Chronic kidney disease — delaying it, not just diagnosing it

In brief

• Chronic kidney disease (CKD) means an eGFR below 60, or kidney damage such as protein in the urine, for more than 3 months.
• It is silent until late, so people with diabetes or high blood pressure, or aged 60 and over, need a yearly eGFR and urine albumin (UACR) test.
• Four pillars slow it: blood pressure below 130/80 mmHg with an ACE inhibitor or ARB, an SGLT2 inhibitor, a statin, and diabetes control.
• Heart disease, not dialysis, is the main cause of death in CKD, so we treat both.
• Avoid regular NSAID painkillers, and pause certain medicines when you are vomiting or not eating (sick-day rules).
• We involve a kidney specialist from stage G3b, or for rapid decline or nephrotic syndrome.

We screen for and manage kidney disease at our Punggol clinic. See our chronic disease care.

What CKD actually is

The kidneys do far more than filter blood. They regulate blood pressure, salt and water, activate vitamin D, and make erythropoietin, the hormone that drives red blood cell production. They also clear medicines and wastes, and support acid-base balance and bone metabolism. So CKD brings high blood pressure, anaemia, bone disease and raised cardiovascular risk.

CKD is defined as either:

• a reduced glomerular filtration rate (GFR), below 60 mL/min/1.73m², for more than 3 months, or
• evidence of kidney damage, most often protein (albumin) in the urine, for more than 3 months, whatever the GFR

Dehydration or an acute illness can lower GFR briefly, so a repeat test weeks later confirms the pattern.

CKD is a spectrum. Early CKD can stay stable for years with good management; late CKD can progress to dialysis or a transplant. Most of our patients are in the early stages; we aim to keep them there.

Why it’s so often diagnosed late

CKD is one of the most under-diagnosed chronic conditions we see. A 2019–2020 Singapore survey found it in 8.8% of adults aged 18–74, and national modelling projects this to triple by 2035. Most cases are early (G1–G2), and Singapore’s national CKD guidance reports that kidney function declines faster each year at these stages than in later ones. Early CKD is when good management helps most.

Most people feel well until kidney function is seriously impaired, often below 30% of normal. Tiredness, itch, poor appetite, nausea, leg swelling, breathlessness and foamy urine are late features, when much damage is irreversible. So we screen higher-risk people while they feel fine.

How we screen for it

Two tests matter, and we use both together:

• Serum creatinine, a blood test used to calculate the estimated GFR (eGFR)
• Urine albumin-to-creatinine ratio (UACR), a spot urine test for albumin leaking through the kidney’s filters, corrected for urine concentration

eGFR alone misses a meaningful share of early kidney disease. Significant albuminuria with a normal eGFR still counts as CKD, and is common in early diabetic kidney disease.

Creatinine alone is less useful because it depends on muscle mass: a small older woman and a muscular young man can share a creatinine value but differ greatly in kidney function. Always ask for the eGFR.

Who should be screened annually

At minimum, we recommend a yearly eGFR and UACR for anyone with:

• diabetes, the biggest single driver of CKD in Singapore
• hypertension
• age 60 or over, because a baseline and trend tell us more than one number later
• a family history of kidney disease, especially polycystic kidney disease, IgA nephropathy and hereditary glomerular diseases
• a past acute kidney injury (AKI): even a resolved AKI roughly doubles long-term CKD risk
• recurrent urinary tract infections or known urological problems (reflux, stones)
• autoimmune disease, especially systemic lupus erythematosus (SLE)
• long-term NSAID or herbal supplement use
• HIV, hepatitis B or C, from both the infection and its treatment
• multiple myeloma or any monoclonal gammopathy

Healthier SG care plans for enrolled patients with diabetes or hypertension should include it.

How we stage it — the KDIGO classification

The international standard, the KDIGO classification, stages CKD on three dimensions: the G stage (GFR), the A stage (albuminuria, measured by UACR), and the cause. Two people with the same GFR can have very different outlooks, depending on their albuminuria and cause.

The GFR stages

The albuminuria stages

The “heat map” — why both dimensions matter

KDIGO combines the two in a colour-coded grid. Risk rises down (worse GFR) and to the right (more albuminuria). Someone at G1A3 (normal GFR, severe albuminuria) has a higher risk of progression and cardiovascular events than someone at G3aA1 (reduced GFR, no albuminuria). Albuminuria shows damage to the glomerular wall that GFR misses.

In plain terms: any GFR below 45 (G3b, G4, G5) sits in the high or very high risk zone whatever the albuminuria. Any A3 albuminuria sits in the high or very high zone whatever the GFR. G3a with A2 or A3 is already high risk. These combinations most need aggressive treatment.

Albuminuria is an early, dynamic signal; GFR is a later, structural one. Together they guide how hard to treat.

Causes of CKD — not just metabolic

In Singapore, diabetic kidney disease accounts for the majority of new dialysis starts, and hypertensive nephrosclerosis is the other major contributor. But a meaningful minority of CKD has other causes, with different treatment.

Metabolic (the big two)

• Diabetic kidney disease usually progresses from albuminuria to falling GFR over years. Good diabetes and blood pressure control, and now SGLT2 inhibitors and finerenone, have changed this course substantially.
• Hypertensive nephrosclerosis: long-standing high blood pressure damages the kidney’s small vessels. Blood pressure control, often with an ACE inhibitor or ARB, is the mainstay.

Non-metabolic causes worth knowing about

• IgA nephropathy: the most common primary glomerular disease worldwide, and particularly common in East and Southeast Asia, including Singapore. It is often found through blood in the urine (visible or microscopic), sometimes after a sore throat or viral illness. Treatment is changing fast, with new targeted options.
• Polycystic kidney disease (PKD), usually autosomal-dominant (ADPKD): inherited, usually found on ultrasound, and family history is a strong clue. Specialist-led treatments (such as tolvaptan) exist for eligible patients.
• Obstructive uropathy: back-pressure from a blockage such as stones, an enlarged prostate, strictures or pelvic masses. Relieving it is the main treatment.
• Chronic pyelonephritis / reflux nephropathy: the long-term result of repeated kidney infections, often from childhood vesicoureteric reflux.
• Drug-induced kidney disease: chronic NSAID use, certain herbal preparations (particularly those containing aristolochic acid), some chemotherapy and antiviral drugs, lithium, and repeated iodinated contrast.
• Autoimmune kidney disease: lupus nephritis in SLE, ANCA-associated vasculitis, anti-GBM disease and others, often with shared nephrology and rheumatology care.
• Multiple myeloma and other monoclonal gammopathies: deposited proteins damage the kidney. We suspect this when CKD comes with anaemia, unexplained bone pain or hypercalcaemia.
• Genetic and congenital conditions: Alport syndrome, Fabry disease, thin basement membrane disease.

Not every patient with CKD has “just” diabetes or high blood pressure. When the picture doesn’t fit (a young patient, family history, unusual urine findings, systemic features), we investigate more widely and involve a specialist earlier.

Age-related GFR decline — not everything below 60 is disease

Kidney function declines with age. From around age 40, GFR falls by about 0.5 to 1 mL/min/1.73m² per year, even without kidney disease. So many people in their 70s and 80s have an eGFR below 60 that reflects ageing kidneys rather than disease.

KDIGO criteria (sustained eGFR <60) still label them “CKD G3”, even with a stable trend and no albuminuria. Some are genuinely fine; others have early progressive disease. We tell them apart by:

• Trend over years, not a single number. A stable eGFR of 55 at age 75, unchanged for 5 years, with no albuminuria and controlled blood pressure, is very different from an eGFR of 55 that has fallen from 72 over 3 years.
• Albuminuria, the tie-breaker. Ageing rarely causes significant albuminuria; any UACR >3 mg/mmol points towards disease.
• Other evidence of kidney damage: structural changes on ultrasound, electrolyte problems, anaemia out of proportion to age, or an active urinary sediment.

If your eGFR is in the 50s in your 70s with no albuminuria, you may not need the intensive care of a 55-year-old with diabetes, the same eGFR and A2 albuminuria. But the medication safety rules still apply (NSAIDs, dose adjustment for kidney-cleared drugs, sick-day rules), and cardiovascular risk still needs active management. If unsure, bring us your results; the trend usually tells the story.

Why treat it — what’s at stake

The main cause of death in people with CKD is cardiovascular disease, not kidney failure. Heart attacks, strokes, heart failure and sudden cardiac death are all more common, and the risk rises with lower eGFR and higher albuminuria. So good CKD care has two goals:

1. Slowing the decline in kidney function, to delay or prevent dialysis
2. Reducing cardiovascular events, the bigger killer

The same treatments often serve both, because kidneys and the cardiovascular system share the same vascular biology. Good control also means safer medicine use, fewer episodes of AKI on top of CKD, and better blood pressure and glucose control. It means fewer symptoms as the disease progresses (anaemia, fatigue, itch, bone pain), better quality of life, and less medical intensity in later years.

Treatment that changes the trajectory — the four pillars

We can now genuinely slow CKD in a way we couldn’t 10 years ago, including in people without diabetes. Four pillars anchor the plan for early-stage CKD.

Pillar 1 — blood pressure control with an ACE inhibitor or ARB

Blood pressure control is the biggest single lever. For most people with CKD, Singapore’s national guidance sets the target at below 130/80 mmHg, or slightly more relaxed (below 140/90) for older people or those at higher risk of falls and complications.

ACE inhibitors (ACEi) and angiotensin receptor blockers (ARBs) are preferred first-line, because they lower both blood pressure and albuminuria, with well-proven kidney and cardiovascular benefit.

• We start low and increase every 2–4 weeks, guided by blood pressure, albuminuria and tolerance.
• We check serum potassium and creatinine about 2–4 weeks after starting and after each dose increase. A modest rise (creatinine up to 30%, a small potassium rise) is expected and is not a reason to stop.
• A dry cough on an ACE inhibitor usually means switching to an ARB: same benefit, no cough.
• We don’t combine an ACEi and an ARB. It doesn’t improve outcomes and raises the risk of low blood pressure and hyperkalaemia (high potassium).

Pillar 2 — SGLT2 inhibitors (the paradigm shift)

SGLT2 inhibitors, first developed for diabetes, have reshaped CKD care. In trials (DAPA-CKD, EMPA-KIDNEY) they produced large reductions in kidney-function decline, kidney failure and cardiovascular events, with or without diabetes. They are now standard care for most people with CKD and persistent albuminuria or meaningfully reduced GFR.

Canagliflozin (Invokana) is also registered in Singapore, but for CKD we prefer the two with dedicated kidney-outcome trials. Canagliflozin also carried a signal of lower-limb amputation risk in one trial programme; see our diabetes medications guide.

• A small early drop in eGFR (up to about 30%) in the first few weeks is expected and is not a reason to stop. The long-term effect is protective.
• Allow at least a few weeks of steady use. The benefit is on the disease course, not on how you feel.
• Side effects: more urinary and genital yeast infections, usually easy to manage with good hygiene and coming in early; and a rare risk of “euglycaemic ketoacidosis” in people with diabetes during prolonged fasting, surgery or major illness.
• Sick-day rules: hold it if you are acutely unwell, vomiting, can’t keep fluids down, or are fasting for a procedure. Restart when you are eating and drinking normally.

Pillar 3 — statin therapy for cardiovascular risk

As cardiovascular disease is the leading cause of death in CKD, cholesterol-lowering treatment is almost always part of the plan. For most people with CKD we aim for LDL cholesterol below 2.6 mmol/L, or below 1.8 mmol/L with established atherosclerotic cardiovascular disease or diabetes with additional risk factors.

Moderate-intensity statins are the workhorse; high-intensity regimens are for higher-risk patients. Advanced CKD may need a dose adjustment for a slightly higher risk of muscle side effects. See our cholesterol and statins guide for targets, individual statins, ezetimibe and PCSK9 inhibitors.

Pillar 4 — glycaemic control if you have diabetes

With diabetes, these kidney-protective medicines sit on top of diabetes treatment:

• HbA1c target of around 7% for most; more flexible (6.5–8%) depending on age, frailty and other conditions.
• Metformin remains first-line for most people with eGFR ≥30, with some dose adjustment.
• SGLT2 inhibitors do double duty: lowering glucose and protecting the kidneys.
• GLP-1 receptor agonists (semaglutide — Ozempic; dulaglutide — Trulicity; liraglutide — Victoza) have cardiovascular and emerging kidney benefit in CKD with diabetes. They suit people who also want to lose weight.
• More in our diabetes pieces.

An emerging add-on — finerenone

Finerenone (Kerendia) is a non-steroidal mineralocorticoid receptor antagonist. In trials (FIDELIO-DKD, FIGARO-DKD), adding it to maximally tolerated ACEi/ARB reduced cardiovascular and kidney outcomes in people with CKD and type 2 diabetes who still had significant albuminuria. It is most useful as a third-line add-on, after ACEi/ARB and an SGLT2 inhibitor are optimised.

• It is registered in Singapore for this use. Since November 2025, eligible patients can get it subsidised through the Medication Assistance Fund (MAF) when a specialist starts it or advises on it; otherwise it is relatively expensive.
• Serum potassium monitoring is essential, as hyperkalaemia is the main risk.

We would discuss it if you still have progressive albuminuria on optimal ACEi/ARB plus an SGLT2 inhibitor, with reasonable potassium levels.

Medications to be careful about

Many prescription medications are cleared at least partly by the kidneys; Singapore’s national CKD guidance puts the figure at more than two-thirds. As kidney function falls, drug levels rise, with more side effects and less predictable responses.

• Avoid NSAIDs (ibuprofen, diclofenac, naproxen, mefenamic acid), prescription or over the counter. An occasional short course is possible, but not regular use. They reduce kidney blood flow and are probably the most common reversible cause of worsening CKD we see.
• Check before any contrast-enhanced scan (CT angiogram, coronary angiogram). Modern low-osmolar contrast is safer, but pre-hydration, contrast volume and dose adjustment matter. Tell the radiology team your kidney function.
• Herbal supplements may contain aristolochic acid or other kidney toxins, and ingredient lists are often incomplete. Show us what you take; “natural” doesn’t mean safe.
• Some antimicrobials (antibiotics, antivirals and antifungals) need dose adjustment: ciprofloxacin, nitrofurantoin (usually avoided in later CKD), trimethoprim-sulfamethoxazole (affects creatinine readings and carries a hyperkalaemia risk), valaciclovir (an antiviral), fluconazole (an antifungal).
• Direct oral anticoagulants (apixaban, dabigatran, rivaroxaban, edoxaban) all need dose awareness in CKD.
• Certain cardiovascular drugs (digoxin, sotalol, atenolol, fenofibrate) need dose adjustment.
• Gabapentin and pregabalin (for nerve pain) need a lower dose in CKD, or they accumulate and cause drowsiness, unsteadiness and confusion.
• Metformin is fine down to an eGFR of about 30, with a lower dose below 45, and is paused during acute illness (below).

Sick-day rules — the “SADMANS” list

A memory aid for medicines to pause during an acute illness (vomiting, diarrhoea, significant infection, poor eating and drinking, prolonged fasting):

• S — Sulphonylureas (gliclazide, glimepiride)
• A — ACE inhibitors
• D — Diuretics and direct renin inhibitors
• M — Metformin
• A — ARBs
• N — NSAIDs (avoid entirely)
• S — SGLT2 inhibitors (“flozins”)

Restart once you are eating, drinking and feeling better. This habit prevents a meaningful share of the acute-on-chronic kidney injury we see after a bad tummy bug or flu.

Lifestyle — what actually helps

The old “renal diet” was often stricter than necessary; the evidence now supports a more nuanced approach.

Salt

• Aim for less than 2 g of sodium a day, roughly under one teaspoon of salt. This helps blood pressure and reduces albuminuria. Going much lower adds little and is hard to sustain.
• The Health Promotion Board’s online sodium tool lists the sodium in common local foods; hawker dishes vary widely between vendors.

Protein

• In early CKD (G1 to G3a), severe protein restriction is not recommended. It doesn’t meaningfully slow progression and risks malnutrition, especially in older people.
• A normal, balanced intake (roughly 0.8 g/kg/day) is fine. Discuss very high-protein diets, such as some weight-loss regimens, with us first.
• In more advanced CKD (G3b and beyond), a moderate protein reduction may help, usually with a dietitian’s input.

Potassium

• Most people with early CKD need no routine potassium restriction.
• If hyperkalaemia develops on an ACE inhibitor or ARB, we usually reduce dietary potassium before stopping the medicine, because its benefit is substantial.
• The DASH diet and salt substitutes (potassium chloride instead of sodium) need caution in more advanced CKD.

Physical activity

• 150 to 300 minutes a week of moderate-intensity activity, as for everyone, is safe and beneficial in early CKD. Brisk walking counts.

Smoking

• Smoking speeds both kidney and cardiovascular decline; quitting is one of the biggest things you can do. Ask us about the I Quit national programme and medicines (nicotine replacement, varenicline, bupropion).

Weight and alcohol

• A 5–10% weight reduction in overweight people improves blood pressure, blood sugar and cardiovascular risk.
• Alcohol within the usual limits (no more than 2 standard drinks a day for men, 1 for women) is acceptable for most. Severe hypertension or other conditions may call for less.

Hydration

• Drink to thirst. Over-drinking to “flush the kidneys” doesn’t help, and occasionally causes hyponatraemia (low sodium) in older people.

The cardiovascular–kidney–metabolic (CKM) connection

The major societies (AHA, KDIGO) increasingly frame CKD, cardiovascular disease and metabolic conditions (type 2 diabetes, obesity) as three expressions of the same underlying process. They share drivers, treatments and complications, which is why SGLT2 inhibitors, GLP-1 receptor agonists and finerenone help across the cluster.

So if you have CKD, we are treating a whole-body process, not just your kidneys, and your plan usually covers blood pressure, cholesterol, glucose, weight and activity together. Our CKM guide covers this in depth.

Follow-up — what good care looks like

Kidney decline varies widely between people. Regular follow-up is how we catch changes early, including those that call for stepping up treatment. How often we test depends on where you sit on the KDIGO heat map above:

These are minimum testing frequencies. We may see you more often while we adjust your medicines: Singapore’s ACE guidance suggests clinic reviews every 6–12 months at moderate risk, every 3–6 months for G3a A2 or G1–G2 A3, and every 1–4 months for G3a A3.

At follow-up we also review your medicines (cost, dosing, side effects) and anything new another clinician has started. We reinforce lifestyle changes, update vaccinations and discuss new symptoms or concerns.

When we’d involve a nephrologist

Most early-stage CKD is managed in primary care. Shared or specialist care becomes more appropriate with:

• G3b, G4 or G5 disease
• a suspected primary kidney disease: glomerulonephritis, autoimmune disease, or IgA nephropathy with active features
• nephrotic syndrome (very high protein loss, low blood albumin and swelling)
• rapid decline: eGFR falling by ≥ 25% from baseline, or by more than 5 mL/min/1.73m²/year
• an acute kidney injury (AKI) that hasn’t fully recovered
• anaemia that appears related to CKD
• resistant or refractory hypertension, particularly if a kidney cause is suspected
• persistent hyperkalaemia despite dietary changes
• kidney stones, cysts or structural abnormalities suggesting a urological cause
• bone or mineral abnormalities developing alongside the CKD

Shared care doesn’t mean we stop looking after you. The nephrologist and we work together, with you in the middle.

Vaccinations

CKD raises the risk and severity of several infections. Recommended vaccinations:

• Influenza, every year
• Pneumococcal (PCV20 or the 2-dose regimen)
• Hepatitis B, particularly important in advanced CKD given possible future dialysis
• Shingrix (shingles): recommended under NAIS from age 60, and from age 18 for those with immunocompromising conditions (subsidised from September 2025); can be considered from age 50 on a self-funded basis
• COVID-19 boosters as recommended
• Tdap every 10 years

We review vaccinations at each visit and can usually update them the same day.

The Singapore context — schemes that help

• Healthier SG Chronic Tier: enrolled patients can access chronic disease consultations and many CKD medicines (ACEi/ARB, SGLT2 inhibitors, statins, metformin) at prices close to polyclinic rates.
• Community Health Assist Scheme (CHAS): means-tested subsidies for consultations and selected medicines. More at chas.sg.
• MediSave: usable for chronic disease consultations and selected medicines, up to the annual limit (currently $500, or $700 for complex chronic conditions; rising to $700 / $1,000 from January 2027).
• National Kidney Foundation Singapore (NKF): supports patients who progress to dialysis, including financial assistance and integrated care programmes. We would discuss this well before it is needed.

Get in touch

Punggol — 658 Punggol East, #01-04, Singapore 820658 · Tel 6312 4589

Joo Chiat — 172 Joo Chiat Road, #01-01, Singapore 427443 · Tel 6920 1952

Email — admin@ktmc.sg

References

Guidelines

• Agency for Care Effectiveness (ACE). Chronic kidney disease — delaying progression and reducing cardiovascular complications. ACE Clinical Guidance, Ministry of Health, Singapore. 27 October 2023. ace-hta.gov.sg
• KDIGO (Kidney Disease: Improving Global Outcomes). 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. kdigo.org
• Ndumele CE, Rangaswami J, Chow SL, et al. Cardiovascular-Kidney-Metabolic Health: A Presidential Advisory From the American Heart Association. Circulation. 2023;148(20):1606-1635.

Landmark trials cited in this guide

• DAPA-CKD investigators (Heerspink HJL, Stefánsson BV, et al.) Dapagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2020;383:1436-1446.
• EMPA-KIDNEY Collaborative Group. Empagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2023;388:117-127.
• Bakris GL, Agarwal R, Anker SD, et al. (FIDELIO-DKD Investigators). Effect of Finerenone on Chronic Kidney Disease Outcomes in Type 2 Diabetes. N Engl J Med. 2020;383:2219-2229.
• Pitt B, Filippatos G, Agarwal R, et al. (FIGARO-DKD Investigators). Cardiovascular Events with Finerenone in Kidney Disease and Type 2 Diabetes. N Engl J Med. 2021;385:2252-2263.
• Perkovic V, Tuttle KR, Rossing P, et al. (FLOW Trial Committees). Effects of Semaglutide on Chronic Kidney Disease in Patients with Type 2 Diabetes. N Engl J Med. 2024;391:109-121.

Singapore epidemiology

• National Registry of Diseases Office, Singapore. Singapore Renal Registry Annual Report.
• Ministry of Health, Singapore. National Population Health Survey 2019/2020.

National programmes

• Health Promotion Board Singapore. Food Composition Online Search — sodium content lookup. focos.hpb.gov.sg
• National Kidney Foundation Singapore. nkfs.org
• Healthier SG and Chronic Tier information. healthiersg.gov.sg

Singapore registration and subsidy of finerenone

• Agency for Care Effectiveness (ACE). Finerenone for treating chronic kidney disease and albuminuria associated with type 2 diabetes. Technology Guidance from the MOH Drug Advisory Committee. Updated 16 September 2025. ace-hta.gov.sg
• National Drug Formulary, Ministry of Health, Singapore. Kerendia film-coated tablet 10 mg (SIN16387P) — product information. ndf.gov.sg

This information is for general education only and is not a substitute for medical advice. Chronic kidney disease management must be individualised based on your stage, underlying cause, comorbidities, and medications — please speak with our team about what’s right for you. v1.1 · October 2026 (v1.0 April 2026) · Review due April 2028.