AKT · Renal & urology/CKD, RRT & cystic

Chronic kidney disease

Sustained (>3 months) reduction in GFR and/or kidney damage (albuminuria) — commonest causes diabetes & hypertension

Overview

Abnormal kidney function or structure present for more than 3 months, classified by the GFR category (G1–G5) and the albuminuria category (A1–A3) — the 'CKD heat map'. The commonest causes are diabetes and hypertension. Management slows progression (BP control, ACE inhibitor/ARB, SGLT2 inhibitor), treats the complications (anaemia, bone disease, acidosis), and reduces cardiovascular risk — the leading cause of death in CKD.

Recognise

Usually asymptomatic until advanced; found on eGFR/albuminuria screening; later — fatigue, oedema, pruritus, nausea, restless legs
Classify by eGFR (G1 ≥90 … G5 30 mg/mmol) — the heat map predicts risk
Complications: anaemia (low EPO), renal bone disease (low vit D/high phosphate/secondary hyperparathyroidism), metabolic acidosis, hyperkalaemia, fluid overload, accelerated CVD

Red flags

A rapid fall in eGFR, accelerated hypertension, or visible haematuria → investigate for a treatable cause (GN, obstruction, malignancy)
Refer to nephrology: eGFR <30, ACR ≥70, rapid progression, uncontrolled complications, or suspected genetic/systemic cause

Differentials & how to tell them apart

Acute kidney injuryacute rise, normal-sized kidneys, no chronic anaemia/bone disease — but AKI-on-CKD coexists

Diabetic nephropathydiabetes + albuminuria + retinopathy — the commonest cause; cross-ref endocrine

Reversible/obstructive causehydronephrosis on USS, post-renal — relieve it

Investigations

eGFR and urine ACR (the two staging axes — confirm chronicity over ≥3 months); urinalysis (haematuria → GN/urological cause); renal ultrasound (small kidneys = chronic; asymmetry/obstruction); FBC (anaemia), bone profile/PTH/vitamin D, HbA1c, lipids; cause-specific tests (immunology, myeloma screen).

Management

BP control + ACEi/ARB + SGLT2 inhibitor; treat complications + CV risk

1Confirm chronicity (eGFR + ACR over ≥3 months), find and treat the cause, and screen for complications. Control BP and start an ACE inhibitor/ARB for albuminuria, plus an SGLT2 inhibitor.Gate: Rapid progression, ACR ≥70, eGFR <30, visible haematuria or uncontrolled complications → refer to nephrology and investigate for a treatable/obstructive/glomerular cause.
2Treat anaemia (iron + ESA), renal bone disease (phosphate binders/vitamin D/PTH), acidosis (bicarbonate) and CV risk (statin); prepare access/transplant work-up for RRT as CKD advances.

BP control + ACE inhibitor or ARB (titrate to max tolerated) — offer if ACR ≥30 (with diabetes) or ACR ≥70, or hypertension + ACR ≥30 — slows progression; monitor K and a tolerated creatinine rise

SGLT2 inhibitor (dapagliflozin) — add for CKD with albuminuria (especially type 2 diabetes / ACR raised) — slows progression and reduces CV/renal events; finerenone as add-on in T2DM albuminuric CKD on RAS+SGLT2i

Treat complications — iron + erythropoiesis-stimulating agent (anaemia), phosphate binders/vitamin D/manage PTH (bone disease), oral bicarbonate (acidosis); atorvastatin for CV risk

Prepare for RRT in advanced CKD — plan dialysis access/transplant work-up as eGFR approaches <15–20; avoid nephrotoxins, adjust drug doses

Key points

Stage CKD on BOTH eGFR (G) and ACR (A) — the heat map. Slow progression with BP control + ACEi/ARB + SGLT2 inhibitor (+ finerenone in T2DM albuminuric CKD). Treat anaemia/bone disease/acidosis. CVD is the leading cause of death. A creatinine rise up to ~30% after starting an ACEi/ARB is acceptable.

Monitor & prognosis

eGFR/ACR trajectory, K and creatinine after ACEi/ARB, Hb, bone profile/PTH, BP, CV risk.

Variable; many remain stable, a minority progress to ESRD; CV death is commoner than reaching dialysis.

Source: NICE NG203 (CKD)