Kidney in systemic disease Flashcards

1
Q

Define the perimeters for diabetic nephropathy

A

300mg/24h on at least 2 occasions separated by 3- 6 months

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2
Q

state the micro and macro vascular complications of diabetes

A
Microvascular
Nephropathy
Retinopathy
Polyneuropathy
Sensory
Motor
Autonomic neuropathy
(Gastroparesis, Silent MI, Urogenital abnormalities)

Macrovascular
Stroke
Coronary heart disease
Peripheral vascular disease

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3
Q

Describe the pathogenesis of Diabetic Nephropathy (7)

A

-Haemodynamic changes-
afferent arteriolar vasodilatation mediated by range of vasoactive mediators e.g IGF-1
hyperfiltration
increased GFR

-Renal hypertrophy
plasma glucose stimulates several growth factors within the kidney

-Mesangial Expansion

-Nodule Formation
nodular diabetic glomerulosclerosis ( Kimmelstiel-Wilson lesion) and diffuse glomerulosclerosis

  • Inflammation
  • Proteinuria (GBM thickening and podocyte dysfunction)
  • Tubulo-interstitial fibrosis
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4
Q

name the appearance on histology of glomerulosclerosis in diabetes

A

Kimmelstiel-Wilson lesion

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5
Q

describe the pattern of GFR and albuminuria in diabetic nephropathy?

A

initial increase as the kidneys undergoes hyperplasia and then decrease
albuminuria rises as GFR falls

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6
Q

Diagnosis of diabetic nephropathy (4)

-indications for biopsy?

A

History of Diabetes Mellitus
Proteinuria
Presence of other diabetic complications eg retinopathy
Renal Impairment in later stages

-haematuria

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7
Q

nephrotic range for proteinuria?

A

> 300 mg/day

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8
Q

treatment of diabetic nephropathy (3)

-mechansim?

A
Glycaemic control
(Maintain tight glycaemic control (HbA1c
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9
Q

3 types of RRT in diabetic nephropathy

A

Simultaneous Kidney-Pancreas Transplant (Type 1 only)

Kidney transplant

Haemodialysis and Peritoneal Dialysis (need tight BG control as the fluid is high in glucose)

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10
Q

Renal vascular hypertension

  • what is it?
  • caused by?
  • 2 types of renovascular disease
A
  • secondary from of hypertension usually due to renal artery stenosis
  • A reduction in renal perfusion pressure activates RAAS which raises systemic arterial BP.

-Fibromuscular dysplasia
Atherosclerotic Renovascular disease

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11
Q

ischaemic nephropathy

-what is it?

A

refers to the reduced GFR associated with reduced renal blood flow beyond the level of auotregulatory compensation
over time can lead to renal atrophy and CKD

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12
Q

Fibromuscular dysplasia

  • what is it?
  • population
  • types
  • associated
  • presentation(4)
A
  • non-atherosclerotic, non-inflammatory disease of the blood vessels that causes abnormal growth within the wall of an artery- rings of sclerosis and eventual renal artery stenosis
  • 15-50 yeas
  • familial, involves both renal arteries

-hereditary conditions e.g Ehlers-Danlos
can involve cerebral arteries and cause carotid artery dissection

-renal symptoms are hypertension and renal artery bruit also get headaches, dizziness and neck pain

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13
Q

Atherosclerotic renovascular disease

  • population
  • risk factors
  • presentation (7)
A
  • older patients, men, caucasians
  • general atherosclerosis

-Renovascular hypertension
AKI after treatment of hypertension (usually with ACEi)
CKD in elderly with diffuse vascular disease
‘Flash’ pulmonary oedema
Microscopic haematuria
Abdominal bruit
Atherosclerotic disease elsewhere

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14
Q

what are the 3 conditions associated with renal artery stenosis?

A

ischaemic nephropathy (IN)

fibromuscular dysplasia (FMD)

atherosclerotic renovascular disease (ARVD)

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15
Q

investigations in ischaemic renal disease?

  • managment
  • contraindicated
A
-Screening tests
Renal ultrasound
Renal artery duplex studies
CT angiography
MR angiography
Angiography

-control BP and reduce CV risk factors
Angioplasty/Angioplasty + stenting/Stenting alone

-ACE inhibitors

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16
Q

Myeloma

  • what is it?
  • pathognesis
  • signs (5) and symptoms (4)
  • investigations (6)
  • renal manifestations (4)
A
  • a cancer of plasma cells (a type of WBC normally responsible for producing antibodies)
  • collections of abnormal plasma cells accumulate in the bone marrow where they interfere with the production of normal blood cells. most cases feature the production of paraprotein- an abnormal antibody which can cause kidney problems
-signs
Anaemia
Hypercalcaemia
Renal Failure
Amyloidosis
Recurrent infections
-symptoms
Bone Pain
Weakness
Fatigue
Weight Loss
-blood film
FBC- CRP
creatinine
protein electrophoresis
Bence-Jones protein in urine
Lytic lesions on skeletal survey

-AKI secondary to hypercalcaemia
Monoclonal immunoglobin deposition disease
Amyloidosis

17
Q

Amyloidosis

  • what is it?
  • classification
  • histology
A

-Generic name for a family of diseases
Characterised by the deposition in extracellular spaces of a proteinaceous material

-Classified by the type of precursor protein that makes up the main component of the fibrils
Renal amyloidoses include primary (AL) amyloid and secondary (AA) amyloid

-Clasically positive Congo red staining showing apple-green birifringence under polarised light

18
Q

Treatment of myeloma in acute renal failure?

  • acute (7)
  • long term (4)
A
Acute
Stop Nephrotoxins
-NSAID’s
-Diuretics in view of risk increasing cast formation
Treat hypercalcaemia
-IV NaCl to volume resuscitate
-IV Pamidronate if required
\+ avoid contrast
long term
-Chemotherapy to reduce tumour load
\+High dose dexamethasone may help reduce tumour load.
-Plasma exchange
-To remove light chains.
Dialysis to support AKI and CKD
19
Q

Vasculitis

  • type that effects kidneys most?
  • name the 4 major subtypes of this
A

-small vessel vasculitis

-necrotising polyangitis
Granulomatosis with polyangitis
Churg-strauss syndrome
microscopic polyangitis

20
Q

necrotising polyangiitis

  • antibody associated
  • effects?
  • population
  • presentation
A
  • ANCA
  • capillaries, venules and arterioles
  • general symptoms; weight loss, anorexia, malaise
21
Q

Granulomatosis with Polyangiitis

  • what is it?
  • presentation
  • signs
  • antibody
A
  • Necrotising granulomatous inflammation which most commonly affects the respiratory tract
  • nasal crusting, sinusitis, persistent rhinorrhea, otitis media, oral/nasal ulcers, bloody nasal discharge
  • bony cartilage destruction- saddle nose
  • c-ANCA
22
Q

Churg-Strauss syndrome

  • what is it?
  • other features
  • antibody
A

-necrotising granulomatous inflammation causing asthma and eosonophilia
lung most common involvement

  • skin involvement= palpable purpura to subcutaneous nodules
  • p-ANCA
23
Q

Microscopic polyangitis

  • what is it?
  • complications
A
  • small vessel vasculitis, no granulomatous inflammation

- pulmonary haemorrhage as a consequence of alveolar capillary involvement

24
Q

Investigations in small vessel vasculitis? (7)

A
Hx
examination
Bloods (CRP, PV, complement, ANCA, virology)
urinalysis
Biopsy (kidney, skin, nasal, lung)
cytoplasmic PR3 (c-ANCA)
perinuclear MPO (p-ANCA)
25
Q

small vessel vasculitis more common in renal disease? (2)

  • findings on urinalysis? (2)
  • on biopsy?
A
  • GPA and MPA
  • Proteinuria and haematuria
  • shows segmental necrotising glomerulonephritis - crescent formation
26
Q

treatment of SV vasculitis? (7)

A
Immunosuppressive therapy:
-IV methylprednisolone
-prednisolone
-cyclophosphamide
-azothioprine
Plasma Exchange
May require renal support
27
Q

SLE

  • what is it?
  • name 5 signs
  • investigations
  • features of renal involvement
A
  • Chronic inflammatory disease of unknown origin, Affecting skin, joints, kidneys, lungs, nervous system, serous membranes
  • Malar rash, photosensitivity, non-erosive arthritis, discoid rash, oral arthritis

-Complement levels (C3 and C4)
Anti-cardiolipin antibody
Anti-phospholipid antibody (lupus anticoagulant)

-Proteinuria/nephrotic syndrome
granular casts/RBC casts
reduced renal function
hypertension

28
Q

Lupus nephritis

  • classified how?
  • describe classes 1-6
  • treatment of proliferative disease immunosuppressive and non- immunosupressive (5)
A

-on renal biopsy

-Class I: Minimal mesangial
Class II: Mesangial Proliferative
Class III: Focal Proliferative
Class IV: Diffuse Proliferative
Class V: Membranous
Class VI: Advanced sclerosing

-Non-immunosuppressive:
ACE/ARB target BP 130/80

Immunosuppressive therapy: 
-Induction
High dose steroids
Cyclophosphamide/ MMF
Azathioprine, rituximab, tacrolimus
-Maintenance
Steroids
MMF/azathioprine