Chronic kidney disease — delaying it, not just diagnosing it

About this guide

Chronic kidney disease (CKD) is one of the most under-diagnosed chronic conditions we see. A Singapore population survey in 2019–2020 put the local prevalence at 8.8% of adults aged 18–74, and national modelling projects this to triple by 2035. Most of those cases are early — CKD stages G1–G2 — and the rate of kidney-function decline in that group has been shown to be faster than in later stages. That last point is important: early CKD isn’t a reason to relax, it’s exactly when good management delivers the most benefit.

Two things have changed substantially in the last decade that patients should know about:

1. We can now genuinely slow the disease in a way we couldn’t 10 years ago — the arrival of SGLT2 inhibitors, originally developed as diabetes medications, has shifted CKD care into an era where we can meaningfully protect kidney function, including in patients who don’t have diabetes.
2. The main killer for people with CKD is cardiovascular disease, not dialysis. Kidney disease and heart disease are now understood as two sides of the same coin — a whole body of work on the cardiovascular–kidney–metabolic (CKM) syndrome reflects this shift. We’ll have a dedicated guide on that soon; this piece focuses on the kidney side.

This guide covers:

• Why CKD goes undetected for so long — and who should be screened
• The KDIGO staging system, and why it uses two dimensions (GFR and albuminuria), not one
• The causes — metabolic (diabetes, blood pressure) but also important non-metabolic causes, plus age-related decline
• The four-pillar treatment approach that changes the disease trajectory
• Medications to be careful about, sick-day rules, and when we’d involve a nephrologist

What CKD actually is

The kidneys do far more than “filter blood.” They regulate blood pressure, balance salt and water, activate vitamin D, produce the hormone erythropoietin that drives red cell production, clear many medications and metabolic waste products, and contribute to acid-base and bone metabolism. When kidney function falls, problems show up across all of those domains — which is why CKD is associated with high blood pressure, anaemia, bone disease, and raised cardiovascular risk.

Chronic kidney disease is defined as either:

• A reduced glomerular filtration rate (GFR) — below 60 mL/min/1.73m² — persisting for more than 3 months, or
• Evidence of kidney damage — most commonly protein (albumin) in the urine — persisting for more than 3 months, regardless of GFR

The “more than 3 months” matters — a one-off dehydration episode or an acute illness can drop the GFR temporarily without meaning chronic disease. A repeat test weeks later confirms the pattern.

CKD is a spectrum, not an on/off condition. Early CKD can be stable for years with good management. Late CKD can progress to the need for dialysis or transplantation. Most patients we see are in the early stages, where the work of the next decade is to keep them there.

Why it’s so often diagnosed late

Here’s the hard truth: patients usually feel well until kidney function is seriously impaired — often below 30% of normal. The symptoms that eventually appear — tiredness, itch, poor appetite, nausea, leg swelling, breathlessness, foamy urine — are late features. By the time they show up, much of the irreversible damage is already done.

This is the case for proactive screening in the people most likely to have kidney disease, while they still feel fine.

How we screen for it

The two tests that matter:

• Serum creatinine — used to calculate the estimated GFR (eGFR). A simple blood test.
• Urine albumin-to-creatinine ratio (UACR) — a single spot-urine sample measuring the amount of albumin leaking through the glomerular filter, corrected for urine concentration.

We use both together. eGFR alone misses a meaningful proportion of early kidney disease — a patient can have significant albuminuria with a perfectly normal eGFR, and that still counts as CKD. That pattern is particularly common in early diabetic kidney disease.

A creatinine value on its own — without the eGFR calculation — is genuinely less useful, because serum creatinine depends on muscle mass. A small older woman and a muscular young man can have the same creatinine with very different kidney function. Always ask for the eGFR.

Who should be screened annually

At minimum, we’d recommend yearly eGFR + UACR for anyone with:

• Diabetes (the single biggest driver of CKD in Singapore)
• Hypertension
• Age 60 or over — kidney function declines with age, and a baseline plus trajectory is more informative than a single number later
• Family history of kidney disease — particularly for polycystic kidney disease, IgA nephropathy, and hereditary glomerular diseases
• A past episode of acute kidney injury — even a resolved AKI roughly doubles the long-term CKD risk
• Recurrent urinary tract infections or known urological abnormalities (reflux, stones)
• Autoimmune disease — especially systemic lupus erythematosus (SLE)
• Long-term NSAID or herbal supplement use
• HIV, hepatitis B or C — treatment-related and infection-related kidney risk
• Multiple myeloma or any monoclonal gammopathy

Screening is also part of Healthier SG for enrolled patients with diabetes or hypertension — it’s one of the things your care plan should include.

How we stage it — the KDIGO classification

Kidney disease isn’t a single number. The current international standard — the KDIGO classification — stages CKD along three dimensions:

• G stage — based on GFR
• A stage — based on albuminuria (UACR)
• Cause — what’s actually driving the kidney damage

This matters because two patients with the same GFR can have very different prognoses depending on their albuminuria and their underlying cause.

The GFR stages

The albuminuria stages

The “heat map” — why both dimensions matter

KDIGO presents the combined picture as a colour-coded grid where risk rises as you move down (worse GFR) and to the right (more albuminuria). A patient at G1A3 (normal GFR, severe albuminuria) carries a higher risk of progression and cardiovascular events than a patient at G3aA1 (reduced GFR, no albuminuria) — which is counter-intuitive if you think of kidneys only as filters. Albuminuria tells you something about the glomerular wall that a GFR alone doesn’t.

In plain terms: any GFR below 30 (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. And G3a combined with A2 or A3 already crosses into high risk. These are the combinations that most need aggressive treatment.

A useful shorthand: albuminuria is an early, dynamic signal; GFR is a later, structural signal. Both matter; together they guide how aggressively to treat.

Causes of CKD — not just metabolic

It’s tempting to think of CKD as a diabetes or hypertension problem. In Singapore those are the big two — diabetic kidney disease alone accounts for the majority of new dialysis starts, and hypertensive nephrosclerosis is the other major contributor. But a meaningful minority of CKD is driven by something else, and the treatment pathway can differ substantially.

Metabolic (the big two)

• Diabetic kidney disease — typically progresses from albuminuria → declining GFR over years. Well-controlled diabetes, blood pressure, and now SGLT2 inhibitors + finerenone have substantially changed this trajectory.
• Hypertensive nephrosclerosis — long-standing raised blood pressure damages the small vessels of the kidney. Controlling blood pressure, 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 prevalent in East and Southeast Asian populations, including Singapore. Often picked up because of visible or microscopic blood in the urine, sometimes following a sore throat or viral illness. Treatment is changing rapidly, with new targeted options in recent years.
• Polycystic kidney disease (PKD) — usually the autosomal-dominant form (ADPKD). Inherited, typically picked up by ultrasound; family history is a strong clue. Specific treatments (e.g. tolvaptan) exist for eligible patients and are specialist-led.
• Obstructive uropathy — back-pressure from a blockage anywhere in the urinary tract: kidney stones, an enlarged prostate, strictures, or pelvic masses. Relieving the obstruction is the main intervention.
• Chronic pyelonephritis / reflux nephropathy — the long-term consequence of repeated kidney infections, often going back to childhood vesicoureteric reflux.
• Drug-induced kidney disease — chronic use of non-steroidal anti-inflammatories (NSAIDs), certain herbal preparations (particularly those containing aristolochic acid), some chemotherapy and antiviral drugs, lithium, and repeated exposure to iodinated contrast.
• Autoimmune kidney disease — lupus nephritis in SLE, vasculitis (ANCA-associated), anti-GBM disease, and others. Often warrants shared care with a nephrologist and rheumatologist.
• Multiple myeloma and other monoclonal gammopathies — deposited proteins damage the kidney. Suspected when CKD is accompanied by anaemia, unexplained bone pain, or hypercalcaemia.
• Genetic and congenital conditions — Alport syndrome, Fabry disease, thin basement membrane disease.

The take-home: not every patient with CKD has “just” diabetes or high blood pressure. When the picture doesn’t fit — young patient, family history, unusual urinary findings, systemic features — the investigation has to be broader, and specialist input earlier.

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

Kidney function declines with age. From around age 40, the GFR falls by approximately 0.5 to 1 mL/min/1.73m² per year, even in people without kidney disease. That means many people in their 70s and 80s have eGFR values below 60 that reflect the kidneys they have, rather than pathology that needs to be chased down.

This is a real clinical dilemma. The KDIGO criteria (eGFR <60 sustained) will classify such patients as “CKD G3” even though the trajectory is stable and the albuminuria is absent. Some of them are genuinely fine; others have the early stage of something progressive.

How we tell the difference:

• Trajectory over years, not a single number. A stable eGFR of 55 at age 75, unchanged for 5 years, with no albuminuria, and blood pressure well controlled, is very different from an eGFR of 55 falling from 72 over 3 years.
• Albuminuria is the tie-breaker. Age-related decline rarely produces significant albuminuria. Any UACR >3 mg/mmol shifts the picture toward pathological disease.
• Other evidence of kidney damage — structural abnormalities on ultrasound, electrolyte disturbances, anaemia out of proportion to age, active urinary sediment.

What this means practically: if your eGFR is in the 50s in your 70s with no albuminuria, you may not need the same aggressive monitoring and treatment as a 55-year-old diabetic patient with the same eGFR and A2 albuminuria. But — and this is important — the medication safety rules still apply (NSAIDs, dose adjustment for renally-cleared drugs, sick-day rules), and cardiovascular risk still needs active management.

If you’re uncertain where you sit, bring your lab results to us; the trajectory usually tells the story.

Why treat it — what’s at stake

CKD is often perceived as a “dialysis countdown.” In reality, the main cause of death in people with CKD is cardiovascular disease, not end-stage kidney failure. Heart attacks, strokes, heart failure, and sudden cardiac death are all more common in CKD, and the risk rises with both lower eGFR and higher albuminuria.

Good CKD management therefore has two goals, held together:

1. Slowing the decline of kidney function — delaying or preventing dialysis
2. Reducing cardiovascular events — the bigger killer

The same treatments often serve both ends. That’s not a coincidence — the kidney and the cardiovascular system share the same vascular biology.

Beyond those two headlines, good control also means:

• Safer medication use — many common medications need dose adjustment in CKD
• Fewer episodes of AKI on top of chronic disease
• Better blood pressure and glucose control
• 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

Over the last decade, the evidence base for how we treat CKD has changed substantially. For patients with early-stage CKD, four pillars now anchor the plan.

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

Blood pressure control is the single biggest lever. The target for most patients with CKD is below 130/80 mmHg, though slightly more relaxed targets (below 140/90) apply in older patients or those at higher risk of falls and complications.

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

Commonly used in Singapore:

Starting and titrating:

• We start at a low dose and titrate upward every 2–4 weeks, guided by blood pressure, albuminuria, and tolerance.
• We check serum potassium and creatinine about 2–4 weeks after starting or each dose increase. A modest rise (creatinine up to 30%, small potassium rise) is expected and is not a reason to stop.
• If you develop a dry cough on an ACE inhibitor, we usually switch to an ARB — same benefit, no cough.
• We don’t combine an ACEi and an ARB — the combination doesn’t improve outcomes and carries a higher risk of hypotension and hyperkalaemia.

Pillar 2 — SGLT2 inhibitors (the paradigm shift)

The arrival of SGLT2 inhibitors — originally developed as diabetes medications — has reshaped CKD care. Trials (DAPA-CKD, EMPA-KIDNEY) showed large reductions in kidney-function decline, onset of kidney failure, and cardiovascular events, in patients with or without diabetes. This has moved SGLT2 inhibitors firmly into the standard-of-care list for most patients with CKD who have persistent albuminuria or meaningfully reduced GFR.

Commonly used in Singapore:

Canagliflozin (Invokana) was historically a third SGLT2 inhibitor available locally but has been withdrawn from the Singapore market following post-market data on lower-limb amputation risk. Patients previously on canagliflozin are usually switched to dapagliflozin or empagliflozin.

Points worth knowing:

• An initial small 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.
• Give it at least a few weeks of consistent use; benefit is on the disease trajectory rather than on how you feel day-to-day.
• Side effects — increased risk of urinary and genital yeast infections (often easy to manage; good hygiene and a low threshold for coming in helps), and a rare risk of “euglycaemic ketoacidosis” in diabetic patients under certain conditions (prolonged fasting, surgery, major illness).
• Sick-day rules — hold the SGLT2 inhibitor if you’re acutely unwell, vomiting, unable to keep fluids down, or fasting for a procedure. Restart when you’re eating and drinking normally.

Pillar 3 — statin therapy for cardiovascular risk

Because cardiovascular disease is the leading cause of death in CKD, lipid-lowering treatment is almost always part of the plan. For most patients with CKD, we aim for:

• LDL cholesterol below 2.6 mmol/L
• Below 1.8 mmol/L if you also have established atherosclerotic cardiovascular disease or diabetes with additional risk factors

Moderate-intensity statins are the workhorse; high-intensity regimens are reserved for higher-risk patients. Dose adjustments may be needed in advanced CKD because of a slightly higher risk of muscle side effects.

For the full detail on lipid management — targets, individual statins, ezetimibe, PCSK9 inhibitors — see our cholesterol and statins guide.

Pillar 4 — glycaemic control if you have diabetes

In patients with CKD and diabetes, the kidney-protective medication stack above sits on top of diabetes treatment. Key points:

• HbA1c target of around 7% for most; more flexible (6.5–8%) depending on age, frailty, and comorbidities.
• Metformin remains the initial first-line agent in most patients with eGFR ≥30 and some dose adjustment.
• SGLT2 inhibitors do double duty here — glucose reduction and kidney protection.
• GLP-1 receptor agonists (semaglutide — Ozempic; dulaglutide — Trulicity; liraglutide — Victoza) have cardiovascular and emerging renal benefit in CKD with diabetes, and are a good choice where weight reduction is also a goal.
• For detail see our diabetes pieces.

An emerging add-on — finerenone

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

Two caveats locally:

• Availability in Singapore remains limited at the time of writing, and it is relatively expensive.
• Monitoring of serum potassium is essential — hyperkalaemia is the main risk.

We’d discuss finerenone with you if you are on optimal doses of ACEi/ARB + SGLT2 inhibitor and still have progressive albuminuria with reasonable potassium levels.

Medications to be careful about

Between two-thirds and three-quarters of prescription medications are cleared, at least in part, by the kidneys. When kidney function falls, drug levels rise — which can cause both more side effects and less predictable responses. A short mental checklist:

• Avoid NSAIDs — ibuprofen, diclofenac, naproxen, mefenamic acid, both prescription and over-the-counter. Short courses occasionally, but not regular use. They reduce kidney blood flow and are probably the single most common reversible worsener of CKD we see.
• Check before any contrast-enhanced scan (CT angiogram, coronary angiogram). Modern low-osmolar contrast is safer than older agents, but pre-hydration, contrast volume management, and dose adjustment matter. Let the radiology team know your kidney function.
• Herbal supplements — some contain aristolochic acid or other nephrotoxins; the ingredient lists are often incomplete. Bring what you’re taking to us rather than assume “natural” means safe.
• Some antibiotics need dose adjustment — ciprofloxacin, nitrofurantoin (usually avoided in later CKD), trimethoprim-sulfamethoxazole (affects creatinine readings and carries hyperkalaemia risk), valaciclovir, fluconazole.
• Direct oral anticoagulants — apixaban, dabigatran, rivaroxaban, edoxaban — all need dose awareness in CKD.
• Certain cardiovascular drugs — digoxin, sotalol, atenolol, fenofibrate — need dose adjustment.
• Neuropathic pain agents — gabapentin and pregabalin in particular — need dose reduction in CKD, or they accumulate and cause drowsiness, unsteadiness, and confusion.
• Metformin — fine down to an eGFR of about 30, with dose reduction below 45. We also hold it during acute illness (see sick-day rules).

Sick-day rules — the “SADMANS” list

A simple mnemonic for medications to hold temporarily during an acute illness (vomiting, diarrhoea, significant infection, reduced oral intake, 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 when you’re eating and drinking normally and feeling better. This one practice prevents a meaningful chunk of the acute-on-chronic kidney injury we see after a bad tummy bug or flu.

Lifestyle — what actually helps

Lifestyle measures in CKD have evolved. The old “renal diet” was often more restrictive than necessary, and the evidence now supports a more nuanced approach.

Salt

• Aim for less than 2 g of sodium per day — roughly less than one teaspoon of salt — which helps blood pressure and reduces albuminuria.
• Don’t drastically under-salt (below about 1.4 g per day) — extreme restriction can drop GFR and blood pressure unsafely.
• The Health Promotion Board’s online sodium tool lists the sodium content of 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 disease progression, and risks malnutrition, particularly in older patients.
• A normal, balanced protein intake (roughly 0.8 g/kg/day) is fine. Very high-protein diets (e.g. some weight-loss regimens) are worth discussing with us first.
• In more advanced CKD (G3b and beyond), a moderate protein reduction may be helpful, and we’d usually loop in a dietitian.

Potassium

• No routine potassium restriction is needed for most patients with early CKD.
• If you develop hyperkalaemia while on an ACE inhibitor or ARB, we usually prefer to reduce dietary potassium before stopping the medication, because the medication benefit is substantial.
• The DASH diet and salt substitutes (which use potassium chloride instead of sodium) need caution in more advanced CKD.

Physical activity

• 150 to 300 minutes per week of moderate-intensity activity — same as the general population — is both safe and beneficial in early CKD. Brisk walking counts.

Smoking

• Smoking accelerates both kidney and cardiovascular decline. Quitting is one of the single biggest things you can do for long-term outcomes.
• The I Quit national programme and pharmacotherapy (nicotine replacement, varenicline, bupropion) are available — please ask us.

Weight and alcohol

• A 5–10% weight reduction in overweight patients improves blood pressure, blood sugar, and cardiovascular risk.
• Alcohol within the usual limits (no more than 2 standard drinks/day for men, 1 for women) is acceptable in most patients; those with severe hypertension or other comorbidities may need to be more restrictive.

Hydration

• Drink to thirst. Drastic over-hydration to “flush the kidneys” is not helpful and occasionally causes hyponatraemia in older patients.

The cardiovascular–kidney–metabolic (CKM) connection

Over the last few years, the major societies (AHA, KDIGO) have increasingly framed chronic kidney disease, cardiovascular disease, and the metabolic conditions (type 2 diabetes, obesity) as three expressions of the same underlying process — with shared drivers, overlapping treatments, and interacting complications. SGLT2 inhibitors, GLP-1 receptor agonists, and finerenone all help across the cluster, which is no coincidence.

We’ve written a dedicated guide — Cardiovascular-kidney-metabolic (CKM) health — why we look at these together — that covers this framework in depth. The short version: if you have CKD, we’re not just treating your kidneys — we’re treating a whole-body process that is pushing on your heart, your blood vessels, and your metabolic regulation at the same time. That’s why the plan usually covers blood pressure, cholesterol, glucose, weight, and activity together.

Follow-up — what good care looks like

Rate of kidney decline varies widely between patients. Regular follow-up is how we catch changes early — including the ones that justify stepping treatment up.

A general guide, adapted from the KDIGO “heat map”:

Beyond the numbers, follow-up is also where we:

• Review how you’re coping with medications (cost, dosing complexity, side effects)
• Reinforce lifestyle changes
• Update vaccinations (see below)
• Review anything new that’s been started by another clinician
• Discuss any 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 when:

• You’re at G3b, G4, or G5 — progressing into later stages of kidney disease
• A primary kidney disease is suspected — glomerulonephritis, autoimmune disease, IgA nephropathy with active features
• Nephrotic syndrome (very high protein loss with low blood albumin and swelling)
• Rapid decline — eGFR falling by ≥ 25% from baseline, or more than 5 mL/min/1.73m²/year
• An episode of acute kidney injury (AKI) that hasn’t fully recovered
• Anaemia that appears related to CKD
• Resistant or refractory hypertension — particularly if a renal cause is suspected
• Persistent hyperkalaemia despite dietary management
• 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 — it means the nephrologist and we work together, with you in the middle.

Vaccinations

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

• Annual influenza
• Pneumococcal (PCV20 or the 2-dose regimen)
• Hepatitis B — particularly important in advanced CKD given the possibility of future dialysis
• Shingrix (shingles) — from age 50, or from 18 with chronic conditions under the current subsidy arrangements
• COVID-19 boosters as recommended
• Tdap every 10 years

We review vaccinations at each visit — if you’re overdue, it’s usually easy to update on the same day.

The Singapore context — schemes that help

• Healthier SG Chronic Tier — enrolled patients can access chronic disease consultations and many CKD medications (ACEi/ARB, SGLT2 inhibitors, statins, metformin) at prices close to polyclinic rates.
• Community Health Assist Scheme (CHAS) — means-tested subsidies for consultations and selected medications. More at chas.sg.
• MediSave — usable for chronic disease consultations and selected medications, up to the annual limit (currently $500, rising to $700 / $1,000 from January 2027).
• National Kidney Foundation Singapore (NKF) — provides support for patients who progress to dialysis, including financial assistance and integrated care programmes. If you’re heading in that direction, we’d discuss this well before it becomes necessary.

Get in touch

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

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

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

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. v1.0 · April 2026 · Review due April 2028.