Glomerular Disease Flashcards

1
Q

What is glomerulonephritis?

A

Inflammation of the glomerulus
Responsible for 15% end stage kidney disease

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2
Q

How is glomerulonephritis diagnosed?

A

Often relies on kidney biopsy and classified following findings

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3
Q

What are features of glomerulonephritis?

A

Harmaturia
Proteinurea
Hypertension
Renal impairment

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4
Q

What is a nephritic state?

A

Active urine sediment dysmorphic rbcs cellular casts
Hypertension
Renal impairment

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5
Q

Nephrotic syndrome

A

Odema
Nephrotic range proteinuria:3.5g per day or 350mg/mmol creatinine
Hypoalbuminemia
Dyslipidaemia

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6
Q

What can glomerulonephritis be separated into?

A

Proliferation and non proliferation

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7
Q

What is proliferation glomerulonephritis?

A

Excessive numbers of cells in glomeruli these include infiltrating leukocytes

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8
Q

Non proliferative glomerulonephritis?

A

Glomeruli look normal or have areas of scarring
They have normal numbers of cells

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9
Q

Diffuse

A

> 50% glomeruli affected

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10
Q

Focal

A

<50% glomeruli affected

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11
Q

Global

A

All glomeruli affected

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12
Q

Segmental

A

Part of the glomerulus affected

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13
Q

What is the most common cause of glomerulonephritis?

A

IgA nephropathy

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14
Q

What is IgA nephropathy characterised by?

A

IgA deposition in mesangium and mesangial proliferation

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15
Q

When is IgA nephropathy most common?

A

In 2nd and 3rd decades of life

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16
Q

What is the presentation of IgA nephropathy?

A

Microscopic haematuria
Microscopic haematuria and proteinuria
Nephrotic syndrome
IgA crescentic glomerulonephritis

17
Q

What is post streptococcal glomerulonephritis?

A

Follows 10-21 days after infection typically throat or skin
Most commonly with lancefeild group A streptococci

Genetic predisposition HLA-DR -DP

18
Q

What is Anti GBM disease?

A

Rare disease caused by circulating anti GBM

Around 10-20% of crecentix glomerulonephritis

19
Q

How does anti GMB disease present?

A

Nephritis
Nephritis lung haemorrhage

20
Q

How is Anti GBM disease diagnosed?

A

Two peaks 3rd decade and and 6/7th decade of life
Diagnosed by demonstrating anti-GBM antibodies in serum and kidney

21
Q

What is treatment for anti-GBM disease?

A

Aggressive immune suppression steroid plasma exchange and chclophophamide

22
Q

Summarise proliferative glomerulonephritides?

A

Present with nephritic state
Haematuria
Variable proteinuria
Hypertension
Renal impatiente
Rapid decline in function that leads to dialysis
Early diagnosis necessary to save nephrons

23
Q

Non proliferative glomerulonephritis?

A

Minimal change disease
Focal and segmental glomerulonephritis
Membranous nephropathy

24
Q

Nephrotic syndrome management?

A

treat oedema: salt and fluid restriction and loop diuretics
Hypertension use renin angiotensisn aldosterone blockade
Reduce risk of thrombosis heparin or warfarin
Reduce infective risk pneumococcal vaccine
Treat dyipidaemia

Specific therapy towards cause of non proliferative glomerulonephritis

25
Minimal change disease?
Commonest form in children Sudden onset odema Remission with steroids Relapse in two thirds of patients
26
Minimal change disease treatment
Prednisone Once remission achieved slow taper over 6 months Initial pelapse treated with steroid course
27
What do subsequent relapses of minimal change disease get treated with?
Cuclophophamide Cyclosporine Tacrilimus Mycophenolaye Rituximab
28
Membranous nephropathy
Commonest cause nephrotic syndrome adults Majority cases occur in isolation Serological markers Antiphospholipidase a2 receptor Theombospondun Secondary causes Malignancies Ale Rheumatoid arthritis Drugs
29
How is membranous nephropathy treated
General measure for at least 6 months Immunosuppressive Cyclophosphamide and steroids for 6 months Tacrilimus Rutuximab Resolves spontaneously in a third of patients
30
30 male referred to the renal clinic by GP for incidental microscopic haematuria. BP 150/90 mmHg. Creatinine 80 µmol/L, eGFR>60 ml/min/1.73m2. Urine dip: RBC+++, Protein ++. Urine protein creatinine ratio=180mg/mmol creatinine Renal US: normal kidney size with no structural abnormalities. what do you do?
You decide to start ACE-I. You also decide to perform a renal biopsy. Renal biopsy confirms IgA nephropathy.
31
30 male referred to the renal clinic by GP for incidental microscopic haematuria. BP 150/90 mmHg. Creatinine 80 µmol/L, eGFR>60 ml/min/1.73m2. Urine dip: RBC+++, Protein ++. Urine protein creatinine ratio=180mg/mmol creatinine Renal US: normal kidney size with no structural abnormalities. following initial treatment At 5 years: serum creatinine 210 µmol/L and eGFR 32 ml/min/1.73m2. 10 years later, serum creatinine 480 µmol/L and eGFR 14 ml/min/1.73m2. Brother considered as kidney donor for living kidney transplantation. what is he suffering from?
Post Infectious Glomerulonephritis
32
Six-year-old boy brought to GP generally unwell, dark urine Puffy face, no rashes no oedema, BP 135/86mmHg Sore throat 2 weeks previously Presumptive diagnosis post-streptococcal nephritis what investigations should be done? how should this be treated?
Hb 130g/L; WCC 11.3 x 109. Urea 11.2mmol/L, creatinine 160μmol/L. Urine microscopy RBC +++, casts +. Complement: low C3. Antibiotics for infection, debatable. Loop diuretics such as frusemide for oedema. Anti-hypertensives e.g. vasodilator drugs.
33
what are different types of crescentic glomerulonephritis?
34
60-year-old woman presents to GP with three-month history of increasing tiredness, anorexia and weight loss. Physical examination revealed a rash on both ankles and lower legs, and bilateral basal crepitations: BP 150/85 mmHg. Urine dipstick: protein+++ and blood++. Serum creatinine 640 µmol/L, eGFR 8 ml/min/1.73m2. what investigations and treatment should be done?
Anti-neutrophil cytoplasmic antibodies positive with MPO-ANCA of >134 units/L. Renal biopsy Focal necrotizing glomerulonephritis. Treatment: High dose steroids Cyclophosphamide Plasma exchange
35
22-year-old woman presents with bilateral leg oedema which has developed suddenly over a week. She also describes breathless and chest pain. Urine dip ++++ protein. what investigations and treatment should be done?
Urine protein creatinine ration 400mg/mmol. Creatinine 60 mmol/l and eGFR of >60 ml/min/1.73m2 Serum Albumin 15 g/L Haemoglobin 154 g/L Cholesterol 9.2 mmol/l Pregnancy test negative. Salt and fluid restrictions. Daily weights. Loop diuretic e.g. Furosemide. Thromboprophylaxis e.g. low molecular weight heparin. Prednisolone 60 mg per day Achieved remission after 8 weeks of treatment. Diuretics and thromboprophylaxis stopped. Prednisolone dose tapered over 6 months.
36
what is focal and segmental glmerulonephritis?
Is not a single disease, rather a syndrome with multiple causes. Presents with nephrotic syndrome. Pathology reveals focal and segmental sclerosis with distinctive patterns e.g. tip lesion, collapsing, cellular, perihilar, and not otherwise specified. Primary (idiopathic) or secondary. Generally steroid resistant. High chance of progression to end stage kidney disease.
37
what is the treatment for focal and segmental glmerulonephritis?
General measures, as previously described. Trail of steroids, positive response , even partial remission, carries better prognosis. Alternative options: cyclosporin, cyclophosphamide, and Rituximab.
38
34-year-old man presented with severe oedema which developed over 3 weeks Investigations Urine PCR 560mg/mmol creatinine Serum albumin 18 g/L Serum creatinine 130 µmol/L, eGFR 56 ml/min/1.73m2 Renal biopsy showed FSGS. what is the treatment?
Diuretics helped to reduce oedema. Prednisolone - no response. Trial of cyclosporin – progressively rising serum creatinine. Serum creatinine at 280 µmol/L and eGFR 26 ml/min/1.73m2 at 8 months from presentation. At 18 months serum creatinine 540 µmol/l and eGFR 11 ml/min/1.73m2. Pre-emptive renal transplantation from brother, early recurrence post-transplant. Plasma exchange and Rituximab. Remission at 3 months post-transplant with serum creatinine 80µmol/L and normal serum albumin.
39
66-year old man presented with cough, breathlessness, and peripheral oedema. He smokes 20 cpd. Urine dip: Proteinuria ++++ Urine protein creatinine ration 580mg/mmol. Serum albumin 20 g/L. Serum creatinine 135mmol/l Renal biopsy: confirms membranous nephropathy. what investigations and treatment should be done?
CT chest/abdomen/pelvis: suggestive of lung cancer. Bronchoscopy and biopsy confirm squamous cell carcinoma. General measures for nephrotic syndrome. No immunesuppression. At 3 months: partial remission following radiotherapy Present with nephrotic syndrome. Renal biopsy is key investigation. Identify cause, if possible. General measures are important in all cases. Specific treatment as appropriate.