Renal pathology Flashcards

1
Q

Types of renal carcinoma

A

Clear cell - well differentiated
Papillary (15%) - dialysis-associated cystic disease, >5mm;
Chromophobe - pale eosinophilic cells.
Also Wilms’ - children, small round blue cells, RUQ mass.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

RF for renal carcinoma

A

Smoking, obesity, hypertension, unopposed oestrogen, heavy metals, CKD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Features of renal carcinoma

A

Haematuria, palpable mass, costovertebral pain.

Paraneoplastic syndrome: polycythaemia, ^Ca, HTN, Cushing’s, amyloid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Classification of (non-neoplastic) renal pathogy

A
  1. Glomerulus:
    - Nephritic
    - Nephrotic
    1. Tubules and interstitium
      • Acute tubular necrosis (acute tubular injury)
      • Pyelonephritis
      • Interstitial nephritis
    2. Blood vessels
      • HUS
      • TTP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Nephrotic syndrome features

A

Proteinuria (3g/24h), hypoalbuminaemia, oedema.
“Swelling” (facial in children), “frothy urine”.
Due to loss of foot processes (only seen on EM).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Primary causes of nephrotic syndrome

A
  1. Minimal Change Disease
  2. Membranous glomerular disease
  3. Focal segmental glomerulosclerosis
    All show loss of foot processes on EM.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Minimal change disease

A

Chidren.
No change on microscopy, no immune deposits, (loss of foot processes on EM).
90% respond to steroids. 5% get ESRF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Membranous glomerular disease

A

Adults.
Diffuse thickening of basement membrane.
EM: lose foot processes, subepithelial deposits.
Immunofluorescence: Ig and complement all along BM.
Poor response to steroids. 40% get ESRF eventually.
Can be 2o to SLE, infection, drugs, cancer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Focal segmental glomulerosclerosis

A

Adults, AC.
Bits of glomerular scarring, with hyalinosis.
Immunofluorescence shows Ig and complement in scarred areas.
50% respond to steroids, but 50% get ESRF.
Can be 2o to obesity or HIV nephropathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Seondary causes of nephrotic syndrome

A
  1. Diabetes (Kimmelstiel Wilson nodules);

2. Amyloidosis (chronic inflam, Ig light chains, macroglossia, heart failure, big liver).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Nephritic syndrome features

A

Haematuria,
dysmorphic RBCs and red cell casts in urine.
?: hyertension, oliguria, proteinuria, ^urea and Cr.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Causes of nephritic syndrome (5)

A
  1. Acute post-infectious GN (after strep)
  2. Rapidly progressive / crescentic GN
  3. IgA nephropathy (Berger disease)
  4. Hereditary nephritis (Alport syndrome)
  5. Thin basement membrane disease (benign familial haematuria)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Acute post-infectious glomerulonephritis

A

1-3 weeks after strep throat or impetigo (Staph aureus or Strep pyogenes (group A beta haemolytic));
Immune complexes damage BM;
Raised ASO titre, low C3;
Biopsy:
LM: ^ cellularity,
FM: granular deposits of Ig and C3 in GBM,
EM: subendothelial humps.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Rapidly progressive / crescentic glomerulonephritis

A

Most aggressive: ESRF in weeks. Pronounced oliguria and renal failure.
All show crescents on LM. Classified by immunological findings.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Type 1 Rapidly progressive (crescentic) GN

A
Anti-GBM Ab, because Goodpasture 
Ab to COL4-A3. HLA-DRB1. 
LM: Obviously crescents. 
FM: Linear IgG deposits in GBM. 
Also lungs (pulmonary haemorrhage).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Type 2 Rapidly progressive (crescentic) GN

A

Immune complexes.
Due to SLE / IgA nephropathy / Acute post-infectious GN.
LM: Obviously crescents.
FM: Granular (lumpy bumpy) IgG immune complexes.

17
Q

Type 3 Rapidly progressive (crescentic) GN

A

Pauci-immune / ANCA associated,
ie. no anti-GBM or immune complexes.
Due to c-ANCA (Wegener’s) or p-ANCA (microscopic polyangiitis).
Vasculitis elsewhere - rashes and pulmonary haemorrhage.

18
Q

IgA nephropathy

A

= Berger disease.
Frank haematuria 1-2 days after upper RTI. Recurrent.
Commonest GN worldwide.
IgA immune complexes deposited in glomeruli.

19
Q

Hereditary nephritis

A

= Alport’s syndrome
X-linked mutn in type IV collagen alpha 5 chain.
Nephritic syndrome + sensorineural deafness + eye problems (lens & cataracts).
5-20yo. Progresses to ESRF.

20
Q

Thin basement membrane disease

A

= benign familial haematuria
ie. usually doesn’t cause nephritic syndrome, renal function usually normal.
AD, type IV collagen alpha 4 chain.
Prevalence 5%.

21
Q

Causes of asymptomatic haematuria

A

Thin basement membrane disease,
IgA nephropathy (Berger),
Alport’s.

22
Q

Acute pyelonephritis

A

Bacterial infection of kidney, usually ascending E. coli.
Fever, flank pain, leukocytes, ?urinary Sx.
Leukocytic casts in urine.
Ciprofloxacin or co-amox.

23
Q

Chronic pyelonephritis

A

Chronic bacteria, inflam, scarring.
Due to
- obstruction: calculi, posterior urethral valves
- vesico-ureteric reflux = reflux nephropathy

24
Q

Acute interstitial nephritis

A

Hypersensitivity reaction to drug,
days after exposure,
fever, rash, haematuria, proteinuria, eosinophilia.

25
Chronic interstitial nephritis
= Analgesic nephropathy ie. old people on lots of NSAIDs. Sx = late.
26
Acute tubular injury
= Acute tubular necrosis. Damage, blockage by casts, ischaemia, ARF. Commonest cause of ARF. Caused by: - ischaemia (burns, septicaemia), - nephrotoxins: drugs, contrast, myoglobin (rhabdomyolysis), heavy metals. Necrosis of short segments of tubules.
27
Thrombotic microangiopathies affecting kidneys
HUS + TTP. Fibrin deposits cause thrombi, Plt and RBC damaged as they pass, and destroyed. ie. thrombocytopaenia (petechiae and other bleeding) and MAHA (pallor and jaundice).
28
Haemolytic uraemic syndrome
Children. Diarrhoea by E. coli 0157:H7 (pettng zoos). Thrombi in kidneys only. Renal failure.
29
Thrombotic thrombocytopaenic purpura
Thrombi all around, incl CNS, so neuro Sx. | Can give renal failure, but not often.
30
Acute kidney injury (ARF)
^Cr, ^urea. | ? -> metabolic acidosis, ^K, fluid overload, hypo-Ca.
31
Pre-renal AKI
``` Most common AKI. Renal hypo-perfusion: - Hypovolaemia - Sepsis - Burns - Acute pancreatitis / other causes of SIRS - Renal artery stenosis ```
32
Renal causes of AKI (3)
- Acute tubular necrosis (commonest renal cause of AKI) - Acute glomerulonephritis - MAHA
33
Chronic kidney disease: (=CRF) | Sx, causes, staging.
``` Progressive irreversible loss of renal function, Uraemia Sx: fatigue, itching, anorexia, confusion. Due to: - DM - Glomerulonephritis - Hypertension / vascular disease - Chronic pyelo (reflux) - PCKD 5 stages based on GFR of 90, 60, 30, 15. ```
34
Adult polycystic kidney disease
10% of PCKD AD: 85% PKD1 for polycystin 1 on Chr16; rest PKD2 on Chr4. Haematuria, flank pain, UTI. Cysts can infect, rupture and haemorrhage. Also berry aenurysms (and liver cysts in PKD1).
35
Lupus nephritis
SLE damages kidneys.