Systemic Disease Flashcards
Leading cause of ESRD
Diabetic neprhopathy
What characterises diabetic nephropathy?
Albuminuria, 300mg/24 hours on at least 2 occasions 3-6 months apart
Microvascular complications of diabetes
Nephropathy
Retinopathy
Neuropathy - gastroparesis, silent MI, urogeital abnormalities
Macrovascular complications of diabetes
Stroke
CHD
PVD
Haemodynamic changes in diabetic nephropathy
Afferent arteriolar vasodilation
Hyperfiltration
Increased GFR
Why does renal hypertrophy happen in diabetic nephropathy?
Plasma glucose stimulates growth factors = mesangial expansion, nodule formation, inflammation, proteinuria, tubulo-interstitial fibrosis
Staining in diabetic nephropathy
Kimmelstiel-Wilson lesion - nodular diabetic glomerulosclerosis
Prevention and treatment of diabetic nephropathy
Glycaemic control
Anti-HT: ACEI or ARB
Statin
What does ACEI do to glomerulus?
Dilates efferent arteriole = reduced intraglomerular pressure = prevent hyperfiltration
What causes renovascular HT?
Renal artery stenosis = reduced renal perfusion = responses to incresae BP
Signs of renovascular HT
Flash pulmonary oedema
Microscopic haematuria
Abdominal bruit
Renovascular disease
Fibromuscular dysplasia
Atherosclerotic renovascular disease
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)
Atherosclerotic renovascular disease
Older males
Obesity, smoking, HT
Also CVD, PVD
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
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