The CKD Clinic

By the end of this chapter you should be able to:

• Perform a structured initial assessment of a new CKD patient, identifying the cause and the reversible factors.
• Stage by CGA, place on the heatmap, and compute the kidney-failure risk equation to set the management intensity.
• Set a monitoring schedule for eGFR and albuminuria scaled to the patient's risk.
• Define progression and rapid progression, and investigate a steepening GFR trajectory.
• Screen proactively for the complications of CKD at the GFR thresholds at which they appear.
• Deliver the proactive clinic basics: progression-slowing therapy, cardiovascular risk, immunisation, and nephrotoxin avoidance.
• Apply the criteria for nephrology referral and the shared-care model with primary care.
• Recognise when a high-risk patient should enter the predialysis pathway.

• The CKD clinic does three things: assess and diagnose, monitor over time, and deliver proactive, structured care — all calibrated to risk.
• The initial assessment identifies the cause (history, examination, urine, bloods, imaging, and selective serology or biopsy) and stages by CGA.
• Always search for reversible or treatable factors — obstruction, nephrotoxins, volume depletion, uncontrolled blood pressure or glucose, and infection.
• Monitoring frequency is scaled to the heatmap: low-risk patients are reviewed annually, high-risk patients every few months.
• The GFR trajectory is the key prognostic signal; a rapid decline — a sustained fall greater than about 5 mL/min per year, or a category drop with a 25% loss — defines progression and triggers investigation.
• A steepening trajectory should prompt a search for a superimposed cause: AKI on CKD, obstruction, a nephrotoxin, or uncontrolled risk factors.
• Albuminuria is followed as a response marker — a falling ACR signals that progression-slowing therapy is working.
• Complications appear at predictable GFR thresholds, so screen proactively from G3a–G3b: anaemia, mineral-bone disorder, acidosis, hyperkalaemia, and cardiovascular risk.
• Most patients with early CKD die of cardiovascular disease before they ever reach dialysis, so cardiovascular risk is a central clinic task.
• Review medications at every visit: avoid nephrotoxins, dose-adjust for function, and give sick-day guidance to hold certain drugs during acute illness.
• Immunise against influenza, pneumococcus, hepatitis B (especially before dialysis), and COVID-19.
• Refer to nephrology for eGFR below 30, severe albuminuria, rapid progression, AKI, refractory hypertension, persistent hyperkalaemia, or a suspected uncommon or hereditary cause.
• Most low-risk CKD is managed in primary care with the basics; nephrology focuses on the higher-risk and on preparation for kidney failure.
• A high kidney-failure risk should move the patient into the predialysis pathway — modality education, access planning, and transplant assessment.

The CKD clinic turns the staging of Chapter 1 and the pathway of Chapter 2 into recurring, practical care. Its work is unglamorous and structured: find out why the kidneys are failing and whether anything is reversible, watch the trajectory closely enough to catch acceleration, screen for the complications before they cause harm, deliver the handful of therapies that slow progression and protect the heart, and decide — by risk, not by reflex — who needs a nephrologist and who can be cared for closer to home.

The initial assessment

A first CKD visit answers two questions: what is the cause, and what can be reversed? The cause is pursued through a focused history — diabetes, hypertension, family history of kidney disease, nephrotoxin and analgesic use, traditional or herbal remedies, recurrent infection or stones, and features of systemic disease — an examination centred on blood pressure, volume, and systemic signs, and a core set of tests: urinalysis with sediment and an albumin-to-creatinine ratio, creatinine and electrolytes, glucose and HbA1c, and a renal ultrasound for size, structure, obstruction, and cysts. Selective serology — immunological screens, paraprotein studies, viral serology — is added when the picture suggests a specific disease, and biopsy is reserved for when the cause is unclear and the result would change management. The patient is then staged by Cause, GFR, and Albuminuria, placed on the heatmap, and given a kidney-failure risk estimate that sets how intensively everything that follows is done.

Finding the reversible

Before settling into long-term management, the clinic looks hard for anything that can be undone, because reversing it may recover function or halt a decline. Obstruction must be excluded on the ultrasound. Nephrotoxins — non-steroidal anti-inflammatories, certain herbal preparations, an unnecessary RAAS-plus-diuretic combination — are stopped. Volume depletion is corrected, blood pressure and glucose brought under control, and infection treated. This reversible-factor search is not a one-off; at every later visit, and especially when the trajectory worsens, the same checklist is run again, because a treatable insult superimposed on CKD is the commonest reason a stable patient suddenly deteriorates.

Monitoring: frequency by risk

How often to monitor follows directly from the heatmap. A patient in a green, low-risk cell needs little more than an annual eGFR and ACR; a patient in a red, very-high-risk cell needs review every few months. Tailoring frequency to risk concentrates attention where it changes outcomes and spares the low-risk patient needless testing and anxiety. The two numbers tracked at every visit are the eGFR and the albuminuria, because between them they capture both how far the disease has come and how fast it is moving.

The trajectory is the signal

Of everything the clinic measures, the GFR trajectory matters most, because it is the speed of the final common pathway made visible. A slow, stable decline is expected in established CKD; a steepening one is a warning. KDIGO defines progression as a drop in GFR category accompanied by a sustained fall of at least 25% from baseline, and rapid progression as a sustained decline of more than about 5 mL/min per year. A trajectory that accelerates past these markers should never be accepted as 'just the CKD getting worse'; it should trigger a search for a superimposed, often treatable cause — an acute kidney injury on the chronic background, a new obstruction, a nephrotoxin, uncontrolled hypertension or glucose — and an intensification of pathway-targeted treatment. The trajectory is both the alarm and the report card.

Albuminuria as the response marker

The albumin-to-creatinine ratio is followed not only to stage but to judge whether treatment is working. Because proteinuria is a mediator of progression, lowering it slows the disease, so a falling ACR after starting RAAS blockade or an SGLT2 inhibitor is evidence the pathway has been slowed, and a persistently high or rising ACR signals that therapy needs intensifying. In this sense the clinic uses albuminuria the way a diabetes clinic uses HbA1c — a modifiable number that both predicts the future and measures the response to what you have done.

Screening for complications before they harm

As GFR falls, the kidney's excretory and endocrine functions fail in a predictable order, so the complications can be screened for before they cause symptoms. From around G3a to G3b onward the clinic begins checking for anaemia, for the mineral-bone disorder through calcium, phosphate, parathyroid hormone, and vitamin D, for metabolic acidosis through bicarbonate, and for hyperkalaemia, while attending to cardiovascular risk throughout. Each of these is a Part 3 topic in its own right, but the clinic's job is the proactive screening — catching the anaemia, the rising phosphate, or the falling bicarbonate at a routine visit rather than at a crisis. And because cardiovascular disease, not dialysis, is the commonest destination of early CKD, cardiovascular risk management is not a side task but a central one.

Proactive, structured care

The therapeutic core of the clinic is to deliver, reliably and to every eligible patient, the things that work: the progression-slowing pillars of Part 2 — blood-pressure control, RAAS blockade, SGLT2 inhibition, proteinuria reduction — cardiovascular risk reduction including statins, treatment of the complications, immunisation against influenza, pneumococcus, hepatitis B, and COVID-19, careful medication review with nephrotoxin avoidance and sick-day guidance, and patient education that turns the person into an active participant in their own care. Doing this consistently is best achieved with a structured review — a checklist or bundle run at each visit — so that nothing high-yield is missed, the kind of governance the well-run CKD service is built on.

Referral and shared care

Not every CKD patient needs a nephrologist, and deciding who does is a core clinic judgement. Referral is warranted for an eGFR below 30, severe albuminuria, rapid progression, an episode of AKI or an unexplained fall, refractory hypertension on multiple agents, persistent abnormal potassium, recurrent or extensive stones, and any suspected uncommon, genetic, or immunological cause, with an active nephritic sediment prompting urgent referral. Most lower-risk CKD — the green and yellow cells — is well managed in primary care with the same basics, in a shared-care model that reserves specialist time for the higher-risk and for the work of preparing for kidney failure. When the kidney-failure risk equation predicts a meaningful chance of reaching end-stage disease, the patient enters the predialysis pathway of Part 5 — modality education, access planning, transplant assessment, and vaccination — begun early enough to be unhurried. The clinic's referral decisions, like its monitoring, are calibrated to risk rather than to a single threshold.

Table 3.1 — The initial CKD assessment

Table 3.2 — Reversible / treatable factors to find

Table 3.3 — Monitoring frequency by risk (heatmap-scaled)

Table 3.4 — Defining progression

Table 3.5 — Complication screening by GFR threshold

Table 3.6 — Criteria for nephrology referral

Visualise & Map

Each chain runs from physiology to a named clinic action; read the arrows as “leads to.”

The trajectory as alarm. The final common pathway runs at a rate → the eGFR slope makes it visible → a steepening slope means the loop has accelerated → ACTION: on rapid progression, search for a superimposed cause and intensify therapy.

Albuminuria as report card. Proteinuria mediates progression → therapy that lowers it slows the pathway → a falling ACR signals response, a rising one signals undertreatment → ACTION: follow the ACR and intensify if it does not fall.

Complications by threshold. Falling GFR → excretory and endocrine functions fail in a predictable order → anaemia, mineral-bone disorder, acidosis, hyperkalaemia appear at set thresholds → ACTION: screen proactively from G3a–G3b, before symptoms.

The second hit. A nephrotoxin or AKI superimposed on CKD → an acute acceleration of decline → often the reason a stable patient deteriorates → ACTION: avoid nephrotoxins, give sick-day guidance, and re-run the reversible-factor check when the trajectory worsens.

Cardiovascular dominance. The uraemic, vascular milieu of CKD → accelerated cardiovascular disease → most early-CKD patients die of cardiovascular disease before reaching ESKD → ACTION: make cardiovascular risk reduction a central clinic task, not an afterthought.

Clinical Reasoning

One triad per mechanism the narrative exposed: the rationale, why it matters, and the clinic action.

Safety & Evidence

Panel A — Red flags

Panel B — Never do

Pitfall 1 — Skipping the reversible search

Pitfall 2 — 'Just the CKD'

Pitfall 3 — Reactive complication care

Pitfall 4 — Forgetting the heart

Pitfall 5 — Referring by threshold alone

Graded statements (by evidence type)

Patient Decisions

Natural-frequency estimates for orientation, from CKD cohorts; they vary with stage, cause, and comorbidity. They show what the clinic's monitoring and care are aimed at, expressed per 100 comparable patients.

Apply & Test

Paste-ready notes. Tick the boxes that apply and delete the rest; make the structured review and the referral reasoning explicit — the basis of a well-governed CKD service.

Template 1 — Structured CKD clinic review

• Stage (CGA): cause ___ , GFR category ___ , albuminuria category ___ ; heatmap risk ___ ; KFRE ___ .
• Trajectory: eGFR ___ (slope ___ mL/min/yr); ACR ___ (trend ___ ); progression: ☐ stable ☐ progressing ☐ rapid.
• Reversible factors checked: ☐ obstruction ☐ nephrotoxins ☐ volume ☐ BP/glucose ☐ infection.
• Complication screen (from G3a–G3b): ☐ Hb ☐ Ca/PO4/PTH/vitD ☐ bicarbonate ☐ potassium.
• Progression-slowing therapy: ☐ BP target ☐ RAAS ☐ SGLT2i ☐ albuminuria response reviewed.
• CV risk: ☐ lipids/statin ☐ BP ☐ glucose; immunisations: ☐ influenza ☐ pneumococcal ☐ hepatitis B ☐ COVID-19.
• Medication review: ☐ nephrotoxins avoided ☐ doses adjusted ☐ sick-day rules given.

Template 2 — Nephrology referral

• Referral trigger: ☐ eGFR < 30 ☐ A3 / heavy proteinuria ☐ rapid progression / AKI ☐ refractory hypertension ☐ persistent hyperkalaemia ☐ recurrent stones ☐ uncommon/hereditary/immunological cause.
• Urgency: ☐ routine ☐ urgent (active nephritic sediment / rapidly rising creatinine).
• Summary: cause/stage/risk ___ ; reversible factors addressed ___ ; current therapy ___ .
• Predialysis pathway indicated (high KFRE): ☐ yes → modality education / access planning / transplant assessment.
• Shared-care plan with primary care: ___ .