile) polycystic kidney disease
Nephronophthisis – medullary cystic kidney disease complex
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46
Cystic Disease of the Kidney:Adult polycystic disease epi
Occurs in 1/500 people
AD inheritance:
• Bilateral
• Presents middle age
47
Cystic Disease of the Kidney: Clinically
Haematuria
UTI
Abdo mass
HTN
48
Cystic Disease of the Kidney: Associated with CRF
Cerebral aneurysms
Subarachnoid haem
Cysts in other organs (liver, pancreas, lung)
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Cystic Disease of the Kidney: Complications
CRF
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Cystic Disease of the Kidney: Management
Supportive
Treat HTN
Some will need dialysis/transplant
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Infantile polycystic disease: Epi
1/20000
| AR inheritance
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Infantile polycystic disease: Clinically
Large abdominal masses (both kidneys affected) at birth
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Infantile polycystic disease: Possible
“Potter” phenotype
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Infantile polycystic disease: Associated with
Liver abnormalities (congenital hepatic fibrosis, biliary dysgenesia, bile duct ectasia).
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Infantile polycystic disease: Evolves into
Death shortly after birth in severe forms
Renal failure
Hypertension
Portal Hypertension
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Simple renal cysts
Common autopsy findings. No clinical significance.
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Other cysts
Dialysis associated cystic disease
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Chronic Renal Disease: Description
Abnormal kidney function/ structure –end result of a number different renal diseases.
• Frequently unrecognised and/or coexisting with other conditions
• Can be asymptomatic till it progresses into end stage renal disease.
59
Chronic Renal Disease: Causes
Diabetes
| Hyperternsion
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Glomerulonephritis 40%
Chronic Pyelonephritis (20%)
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Polycystic disease 9%
Multisystem diseases 9%
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Acute Renal Failure → Description
Rapid reduction of in renal excretory function ( within 48 hr)
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Acute Renal Failure → Clinically
Absolute increase in serum creatinine >=m0.3 mg/dl serum urea, CR, K with anuria/ oliguria (<15ml/hr)
Reduction urine output (oliguria) less than 0.5 ml/kg per hour for more than 6 hr
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Acute Renal Failure → Clinical presentations
Oliguric phase – metabolic acidosis, increased Urea]Recovery pahse – polyuria
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Acute Renal Failure → Prerenal (renal perfusion)
Shock, Renal artery stenosis
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Acute Renal Failure → Renal causes (parenchyml structures)
ATN
Acute GN
Acute inst nephritis
CRF
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Acute Renal Failure → Post Renal (urine output)
Obstructive lesions
Stones
Tumours
68
Nephrolithiasis: Description
Stone formation either in the kidney or renal tract
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Nephrolithiasis: Epi
* 20-30 yrs M>F
* 5% of population
* Reoccurrence - 40 to 70%
* Symptomatic – 50% will cause some problem with 5 years of discovery
70
Nephrolithiasis: Stone types
* Calcium oxalate
* Triple phosphate (magnesium ammonium calcium phosphate)
* Urate
* Cystine
71
Nephrolithiasis: Calcium oxalate
Hypercalcaemia/Idiopathic hypercalciuria 75%
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Nephrolithiasis: Triple phosphate (magnesium ammonium calcium phosphate)
Proteus infection which splits urea into ammonium (Staghorn calculus) 15%
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Nephrolithiasis: Urate
Hyperuricaemia (GOUT) 6%
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Nephrolithiasis: Cystine
In born error of metabolism 1%
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Nephrolithiasis:Predisposition to conditions
Dehydration
Sarcoidosis hypercalcaemia (Granuomas produce VitD)
Cushing disease hypercalcemi
Oxalate rich food broccoli, celery
Bladder obstruction urine stasis, stagnant urine
Polycystic disease congenital disorder
Medullary sponge kidney congenital disorder
Calycael diverticula congenital disorder
Urinary diversions crystallation on exposed metallic surgical clips
Stents, catheters crystallisation on foreign substances
76
Renal Tumours: Types
Childhood –Wilm’s tumour
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Renal Tumours: Benign
Papillary adenomas. Fund at autopsy (<5mm), Fibroma
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Renal Tumours:Malignant -
Renal cell Carcinoma (80%) TCC (20%)
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Renal Tumours: Renal cell carcinoma risk factors
Smoking
HTN
Obesity
Heavy Metals
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Renal Tumours:Von Hippel Lindau syndrome
Haemangioblastoma of cerebellum
Retina
Renal cyst
Bilateral RCC
81
Renal Tumours:Clinical presentation of Renal tumours
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Paraneoplastic conditions
e.g.
• Polycythemia
• Hypercalcaemia
• Liver
• Dysfunction
• Cushing syndrome
• Amyloidosis
Palpable mass
Haematuria
Backpain
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82
Renal Tumours: Histotypes
Clear cell
| Papillary and chromophobe
83
Renal Tumours:Survival
5 yrs 70% if no mets, 45% if mets
84
Renal Tumours: Microscopic findings
Clear cytoplasm and sharply outlined cell membrane
