Synopsis
Identify diabetic kidney disease from albuminuria and filtration trends, exclude important alternative diagnoses, and combine renal, cardiovascular and glycaemic protection without provoking acute kidney injury or hyperkalaemia.
- Screen diabetic kidney disease with both estimated glomerular filtration rate and urine albumin-to-creatinine ratio because either may be abnormal while the other remains apparently normal.
- Confirm a new moderately raised albumin-to-creatinine ratio on an early-morning sample after excluding urinary infection, menstruation, fever, strenuous exercise and acute decompensation.
- Diabetes is not proof of causation: haematuria, abrupt filtration loss, nephrotic syndrome, systemic features or an atypical time course should prompt investigation for non-diabetic kidney disease.
- Offer an ACE inhibitor or angiotensin receptor blocker to eligible people with diabetic CKD and albuminuria, titrating to the maximum tolerated dose while monitoring creatinine and potassium.
- Never combine an ACE inhibitor with an angiotensin receptor blocker; dual renin–angiotensin blockade increases acute kidney injury and hyperkalaemia without a safe routine role.
- An SGLT2 inhibitor may provide kidney and heart protection even when eGFR is too low for a strong glucose-lowering effect; prescribe to the current indication and teach ketone-focused sick-day rules.
- Finerenone is an option for selected adults with type 2 diabetes and stage 3 or 4 albuminuric CKD despite optimised standard care, but potassium and renal eligibility determine safe initiation and continuation.
- HbA1c becomes less reliable in advanced CKD, anaemia, erythropoietin treatment and dialysis; use glucose or CGM patterns and reduce hypoglycaemia-prone medicines as renal clearance falls.
- Kidney protection also includes blood-pressure control, smoking cessation, lipid management, avoidance of nephrotoxins, vaccination, cardiovascular prevention and preparation for renal replacement or supportive care when progression continues.
Key red flags
Visible or persistent microscopic haematuria, active urine sediment, abrupt creatinine rise, rapid eGFR loss, nephrotic syndrome or systemic inflammation suggests another or additional renal disorder.
Oedema, breathlessness, nausea, itch, cognitive change, pericarditic pain or severe fatigue can accompany advanced kidney failure and need urgent severity assessment.
Muscle weakness, palpitations or syncope may accompany severe potassium elevation, but dangerous hyperkalaemia can be asymptomatic; laboratory surveillance is essential after RAAS-active medicines.
ACE inhibitors, angiotensin receptor blockers and finerenone are unsuitable around pregnancy; early specialist medicine replacement and renal–obstetric planning are required.
Investigation priorities
Quantify albumin loss and assign the albuminuria component of CKD risk.
Management branches
Routine diabetes review identifies an abnormal urine albumin-to-creatinine ratio, eGFR or creatinine trend.
- Check prior results, volume status, acute illness, urinary infection, recent exercise, medicines and blood pressure to distinguish chronic disease from a transient or acute change.
- Repeat albuminuria using the recommended early-morning strategy and establish eGFR chronicity, while obtaining urinalysis and targeted tests for atypical features.
- Stage risk using both albuminuria and filtration categories, communicate that kidney and cardiovascular risks are linked, and record a personalised monitoring interval.
- Refer or seek nephrology advice for rapid progression, heavy albuminuria, haematuria, resistant hypertension, uncertain cause, electrolyte difficulty or high kidney-failure risk under current NICE criteria.