What are features of glomerulonephritis?
What is the difference between nephrotic and nephritic syndrome?
Nephrotic - proteins in the urine
Nephritic - inflammation of the kidney
What is macroscopic and microscopic haematuria?
•Macroscopic, tea- or cola colored or frank blood
•Microscopic, =>5 RBC per high power field
What is the duration of haematuria?
Can be transient or persistent
What is the more likely syndrome for haematuria - nephritic or nephrotic syndrome?
What is the source of blood in the urine?
•Source: kidney, ureter, bladder, prostate, urethra
What is the finding of microscopy on persistent microscopic haematuria?
•In glomerulonephritis: persistent micorscopic haematuria, microscopy shows dysmorphic RBC (Mickey-mouse-like)
What are the types of proteinuria?
•Glomerular or tubular
•Albuminuria or proteinuria
•Persistent or transient
Which is more common for proteinuria - nephritic syndrome or nephrotic syndrome?
They are equal
How do you determine proteinuria?
•Urine protein creatinine ratio or 24 hour urine collection
What is the definition of persistent proteinuria?
More than 1 gram/mmol creatinine
What is defined as hypertentsion?
What condition is more likely to present with hypertension? Renal insufficiency? Nephritis or nephrotic syndrome?
Renal insufficiency can be mild or severe
May have slow or rapid deterioration
What are the features of nephritic state?
•Active urine sediment: haematuria, dysmorphic RBCs, cellular casts
What are the features of nephrotic syndrome?
•Proteinuria >3.5 g/day
•Can be caused by primary (idiopathic) glomerular disease or secondary glomerular diseases
What is the differential diagnosis for nephrotic syndrome?
•Congestive Heart Failure (JVP raised, normal albumin, minimal proteinuria)
•Hepatic Disease (abnormal LFTs, no proteinuria)
What are the different classifications of glomerulonephritis?
•Aetiology: autoimmune, infection, malignancy, drugs, others
•Primary versus secondary i.e. kidney alone or part of multisystem disease.
What is the difference between proliferative and non-proliferative glomerulonephritis?
Proliferative: Excessive numbers of cells in the glomeruli - these include infiltrating leucocytes
Non-proliferative: Glomeruli look normal or have areas of scarring. They have normal numbers of cells
What is the definition of glomerulonephritis that is, diffuse, focal, global and segmental?
•Diffuse: >50% of glomeruli affected
•Focal: <50% of glomeruli affected
•Global: all the glomerulus affected
•Segmental: part of the glomerulus affected
Which glomerulonephritis syndrome causes urinary sediment abnormalitites and proteinuria?
What types of glomerulonephritis cause nephrotic syndrome?
Minimal change disease
What types of glomerulonephritis cause a nephritic state?
•Anti-neutrophil cytoplasmic antibody (ANCA) associated glomerulonephritis
What are the different types of proliferative glomerulonephritis?
• Diffuse proliferative - post-infective nephritis
• Focal proliferative - mesangial IgA disease
• Focal necrotizing (crescentic) nephritis
• Membrano-proliferative nephritis
What are the features of post-streptococcal glomerulonephritis?
Follows 10 - 21 days after infection typically of throat or skin
•Most commonly with Lancefield group A Streptococci.
•Genetic predisposition: HLA-DR, -DP, -DP.
What are the drugs sued to treat post-infective glomerulonephritis?
•Antibiotics for infection, debatable.
•Loop diuretics such as frusemide for oedema
•Vasodilator drugs (e.g. amlodipine) for hypertension
What is the most common cause of glomerulonephritis?
What is IgA nephropathy characterised by?
IgA deposition in the mesangium and mesangial proliferation
Who is IgA most common in?
2nd and 3rd decade of life
Men more commonly affected
What is the prognosis of IgA nephroapthy?
•Up to 40% of cases can progress to end stage kidney disease.
What is the presentation of IgA nephropathy?
•Micoscopic haematuria + proteinuria
•In rare cases - Nephrotic syndrome (it usually presents with nephritic syndrome)
•IgA crescentic glomerulonephritis
What are the causes of crescentic glomerulonephritis?
ANCA associated - anti neutrophil cytoplasmic antibody assocaited:
1. Microscopic polyangitis
2. Granulomatosis with polyangitis
3. Eosinophilic granulomatosis with polyangitis
•Anti-glomerular basement membrane (GBM) e.g. anti-GBM nephritis or Goodpasture’s syndrome
•1. IgA vasculitis.
•2. post-infection glomerulonephritis.
What percentage of crescentic glomerulonephritis is caused by anti-GBM?
What is the presentation of antiGBM glomerulonephritis and goodpastures syndrome?
•Nephritis (anti-GBM glomerulonephritis)
•Nephritis+ lung haemorrhage (Goodpasture’s syndrome).
Two peaks: 3rd decade of life and 6th/7th decade of life
How is Anti-GBM disease diagnosed?
•Diagnosed by demonstrating anti-GBM antibodies in serum and kidney
How is anti-GBM treated?
•Treatment: aggressive immunesuppression: steroid, plasma exchange, and cyclophosphamide.
Give examples of the possible immunosuppression treatment for crescentic glomerulonephritis management
•Cytotoxic e.g. Cyclophosphamide
•B-cell therapy e.g. Rituximab
What is the prognosis for crescentic glomerulonephritis?
•Prognosis is good provided treatment is started early enough
Summary for proliferative glomerulonephritides
•Present with nephritic syndrome
•Blood on dipstix – variable proteinuria
•Can cause rapid decline in renal function leading to dialysis
•Early diagnosis and appropriate treatment
What are the examples of non-proliferative glomerulonephritis?
•Minimal Change Disease
•Focal and segmental glomerulonephritis
What are the general measures in managing nephrotic syndrome management?
Risk of thrombosis?
Risk of infection?
•Treat oedema: salt and fluid restriction and loop diuretics.
•Hypertension: use Renin-Angiotensin-Aldosterone-blockade.
•Reduce risk of thrombosis: Heparin or Warfarin.
•Reduce risk of infection e.g. pneumococcal vaccine.
Treat dyslipidemia e.g. statins
•Specific therapy towards cause of the non-proliferative glomerulonephritis
What is the commonest form of non-proliferative glomerulopathy in children?
Minimal change nephrotic syndrome
What is the onset of minimal change nephrotic syndrome?
Sudden onset of oedema - days
Describe proteinuria in minimal change nephrotic syndrome
•Complete loss of proteinuria with steroids
What is relapse rate for minmal change?
•Two thirds of patients relapse
What is the treatment of minimal change?
•Prednisolone – 1mg/kg for up to 16 weeks.
•Once remission achieved , slow taper over 6 months.
•Initial relapse treated with further steroid course.
•Subsequent relapses treated with
What is the prognosis for minimal change glomerulopathy?
•Despite relapsing behaviour, prognosis is favourable.
•Risk of end stage kidney disease is low.
Steroids toxicity as multiple exposure
What is the presentation of focal and segmental glomerulonephritis?
Not a single disease - a syndrome with multiple causes
Presents with nephrotic syndrome
What are the distinctive patterns of focal and segmental glomerulonephritis?
•Pathology reveals focal and segmental sclerosis with distinctive patterns e.g.
tip lesion, collapsing, cellular, perihilar, and not otherwise specified
Can be either primary or secondary
What is the treatment for focal and segmental glomerulosclerosis?
•General measures, as previously described.
Generally steroid resistant
•Trail of steroids, positive response , even partial remission, carries better prognosis.
Alternative options: cyclosporin, cyclophosphamide, and Rituximab
What is the commonest cause of nephrotic syndrome in adults?
Most of the cases occur in isolation (idiopathic)
What are the serological markers for membranous nephropathy?
•Anti-phospholipase A2 receptor (PLA2R) antibody positive in 70% of idiopathic cases
•Thrombospondin type 1 domain containing 7A (THSD7A).
What are the secondary causes of membranous nephropathy?
Drugs: NSAIDs, Gold, Penicillamine
What is the treatent for membranous nephropathy?
•General measures for at least 6 months.
•Immunesuppression if symptomatic nephrotic syndrome, rising proteinuria or deteriorating renal function.
•Cyclophosphamide and steroids (alternate months) for 6 months.
•Resolves spontaneously in a third.
•Prognosis good in treated patients whose proteinuria resolves
•About 25% are on dialysis at 10 years
•Can recur in renal transplants
Summary for non-proliferative glomerulonephritis
•Present with nephrotic syndrome.
•Renal biopsy is key investigation.
•Identify cause, if possible.
•General measures are important in all cases.
•Specific treatment as appropriate.