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Renal > Kidneys in Systemic Disease > Flashcards

Kidneys in Systemic Disease Flashcards

1
Q

What is needed to diagnose diabetic kidney disease?

A

Persistent albuminuria 300mg/24hours at least two samples 3-6 months apart

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2
Q

Describe the pathogenesis of diabetic nephropathy

A

Haemodynamic changes - increased GFR as afferent arteriolar vasodilation is mediated by vasoactive mediators
Renal hypertrophy - plasma glucose stimulates growth factors in the kidney

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3
Q

What do haemodynamic changes and renal hypertrophy lead to?

A

Mesangial expansion, nodule formation, proteinuria and tubule-interstitial fibrosis

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4
Q

How is diabetic nephropathy treated?

A

BP target 120/70
ACEi or ARB
Lipid control
Kidney/pancreas transplant

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5
Q

Define vasculitis

A

Inflammation of blood vessels

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6
Q

Why is ANCA vasculitis often misdiagnosed initially?

A

Presents with very vague symptoms and prodromal symptoms may last months before specific organ involvement

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7
Q

Name the three types of ANCA vasculitis

A
  • eosinophilic granulomatosis polyangiitis
  • granulomatosis with polyangiitis
  • microscopic polyangiitis
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8
Q

Describe eosinophilic GPA

A

Presents with last onset asthma, rhinosinusitis, palpable purpura, subcutaneous nodules

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9
Q

What is granulomata?

A

Dead tissue that does not function due to macrophage

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10
Q

Describe GPA

A

Nasal crusting, saddle nose, blood discharge, ulcers, sinusitis

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11
Q

Describe microscopic polyangiitis

A

Cough, hoarseness, SOB, haemoptysis

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12
Q

How will ANCA vasculitis affect the kidneys?

A

Haematuria and proteinuria

Biopsy will show segmental necrotising glomerulonephritis

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13
Q

How is ANCA vasculitis diagnosed?

A

Immunology - GPA (anti-PR3) Microscopic (anti-MPO)

Virology

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14
Q

Describe the treatment of ANCA vasculitis

A

Immunosuppression (cyclophosphamide/rituximab)
Plasma exchange
Supportive (dialysis and ventilation)

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15
Q

What percentage of patients with SLE will develop nephrotic syndrome?

A

50%

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16
Q

What antibodies are associated with SLE?

A

ANA
dsDNA
Sm

17
Q

Describe the classification of SLE renal disease

A 
I - minimal mesangial proliferation 
II - mesangial proliferation 
III - focal proliferative
IV - diffuse proliferative 
V - membranous 
VI - advanced sclerosing
18
Q

What is the treatment for class I and II SLE renal disease?

A

I - extra renal manifestations treated

II - if >3g proteinuria steroids, BP control

19
Q

What is the treatment for class III and IV SLE renal disease?

A

III - steroids and either cyclophosphamide or MMF

IV - maintenance, azathioprine/MMF and low dose steroids

20
Q

What is the treatment for membranous SLE renal disease?

A

Steroids, cyclophosphamide/MMF/Azathioprine

21
Q

What should all patients with SLE be on?

A

Hydroxychloroquine

22
Q

What are dysproteinaemias?

A

Overproduction of immunoglobulin by clonal expansion of cells from B cell lineage

23
Q

What are the sub-types of dysproteinaemias?

A

Deposition,
Complement and cytokine activation
Precipitation/crystallisation

24
Q

Describe the pathology of myeloma

A

Lymphoid disease where DNA damage leads to multiple myeloma cell formation. M proteins are produced instead of antibodies due to abnormal plasma cells collecting in the bone marrow

25
Q

What are the clinical manifestations of myeloma?

A

Bone pain, weakness, fatigue, anaemia, infections, hypercalcaemia, renal failure and lytic bone lesions

26
Q

What are the red flags for myeloma?

A

Back pain and renal failure

27
Q

State the renal manifestations of myeloma

A
  • M proteins clog up renal tubuli
  • amyloidosis
  • dehydration
  • hypercalcaemia
28
Q

How is myeloma diagnosed?

A

Serum protein electrophoresis/free light chains
Bence Jones Protein
Bone marrow/skeletal/renal biopsy

29
Q

How is myeloma managed?

A 
Chemotherapy 
Stem cell transplant 
Plasma exchange 
Dialysis 
Stop nephrotoxic drugs and treat hypercalcaemia
30
Q

What is given to treat hypercalcaemia?

A

IV NaCl

Pamidronate

31
Q

Define amyloidosis

A

Deposition of extracellular amyloid (insoluble protein fibrils) in tissues/organs. The precursor is soluble but abnormal folding and aggregation leads to amyloid.

32
Q

Name four common forms of amyloidosis

A
  • light chain (AL)
  • systemic (AS)
  • dialysis
  • hereditary
33
Q

Describe AL

A

Abnormal Ig light chains from plasma cells enter the blood and deposit in kidneys, heart, bowel, skin and nerves

34
Q

Describe AA

A

Acute phase protein - serum amyloid protein associated with inflammatory disease affects liver, spleen and adrenal glands

35
Q

How does amyloidosis present?

A 
Nephrotic syndrome 
Cardiomyopathy 
Neuropathy 
Malabsorption 
Hepato/splenomegaly
36
Q

What investigations are carried out in suspected amyloidosis?

A

Urinalysis and PCR
Blood tests (renal function, protein electrophoresis, inflammatory markers)
Renal biopsy (congo red staining - apple green)
SAP scan

37
Q

What is a SAP scan?

A

Scintigraphy with radio labelled serum amyloid shows extent of disease

38
Q

How is amyloidosis managed?

A

Immunosuppression and treat the underlying condition

Renal (20 decks)

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