Flashcards in Renal pathology Deck (35):
Types of renal carcinoma
Clear cell - well differentiated
Papillary (15%) - dialysis-associated cystic disease, >5mm;
Chromophobe - pale eosinophilic cells.
Also Wilms' - children, small round blue cells, RUQ mass.
RF for renal carcinoma
Smoking, obesity, hypertension, unopposed oestrogen, heavy metals, CKD.
Features of renal carcinoma
Haematuria, palpable mass, costovertebral pain.
Paraneoplastic syndrome: polycythaemia, ^Ca, HTN, Cushing's, amyloid.
Classification of (non-neoplastic) renal pathogy
2. Tubules and interstitium
- Acute tubular necrosis (acute tubular injury)
- Interstitial nephritis
3. Blood vessels
Nephrotic syndrome features
Proteinuria (3g/24h), hypoalbuminaemia, oedema.
"Swelling" (facial in children), "frothy urine".
Due to loss of foot processes (only seen on EM).
Primary causes of nephrotic syndrome
1. Minimal Change Disease
2. Membranous glomerular disease
3. Focal segmental glomerulosclerosis
All show loss of foot processes on EM.
Minimal change disease
No change on microscopy, no immune deposits, (loss of foot processes on EM).
90% respond to steroids. 5% get ESRF.
Membranous glomerular disease
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.
Focal segmental glomulerosclerosis
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.
Seondary causes of nephrotic syndrome
1. Diabetes (Kimmelstiel Wilson nodules);
2. Amyloidosis (chronic inflam, Ig light chains, macroglossia, heart failure, big liver).
Nephritic syndrome features
dysmorphic RBCs and red cell casts in urine.
?: hyertension, oliguria, proteinuria, ^urea and Cr.
Causes of nephritic syndrome (5)
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)
Acute post-infectious glomerulonephritis
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;
LM: ^ cellularity,
FM: granular deposits of Ig and C3 in GBM,
EM: subendothelial humps.
Rapidly progressive / crescentic glomerulonephritis
Most aggressive: ESRF in weeks. Pronounced oliguria and renal failure.
All show crescents on LM. Classified by immunological findings.
Type 1 Rapidly progressive (crescentic) GN
Anti-GBM Ab, because Goodpasture
Ab to COL4-A3. HLA-DRB1.
LM: Obviously crescents.
FM: Linear IgG deposits in GBM.
Also lungs (pulmonary haemorrhage).
Type 2 Rapidly progressive (crescentic) GN
Due to SLE / IgA nephropathy / Acute post-infectious GN.
LM: Obviously crescents.
FM: Granular (lumpy bumpy) IgG immune complexes.
Type 3 Rapidly progressive (crescentic) GN
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.
= Berger disease.
Frank haematuria 1-2 days after upper RTI. Recurrent.
Commonest GN worldwide.
IgA immune complexes deposited in glomeruli.
= 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.
Thin basement membrane disease
= benign familial haematuria
ie. usually doesn't cause nephritic syndrome, renal function usually normal.
AD, type IV collagen alpha 4 chain.
Causes of asymptomatic haematuria
Thin basement membrane disease,
IgA nephropathy (Berger),
Bacterial infection of kidney, usually ascending E. coli.
Fever, flank pain, leukocytes, ?urinary Sx.
Leukocytic casts in urine.
Ciprofloxacin or co-amox.
Chronic bacteria, inflam, scarring.
- obstruction: calculi, posterior urethral valves
- vesico-ureteric reflux = reflux nephropathy
Acute interstitial nephritis
Hypersensitivity reaction to drug,
days after exposure,
fever, rash, haematuria, proteinuria, eosinophilia.
Chronic interstitial nephritis
= Analgesic nephropathy
ie. old people on lots of NSAIDs.
Sx = late.
Acute tubular injury
= Acute tubular necrosis.
Damage, blockage by casts, ischaemia, ARF.
Commonest cause of ARF.
- ischaemia (burns, septicaemia),
- nephrotoxins: drugs, contrast, myoglobin (rhabdomyolysis), heavy metals.
Necrosis of short segments of tubules.
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).
Haemolytic uraemic syndrome
Diarrhoea by E. coli 0157:H7 (pettng zoos).
Thrombi in kidneys only.
Thrombotic thrombocytopaenic purpura
Thrombi all around, incl CNS, so neuro Sx.
Can give renal failure, but not often.
Acute kidney injury (ARF)
? -> metabolic acidosis, ^K, fluid overload, hypo-Ca.
Most common AKI.
- Acute pancreatitis / other causes of SIRS
- Renal artery stenosis
Renal causes of AKI (3)
- Acute tubular necrosis (commonest renal cause of AKI)
- Acute glomerulonephritis
Chronic kidney disease: (=CRF)
Sx, causes, staging.
Progressive irreversible loss of renal function,
Uraemia Sx: fatigue, itching, anorexia, confusion.
- Hypertension / vascular disease
- Chronic pyelo (reflux)
5 stages based on GFR of 90, 60, 30, 15.
Adult polycystic kidney disease
10% of PCKD
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).