Uropathology Flashcards
Painless haematuria Ddx?
Malignany
Glomerulonephritis
Drugs which cause urine discolouration?
Rifampicin, metronidazole, nitrofurantoin, warfarin, phenytoin
ACR > 70 ?
strongly suggestive of glomerular pathology.
Referals for haematuria?
MACROSCOPIC USUALLY = BLADDER
MICROSCOPIC USUALLY = RENAL
Haematuria - investigations not to forget?
SERUM CREATININE
PROTEINURIA (PCR OR ACR)
What are mesangial cells?
make up the vascular pole ‘stalk’. They sit between the capillaries. Mesangial cell nuclei are very heterochromatic and dark.
Glomerulonephritis - pathophysiology?
(1) Proliferation of glomerular cells (epithelial + mesangial cells)
(2) ==> leading to BM thickening or podocyte foot process effacement
(3) Associated tubulo-interstitial damage
Primary causes of GN?
Intrinsic to kidney: Membranous, minimal change, FSGS
Secondary causes of GN?
- Infection - bacterial, viral, parasitic
- Autoimmune disease -eg. lupus
- Drugs
- Malignancy - eg. multiple myeloma
Nephrotic syndrome?
Proteinuria (> 3 g/24 hr)
Hypoalbuminaemia (< 30 g/L)
Oedema
Nephritic syndrome?
Haematuria
Oligouria
Hypertension
What does nephrotic syndrome result it?
- Hypercholestralaemia - predisposing to ACS and stroke
- Increased risk of thrombosis due to loss of antithrombin III, protein C and S and associated rise in fibrinogen levels
- Increased infections - renal loss of immunoglobulins
- Hypocalcaemia due to vitD binding protein lost in urine
Nephrotic - type of GN?
Non-proliferative
Nephritic type of GN?
Proliferative
What presents with pure nephritic syndrome?
(all As)
ANCA+ve ones (Rapidly progressive GN/crescenteric)
IgAnephropathy
Alport’s syndrome
Lupus nephritis
Anti-GBM
Most common causes of nephrotic syndrome?
Children = minimal change disease.
Adults = focal segmental glomerulosclerosis.
Overall = Membranous GN
General approach to treating GN?
Steroids +/- cyclophosphamide
Reducing proteinuria: with an ACEi or ARB
Preventing VTEs: with aspirin, plus anticoagulation in anyone with albumin <20g/L
Treating hyperlipidaemia: with statins if indicated
If refractory / complications: consider dialysis
Minimal change disease?
- PP and Tx
fusion of podocytes and effacement of epithelial foot processes.
Treatment: steroids steroids and steroids.
Focal segmental glomerulosclerosis?
PP and Tx
Biopsy: scarring of some segments of some glomerulus (hence FOCAL and SEGMENTAL.
Treatment: ACEi/ARB and BP control, steroids
Membranous nephropathy
PP, biopsy and Tx?
Can by primary or secondary to malignancy, autoimmune disease, infection (hep B/C) etc.
Biopsy: diffusely thickened GBM due to Ig deposits, subepithelial deposits of immune complexes (under the podocytes), spike & dome pattern; anti-PLA2R positive
Treatment: ACEi/ARB and BP control; steroids + cyclophosphamide
Membranoproliferative glomerulonephritis
PP and Tx?
proliferation of mesangial cells on light microscopy, may see immune complex deposition
Treatment: ACEi/ARB and BP control; steroids
IgA nephropathy
PP and Tx:
Classically causes macroscopic haematuria just a few days post viral infection.
Biopsy: IgA and C3 deposition in the mesangium.
Treatment: if mild none, otherwise ACEi + steroids in progressive disease.
Post-streptococcal (Diffusely Proflierative)
- What is it?
- Biopsy?
- Treatment?
Streptococcal infection 1-3 weeks before. Patients classically - Low C3, AntiStreptolysin O Test positive.
Biopsy: Immune complex deposition in glomeruli. Granular appearance.
Treatment: None needed usually. Monitor for hypertension.
HSP (in children mostly)
Related to IgA. More systemic IgA vasculitis.
Presents with tetrad of non-blanching purpuric rash, abdominal pain, polyarthritis and renal impairment which manifests similarly to IgA nephropathy.
Treatment: usually supportive and analgesia for arthralgia
Prognosis: usually excellent. Monitor BP and urinalysis to detect progressive renal involvement. ⅓ can relapse.