- MCC of end stage kidney disease
- Decrease insulin → hyperglycaemia → HTN + kidney dysfunction → kidney failure
Stages of diabetic nephropathy
- 1 – early stage, normal GFR
- 2 – microalbuminuria
- 3 – clinical proteinuria
- 4 – Nephrotic syndrome + HTN
- 5 – renal impairment
- 6 – end stage renal failure
Pathophysiology
- ↑Pressure state – due to DM (HTN)→ ↑GFR
- ↑BP → ↑flow through glomerulus → mesangial expansion
- Mesangial expansion – high pressure results in damage of mesangium
- Cells secrete cytokines → inflam and O2 radicals → endoth dysfunction → hypertrophy + matrix accumulation
- Mesangial expansion – high pressure results in damage of mesangium
- When mesangium expands, space between podocytes exands – decreased surface area for filtration
- Filtration system is leaky – microalbuminuria (30-300mg/24h) and proteinuria
- ↑BP → ↑flow through glomerulus → mesangial expansion
- Nephron ischemia – decreased GFR
- Blood supply to lobule of nephron is from vasoconstriction of efferent arteries due to activation of RAAS – this decreases over time → ischemia → atrophy
Clinical features
- Severe tiredness, headaches, N+V, loss of app, itchy skin, leg swelling
Diagnosis
- Renal hypertrophy, glomerular lesions ( KW lesions )
- Microalbuminuria, proteinuria, glom hyperfiltration, progressive loss of GFR
- Screening – urine albumin:creatinine ratio
- USS – hypertrophy
Treatment
- Treat DM (keep HbA1c <7% and LDL <3.0)
- Microalbuminuria – ACEI + ARBs
-
- Decrease intraglomerular pressure and therefore decrease proteinuria
- End stage renal disease – dialysis + transplant
Complications
- Neurogenic bladder, renovascular disorders, papillary necrosis, FSGS