Diabetic nephropathy
Microvascular glomerular damage from chronic hyperglycaemia
Overview
Progressive glomerular damage from diabetes — the leading cause of end-stage renal disease. Earliest marker is moderately increased albuminuria (raised ACR); progresses through proteinuria to declining eGFR. Slowed by glycaemic and BP control with renin-angiotensin blockade and SGLT2 inhibition.
Recognise
- Rising urine albumin:creatinine ratio (ACR) — the earliest sign — then frank proteinuria and falling eGFR
- Often with retinopathy (the two track together); hypertension
- Progresses to CKD/ESRD; nephrotic-range proteinuria in advanced disease
Red flags
- Rapidly rising creatinine, haematuria, or absence of retinopathy → consider a non-diabetic renal cause (refer/biopsy)
- Hyperkalaemia/AKI on ACE-i/ARB → monitor U&Es
Differentials & how to tell them apart
Investigations
Annual ACR (early-morning) and eGFR; BP. Retinal screen (retinopathy usually coexists). Exclude other causes if atypical.
Management
ACE-inhibitor/ARB for albuminuria + SGLT2 inhibitor + tight glucose/BP control
- 1Optimise glucose and BP. Start an ACE-inhibitor or ARB once ACR is raised (titrate to max tolerated); add an SGLT2 inhibitor for additional renoprotection.Gate: Do NOT combine an ACE-inhibitor with an ARB; monitor U&Es/potassium after starting/up-titrating (a small creatinine rise is expected, but a >25–30% rise or hyperkalaemia means stop/seek advice)
- 2Refer to nephrology for advanced CKD/uncertain cause; manage CKD complications; prepare for renal replacement in ESRD.
Key points
ACR is the early signal and retinopathy usually accompanies it — its ABSENCE should make you doubt a purely diabetic cause. ACE-i/ARB + SGLT2 are the renoprotective spine.
Monitor & prognosis
Annual ACR/eGFR; U&Es after RAS blockade changes.
Slowed but not reversed; leading cause of ESRD.
Source: NICE NG28/NG203 (CKD); SGLT2 renal trials