Systemic Disease Flashcards by Ailsa Campbell

Leading cause of ESRD

Diabetic neprhopathy

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What characterises diabetic nephropathy?

Albuminuria, 300mg/24 hours on at least 2 occasions 3-6 months apart

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Microvascular complications of diabetes

Nephropathy
Retinopathy
Neuropathy - gastroparesis, silent MI, urogeital abnormalities

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Macrovascular complications of diabetes

Stroke
CHD
PVD

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Haemodynamic changes in diabetic nephropathy

Afferent arteriolar vasodilation
Hyperfiltration
Increased GFR

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Why does renal hypertrophy happen in diabetic nephropathy?

Plasma glucose stimulates growth factors = mesangial expansion, nodule formation, inflammation, proteinuria, tubulo-interstitial fibrosis

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Staining in diabetic nephropathy

Kimmelstiel-Wilson lesion - nodular diabetic glomerulosclerosis

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Prevention and treatment of diabetic nephropathy

Glycaemic control
Anti-HT: ACEI or ARB
Statin

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What does ACEI do to glomerulus?

Dilates efferent arteriole = reduced intraglomerular pressure = prevent hyperfiltration

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What causes renovascular HT?

Renal artery stenosis = reduced renal perfusion = responses to incresae BP

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Signs of renovascular HT

Flash pulmonary oedema
Microscopic haematuria
Abdominal bruit

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Renovascular disease

Fibromuscular dysplasia

Atherosclerotic renovascular disease

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Fibromuscular dysplasia

Part of renovascular disease
Females age 15-50
Bilateral renal arteries if familial
Associated with Ehler-Danlos and Marfan’s
Can involve cerebral arteries (carotid artery dissection)

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Atherosclerotic renovascular disease

Older males
Obesity, smoking, HT
Also CVD, PVD

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Ischaemic nephropathy

Due to renovascular HT and renovascular disease
Reduced GFR associated with reduced renal blood flow
Renal atrophy and progressive CKD
US, CT, MR

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Treatment of renovascular disease and HT

Reduce CV risk factors
Reduce BP
Angioplasty and stenting
ACEI (only in UNILATERAL renal artery stenosis)

ACEI is contraindicated in what?

Bilateral renal artery stenosis

What is MM?

Cancer of plasma cells (produce Abs) - accumulate in bone marrow = interferes with production of blood cells
Production of paraprotein (abnormal Ab)

Symptoms of MM

Bone pain
Weakness
Fatigue
Weight loss

Signs of MM

Normocytic anaemia
Hypercalcaemia
Renal failure
Amyloidosis
Recurrent infections (chest, UTI)

Investigations for MM

Normocytic anaemia
Rouleaux formation (stacks of RBCs)
Raised CRP/PV
Renal impairment, ESKD
Electrophoresis
BJP in urine
Lytic lesions on skeletal survey

Who gets MM?

Males 80
Females 70
Black

Renal manifestations of MM

AKI
Paraprotein deposition = AKI/CKD
Paraprotein casts
Amyloidosis

Amyloidosis

Protein in EC spaces - heart, kidney, brain, eye

Histology of amyloidosis

Congo red stain - apple green birefringence

Primary and secondary amyloidosis

Primary - AL fibrils | Secondary - AA fibrils (chronic inflammation, MM/IBD/RA)

Treatment of MM and AKI

``` Stop nephrotoxins (NSAID, diuretic) Treat hypercalcaemia - IV NaCl, IV Pamdronate Avoid contrast Chemo and steroids to reduce tumour load Plasma exchange Dialysis ```

GPA

``` Granulomatosis with Polyangitis Wegener's cANCA (PR3) Necrotising granulomatous inflammation affecting resp tract = nasal crusting, sinusitis, rhinorrhoea, OM, bloody nasal discharge, pulmonary haemorrhage Saddle nose deformity Crescents ```

EGPA

Eosinophilic Granulomatosis with PolyAngitis Churg-Strauss Necrotising granulomatous inflammation Late onset asthma and eosinophilia, skin involvement, pulmonary haemorrhage. Kidney involvement less common. pANCA (MPO)

MPA

Microscopic PolyAngitis NO granulomatous inflammation Pulmonary haemorrhage Crescents

Treatment for kidney involvement in vasculitis

Immsup - steroids, cyclophosphamide Plasma exchange (removes ANCA) Dialysis

Investigations for lupus

Raised C3 and C4 Anti-phospholipid Anti-dsDNA

Nephritic or nephrotic syndrome in vasculitis?

Nephritic

Nephritic or nephrotic syndrome in SLE?

Nephrotic