SLIME
Week 4: Renal Medicine
Nephritic and nephrotic syndrome.
Proteinuria:
Normal protein loss: <150mg/day
Microalbuminuria: 30-300mg/day (early sign of diabetic nephropathy)
Proteinuria: 300mg – 4.5g/day ( if >2g/day + microscopic haematuria +/- renal impairment  renal biopsy)
Protein loss <2g/day could be glomerular or tubular or overflow proteinuria
Protein loss >2g/day is usually glomerular.
Causes of proteinuria:
o Myeloma (Bence-Jones protein- immunological light chains)
o Diabetic nephropathy (initially microalbuminuria)
o Glomerulonephritis
o Amyloidosis
o Drugs (NSAIDs, DMARDs)
o SLE (lupus nephritis)
Nephrotic syndrome
o
o
o
o
Proteinuria
(protein: creatinine ratio (PCR) greater than 200 mg/mmol)
Oedema
(children usually present with facial swelling, adults with peripheral oedema)
Hypoalbuminaemia
(serum albumin <25g/L)
Hyperlipidaemia
(total cholesterol >10 mol/L)
Causes:
Primary renal causes:
o Glomerulonephritis:
o Minimal change disease,
o Membranous nephropathy,
o Focal segmental glomerulonephritis
Secondary renal causes:
o Diabetes mellitus
o Renal amyloid
o Drugs (NSAIDs, DMARDs)
o SLE
o Post-infective e.g. HIV, TB
Complications:
o Hypercoagulability  DVT / renal vein thrombosis and dramatic worsening of Renal function.
o Infection: as hypogammaglobulinaemia and impaired immune system.
Treatment:
o Salt and fluid restrict (refer to dietician)
o Diuretics to reduce oedema (care not to cause hypovolaemia which will worsen renal function)
o ACEi to reduce protein loss and any hypertension
o Statins
o Warfarin (evidence base: only warfarinise post-VTE, however, some warfarinise if alb <20)
o Minimal change disease responds to steroids.
o Other glomerulonephritides respond to immunosuppressants e.g. cyclophosphamide.
SLIME
Week 4: Renal Medicine
Nephritic and nephrotic syndrome.
Nephritic Syndrome
o
o
o
o
o
Haematuria
(Mild proteinuria (not enough to cause hypoalbuminaemia))
Oedema (unable to excrete water) occasional oliguria
Hypertension
Uraemia (varies according to GFR)
↓GFR  oliguria  Na retention  HTN
Causes:
Primary renal causes:
o Glomerulonephritis:
o Rapidly progressive glomerulonephritis
Secondary renal causes:
o Post-streptococcal GN (2-3 weeks post B-haemolytic strep throat infection)
o Multisystem systemic diseases - eg systemic lupus erythematosus, vasculitis, Henoch-Schönlein
purpura, Goodpasture syndrome, Wegener granulomatosis
Treatment:
o Diuretics
o ACEi
o Dialysis may be needed for uraemia.
o Treatment dependent on underlying cause
Glomerulonephritis
A range of immune-mediated inflammatory disorders that cause inflammation within the glomerulus and
other compartments of the kidney.
Features raising suspicion of GN:
o Proteinuria + Haematuria (especially red cell casts)
o +/- Renal impairment
Primary GN: affects only both kidneys symmetrically.
Secondary GN: systemic illness, also causing GN e.g. Wegner’s granulomatosis, SLE, Diabetes.
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Primary glomerulonephritis classified according to:
– Clinical syndrome e.g. rapidly progressive GN
– Histopathological appearance e.g. minimal change GN
– Underlying aetiology. E.g. lupus nephritis
•
Glomerulonephritides may be:
– Minimal change.
– Diffuse: affecting all glomeruli.
– Focal: affecting only some of the glomeruli.
– Segmental: only affecting parts of an affected glomerulus.
SLIME
Week 4: Renal Medicine
Nephritic and nephrotic syndrome.
Acute GN
o Rapidly progressive GN
o Nephritic syndrome.
o Crescentic-shaped proliferation of cells in the Bowman’s capsule
o Commonly seen in vasculitidies
 Wegner’s
 Goodpasture’s syndrome (ARF and pulm haemorrhage caused by anti GBM)
 Post-infectious GN after strep infection.
o Develops to renal failure within days
o Needs aggressive Tx early.
o Membraneous GN
o Nephrotic syndrome
o Electron microscope: Thickened glomerular basement membrane due to immune deposition
o Causes:
 SLE
 Drugs
 Infection
 Malignancies
o Minimal change GN
o Nephrotic syndrome
o Light microscope: fused podocyte foot processes
o Commonest in children.
Chronic GN
Small shrunken kidneys  CRF with GN on biopsy
Often don’t biopsy as won’t change management and poses risk to kidneys.
Ix:
o
o
o
o
o
Renal function (serum creatinine, GFR)
Dipstick urine (protein, blood)
Microscopy for casts
24h urine protein excretion
Renal US for size
Significant proteinuria >1g/day suggests GN
Is this primary or secondary?
o pANCA, (WG)
o anti-GBM (Goodpasture’s)
o anti dsDNA (SLE)
o ANA , Scl-70 (scleroderma)
o Biopsy unless kidneys are small.
Treatment:
Minimal change GN
o Corticosteroids
o Relapses needs immunosuppression
Membranous GN
o Steroids and chlorambucil
o May resolve spontaneously, or RF.
Rapidly progressive GN
o Corticosteroids, cyclophosphamide and
plasmaphoresis.
o BP control to avoid further damage.
SLIME
Week 4: Renal Medicine
Nephritic and nephrotic syndrome.
HISTOLOGY
Normal kidney
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Electron micrography shows foot processes of the glomerular endothelial cells.
Minimal change disease.
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No change on light microscopy
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Electron microscopy shows fusion of foot processes (podocytes)
Diabetic nephropathy
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Sclerotic lesions.
Rapidly progressive GN
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Cresentic shaped proliferation of cells in Bowman’s capsule
Membranous GN
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Electron microscope: thickened glomerular basement membrane due to immune deposition
Clinical Scenario
A 24 year old man presents to clinic because he has been feeling more tired recently. He has no systemic
symptoms on questioning. The only thing he has noticed is that his urine is more frothy than normal, but he
has no urinary symptoms and has not noticed any blood. He is normally fit and well and on no regular
medication. He does not smoke and drinks alcohol socially. Examination is unremarkable. A urine dip
shows +++ protein
What are your main differential diagnoses for this gentleman? (make sure these include all important
differentials that must be ruled out)
How would you investigate this gentleman?
What would your management plan be for this gentleman?
What are the features of nephrotic syndrome and nephritic syndrome?
What are the complications of nephrotic syndrome?