Chronic Kidney Disease

Chronic kidney disease is abnormal kidney structure or function present for more than three months, with implications for health.

It is classified by cause, GFR category (G1–G5) and albuminuria category (A1–A3): the "CGA" system, because albuminuria independently predicts progression and cardiovascular risk, and staging on GFR alone substantially underestimates risk in a patient with heavy proteinuria.

• G1: GFR ≥90 with evidence of kidney damage; G2: 60–89; G3a: 45–59; G3b: 30–44; G4: 15–29; G5: below 15 (kidney failure)

• A1: ACR below 3 mg/mmol; A2: 3–30; A3: above 30

The commonest causes are diabetes and hypertension, followed by glomerulonephritis, polycystic kidney disease, obstructive uropathy and recurrent pyelonephritis. Most patients with chronic kidney disease die of cardiovascular disease rather than reaching dialysis, which is why cardiovascular risk management is not a secondary consideration but a central part of treatment.

• eGFR and urine albumin-to-creatinine ratio, both required for staging, and both confirmed on repeat over at least three months to establish chronicity and to distinguish from acute kidney injury
• Urinalysis for haematuria and proteinuria; the combination of haematuria and proteinuria suggests glomerular disease and warrants nephrology referral
• Renal ultrasound to assess size, symmetry and obstruction; small echogenic kidneys support chronicity, while asymmetry suggests renovascular disease and normal-sized kidneys in advanced disease suggest diabetes, amyloid or polycystic disease
• Cause-directed investigations: HbA1c, blood pressure, autoimmune screen, myeloma screen in older patients with unexplained disease, hepatitis and HIV serology where relevant
• Complication screening, which should be systematic: FBC for anaemia, calcium, phosphate, PTH and vitamin D for mineral and bone disorder, bicarbonate for metabolic acidosis, potassium, and lipids
• Track the rate of decline rather than single values; a rapid fall (more than 5 mL/min/1.73m² per year) changes management and prompts referral
• Medication review at every visit, since nephrotoxins and inappropriately dosed drugs are a major modifiable cause of progression

Slowing progression, which is the central goal:

• Blood pressure control, generally targeting below 130/80 mmHg where tolerated, and lower in significant proteinuria
• ACE inhibitor or ARB for proteinuric chronic kidney disease and for diabetic kidney disease, titrated to the maximum tolerated dose. Expect a creatinine rise of up to 25–30% after initiation, which is acceptable and reflects the intended haemodynamic effect; a larger rise warrants investigation for renovascular disease
• SGLT2 inhibitors are now a cornerstone of treatment, with clear benefit in slowing progression in both diabetic and non-diabetic chronic kidney disease, and additional cardiovascular and heart failure benefit
• Glycaemic control in diabetes, with agent selection accounting for renal clearance
• Finerenone for diabetic kidney disease with albuminuria, as an additional option
• Dietary sodium restriction, smoking cessation, weight management and exercise
• Avoid nephrotoxins: NSAIDs, unnecessary contrast, aminoglycosides; adjust drug doses for renal function and provide sick-day guidance for holding ACE inhibitors, ARBs, diuretics, metformin and SGLT2 inhibitors during acute illness

Managing complications:

• Anaemia: iron studies first and iron replacement before considering erythropoiesis-stimulating agents, targeting a haemoglobin around 100–120 g/L rather than normalising it, since higher targets increase cardiovascular events
• Mineral and bone disorder: dietary phosphate restriction and phosphate binders taken with meals, activated vitamin D and calcimimetics for secondary hyperparathyroidism
• Metabolic acidosis: oral sodium bicarbonate where bicarbonate is persistently below about 22 mmol/L, which slows progression and reduces muscle wasting
• Hyperkalaemia: dietary advice, potassium binders where needed to allow continuation of prognostically important ACE inhibitors and ARBs rather than stopping them
• Cardiovascular risk: statin therapy for essentially all patients, and active management of all modifiable risk factors

Advanced disease:

• Timely nephrology referral: generally for G4 and above, rapid progression, heavy proteinuria, unexplained disease, refractory hypertension, or persistent haematuria, allowing planning rather than crisis management
• Preparation for renal replacement therapy well before it is needed, including modality choice, dialysis access creation, and pre-emptive transplant assessment, which offers the best outcomes
• Conservative kidney management is an appropriate and actively chosen pathway for frail or comorbid patients, focusing on symptom control and quality of life, and should be discussed rather than presented as the absence of treatment

Referral: nephrology per the criteria above; dietitian for phosphate, potassium and protein management; cardiology where cardiovascular disease coexists.