- Chronic kidney disease (CKD) affects an estimated 35+ million U.S. adults, and most don't know they have it because it is usually silent in the early stages.
- CKD is staged by eGFR (G1-G5) and by albuminuria (A1-A3); since 2021, the recommended eGFR equations no longer use race as a variable.
- Diabetes and high blood pressure cause the majority of CKD; simple blood (eGFR) and urine (albumin) tests can detect it years before symptoms appear, so people at risk should be screened.
- Modern treatment slows progression: blood pressure and glucose control, ACE inhibitors or ARBs, and SGLT2 inhibitors (now a standard, clinician-directed part of CKD care), with finerenone and GLP-1 medicines as additional options for some patients.
- Do not stop prescribed kidney or blood pressure medicines on your own, and avoid NSAIDs and other nephrotoxins unless your clinician approves them.
- Certain symptoms — confusion, severe fatigue or weakness, an irregular heartbeat, a marked drop in urine output, or severe shortness of breath from fluid overload — are urgent; seek emergency care. This article is educational, not medical advice.
An estimated 35 million or more American adults have chronic kidney disease, yet as many as 9 in 10 don’t know they have it. According to the CDC, chronic kidney disease — often abbreviated CKD — is one of the most underdiagnosed conditions in the country, silently damaging the kidneys for years before symptoms appear. By the time many people are diagnosed, significant and often irreversible kidney damage has already occurred. Early detection and management are the most powerful tools available to slow progression and preserve kidney function. This article is educational information, not medical advice; use it to have a better-informed conversation with your own clinician. For more on chronic conditions, see our medical conditions guide.
The short version: CKD means the kidneys are gradually losing their ability to filter the blood. It is usually silent early, so people at risk — especially those with diabetes or high blood pressure — should be screened with simple blood (eGFR) and urine (albumin) tests. It is staged by eGFR (G1-G5) and albuminuria (A1-A3). Progression can be slowed, sometimes dramatically, with blood pressure and glucose control, ACE inhibitors or ARBs, and SGLT2 inhibitors, plus newer options for some patients. Do not stop prescribed medicines or start supplements on your own. This is general education, not a substitute for your clinician’s advice, and it contains no medication dosing.
What Is Chronic Kidney Disease?
Chronic kidney disease is a condition in which the kidneys gradually lose their ability to filter waste and excess fluid from the blood. Your kidneys — two fist-sized organs near the middle of your back — filter a large volume of blood every day, removing waste products, balancing electrolytes, helping regulate blood pressure, stimulating red blood cell production, and supporting bone health. When kidney function declines, these processes are compromised.
CKD is defined as kidney damage or reduced kidney function lasting three months or more. The damage can be structural (detected through imaging or biopsy), indicated by markers like protein in the urine (proteinuria/albuminuria), or shown by a reduced glomerular filtration rate (GFR) — the primary measure of how well your kidneys are filtering blood. A normal estimated GFR (eGFR) is generally above 90 mL/min/1.73m². CKD is diagnosed when eGFR stays below 60, or when there is other evidence of kidney damage (such as albumin in the urine) that persists for at least three months, regardless of eGFR.
The NIDDK notes that CKD typically progresses slowly over years, and the rate of progression varies enormously depending on the underlying cause, the severity at diagnosis, and how effectively risk factors are managed. Some people with CKD maintain stable kidney function for decades; others progress to kidney failure within years.
Stages of Chronic Kidney Disease
CKD is classified by eGFR into five stages (labeled G1 through G5), with higher stages indicating more severe kidney impairment:
- Stage G1 (eGFR 90+): Normal or high eGFR but with evidence of kidney damage (such as albumin in the urine or structural abnormalities). Kidneys still filter normally despite some damage.
- Stage G2 (eGFR 60-89): Mildly decreased eGFR with evidence of kidney damage. Still no symptoms in most cases.
- Stage G3a (eGFR 45-59) and G3b (eGFR 30-44): Moderately decreased kidney function. Complications like anemia and bone-mineral disease may begin. This is where many people are first diagnosed.
- Stage G4 (eGFR 15-29): Severely decreased function. Symptoms become more prominent. Preparation for dialysis or transplant should begin.
- Stage G5 (eGFR below 15): Kidney failure (historically called end-stage renal disease). Dialysis or a kidney transplant is generally needed to sustain life.
Modern staging (the KDIGO framework) also grades albuminuria alongside eGFR, because how much protein is leaking into the urine strongly predicts risk. Albuminuria categories are A1 (normal to mildly increased, ACR under 30 mg/g), A2 (moderately increased, 30-300 mg/g), and A3 (severely increased, above 300 mg/g). Combining the eGFR stage (G) with the albuminuria stage (A) gives a fuller picture of prognosis than eGFR alone. Knowing your stage is essential for guiding treatment intensity and planning. The National Kidney Foundation provides resources to help you understand what each stage means for your daily management and long-term outlook.
A note on how eGFR is calculated: the 2021 race-free equations
eGFR is estimated from a blood creatinine level using a calculation. Historically, those equations included a race adjustment that could report higher kidney function for Black patients. In 2021, a joint National Kidney Foundation and American Society of Nephrology task force recommended new eGFR equations that do not use race as a variable, and U.S. laboratories have widely adopted them. If you have older kidney test results, your eGFR may have been recalculated under the newer, race-free equation, so ask your clinician which method your lab uses if you are comparing values over time. A cystatin C blood test can also be used, sometimes together with creatinine, to estimate GFR more precisely in certain situations.
Causes and Risk Factors
Diabetes is the leading cause of CKD, responsible for a large share of new kidney failure cases. High blood sugar damages the tiny blood vessels in the kidneys (the glomeruli) over time — a process called diabetic kidney disease. High blood pressure is the second leading cause. Elevated blood pressure damages kidney blood vessels, reducing their filtering capacity, and CKD in turn raises blood pressure — a harmful cycle.
Other causes include glomerulonephritis (inflammation of the kidney’s filtering units), polycystic kidney disease (a genetic condition causing fluid-filled cysts), recurrent kidney infections, kidney stones causing obstruction, prolonged urinary tract obstruction (from an enlarged prostate, for example), and autoimmune diseases like lupus. Certain medications — including long-term or high-dose NSAID use — can damage the kidneys.
Risk factors beyond diabetes and hypertension include age over 60, family history of kidney disease, cardiovascular disease, obesity, and smoking. Kidney disease also disproportionately affects some communities — including Black, Hispanic, and Native American populations — reflecting a mix of higher rates of diabetes and hypertension, genetic factors (such as APOL1 variants), and social and access-related factors, rather than race itself being a biological cause. According to the Mayo Clinic, having multiple risk factors multiplies your likelihood of developing CKD.
Symptoms
CKD earns its reputation as a “silent disease” because symptoms typically don’t appear until the kidneys have lost significant function. In the early stages (G1-G3a), most people feel completely normal. As the disease progresses, symptoms develop gradually and can be vague enough to be attributed to other causes.
Common symptoms in more advanced CKD include fatigue and weakness (from anemia and toxin buildup), swelling in the feet, ankles, and hands (from fluid retention), changes in how much you urinate, foamy or bubbly urine (from excess protein), persistent itching, nausea and vomiting, loss of appetite, a metallic taste in the mouth, difficulty concentrating, muscle cramps, and sleep problems.
Because symptoms are so nonspecific, the CDC recommends regular screening for people at risk — particularly those with diabetes, hypertension, cardiovascular disease, or a family history of kidney disease. Simple blood and urine tests can detect CKD long before symptoms emerge.
Seek urgent or emergency care (call 911 or go to an emergency department) if you or someone with kidney disease develops:
- Confusion, extreme drowsiness, or difficulty staying awake, severe fatigue, or profound muscle weakness — these can be signs of a dangerous buildup of toxins (uremia) or of severe electrolyte problems
- An irregular, very slow, or racing heartbeat, palpitations, or chest pain — severely high potassium (hyperkalemia) can cause life-threatening heart rhythm disturbances
- Severe shortness of breath, or trouble breathing when lying flat, especially with rapid swelling — a sign of severe fluid overload
- A marked drop in urine output or no urine, or sudden severe swelling
- Seizures, or fainting
These are potential emergencies. Do not wait for a scheduled appointment, and do not try to treat them at home.
Diagnosis and Monitoring
Two tests are central to CKD diagnosis and monitoring. A blood test for creatinine is used to calculate your eGFR, which tells you how well your kidneys are filtering. A urine test for albumin (a type of protein) detects kidney damage — healthy kidneys keep albumin in the blood, and its presence in urine indicates the filtration system is leaking.
The albumin-to-creatinine ratio (ACR) from a spot urine sample is the preferred test for albuminuria. An ACR above 30 mg/g is considered abnormal. Higher levels of albuminuria are associated with faster CKD progression and higher cardiovascular risk. Both eGFR and ACR should be monitored regularly — together, they provide a comprehensive picture of kidney health and, as noted above, define your KDIGO risk category.
Additional tests may include a complete metabolic panel (for electrolytes such as potassium, plus calcium and phosphorus), complete blood count (for anemia), parathyroid hormone levels, lipid panel, and a kidney ultrasound to evaluate size and structure. The NIDDK notes that a kidney biopsy may be needed in some cases to determine the specific cause of CKD, particularly when the cause is unclear or when a treatable condition like glomerulonephritis is suspected.
Slowing CKD Progression
While kidney damage that has already occurred generally can’t be reversed, slowing progression is very achievable — and in some cases, progression can be nearly halted. Treatment is directed by your clinician and individualized; the overview below is educational and does not include dosing. The two most important foundations are blood pressure control and, in people with diabetes, blood sugar control.
Blood pressure targets for many CKD patients are around or below 130/80 mmHg, individualized to the person. ACE inhibitors and ARBs are often the preferred blood pressure medications in CKD with albuminuria because they provide kidney protection beyond blood pressure reduction — they reduce protein leakage and slow eGFR decline. These medications are a cornerstone of CKD treatment when tolerated. Do not start, stop, or change them on your own; your clinician will monitor your kidney function and potassium when adjusting them.
A major advance in CKD care has been SGLT2 inhibitors (such as dapagliflozin and empagliflozin). Originally developed for diabetes, they have shown substantial kidney- and heart-protective effects in people with CKD — including many people without diabetes. Landmark trials such as DAPA-CKD and EMPA-KIDNEY, published in the New England Journal of Medicine, showed meaningful reductions in the risk of kidney function decline, kidney failure, and related cardiovascular events across a broad CKD population. As a result, SGLT2 inhibitors are now recommended by major guidelines (including KDIGO) as a standard part of treatment for many people with CKD, especially those with albuminuria. Whether one is right for you, and at what point, is a decision for your clinician.
Additional options have expanded the toolkit further. Finerenone, a nonsteroidal mineralocorticoid receptor antagonist, has been shown in the FIDELIO-DKD and FIGARO-DKD trials to slow progression and reduce cardiovascular events in people with CKD associated with type 2 diabetes, and it is often used alongside an ACE inhibitor or ARB and an SGLT2 inhibitor. GLP-1 receptor agonists such as semaglutide, long used for diabetes and weight management, showed kidney and cardiovascular benefit in people with type 2 diabetes and CKD in the FLOW trial. These medicines are not appropriate for everyone and require clinician oversight and monitoring; think of them as tools your nephrologist or primary care clinician may add to a personalized plan, not something to obtain or dose on your own. Understanding medication costs is important when planning long-term CKD treatment, since several of these are brand-name drugs.
Diet and Lifestyle for CKD
Dietary management becomes increasingly important as CKD progresses, and it should be individualized — ideally with a renal dietitian — because the right diet depends on your stage and lab values. In earlier stages, a heart-healthy diet lower in sodium (commonly a target under about 2,300 mg daily) is a primary recommendation. As kidney function declines, additional attention to potassium, phosphorus, and protein may be needed, but you should not impose strict restrictions on yourself without guidance, as that can cause other problems.
Protein intake is a nuanced topic. Excess protein increases the workload on damaged kidneys, and some protein moderation is often advised in later stages to help slow progression. However, too little protein can lead to muscle wasting and malnutrition, particularly in older adults. A renal dietitian can help you find the right balance for your situation rather than a one-size-fits-all rule.
Staying appropriately hydrated (unless your clinician advises fluid restriction), maintaining a healthy weight, exercising regularly, quitting smoking, limiting alcohol, and avoiding nephrotoxic medications are all important. In particular, avoid over-the-counter NSAIDs like ibuprofen and naproxen unless your clinician has approved them, and be cautious with certain herbal supplements and high-dose vitamins, some of which can harm the kidneys. The National Kidney Foundation offers detailed dietary guidance for each stage of CKD.
Complications of CKD
As kidney function declines, numerous complications can develop. Cardiovascular disease is the leading cause of death in people with CKD — often exceeding the risk of ever reaching kidney failure. Even mild CKD raises the risk of heart disease and stroke. Aggressive management of blood pressure, cholesterol, and blood sugar is critical.
Anemia develops because damaged kidneys produce less erythropoietin, the hormone that stimulates red blood cell production. Treatment may include iron supplementation, erythropoiesis-stimulating agents (ESAs), and, in some cases, newer oral agents (HIF-PH inhibitors) — all clinician-directed. Bone-mineral disease (renal osteodystrophy) occurs because the kidneys can’t properly balance calcium, phosphorus, and vitamin D; untreated, this can lead to bone weakness and fractures.
Electrolyte imbalances — particularly elevated potassium (hyperkalemia) — can be dangerous, as high potassium can cause life-threatening heart rhythm disturbances (see the red-flag box above). Fluid overload leads to swelling, shortness of breath, and higher blood pressure. Metabolic acidosis (excess acid in the blood) can accelerate kidney decline and muscle wasting. Each of these complications requires specific monitoring and management.
Dialysis and Transplant
Dialysis
When kidneys can no longer sustain health — typically at stage G5, when eGFR drops below 15 — renal replacement therapy is needed. Hemodialysis, the most common form, filters blood through a machine, often about three times per week with sessions lasting roughly four hours; it is typically performed at a dialysis center, though home hemodialysis is an option for some. Peritoneal dialysis uses the lining of your abdomen as a filter and can be performed at home, daily or overnight, offering more flexibility.
Planning for dialysis should begin well in advance — ideally in stage G4. This includes creating a dialysis access (for example, an arteriovenous fistula, which takes weeks to mature), education about dialysis options, and discussions about whether transplant is possible. According to the NIDDK, early planning leads to better outcomes and smoother transitions. Some patients, particularly those who are older or have other serious illnesses, may also discuss conservative (non-dialysis) management with their care team; this is a personal, values-based decision to make with your clinicians and family.
Kidney Transplant
Kidney transplantation is the preferred treatment for kidney failure in eligible patients. A transplanted kidney generally provides better quality of life and longer survival than long-term dialysis. Kidneys can come from deceased donors (wait times vary widely by region and blood type) or living donors (who can be family members, friends, or altruistic strangers). Pre-emptive transplant — performed before dialysis is needed — tends to produce the best outcomes.
After transplant, lifelong immunosuppressive medications are required to prevent rejection. These medications have side effects, including increased infection risk and higher rates of certain cancers, but for most eligible people, the benefits of transplant far exceed the risks. Tens of thousands of kidney transplants are performed each year in the United States, and getting evaluated early — before or soon after reaching advanced CKD — can widen your options.
Frequently Asked Questions
Can chronic kidney disease be reversed?
In most cases, established CKD cannot be reversed because scarring is permanent. However, if the underlying cause is identified and treated early — such as relieving an obstruction or controlling an autoimmune flare — some recovery of function is possible. More importantly, progression can often be significantly slowed or even nearly halted with proper, clinician-directed treatment, keeping many people off dialysis for years or indefinitely.
How do I know if I have chronic kidney disease?
The only reliable way to know is through blood and urine tests — a blood test for eGFR and a urine test for albumin (ACR). Since CKD causes no symptoms until advanced stages, regular screening is essential if you have risk factors. Ask your doctor about kidney function testing, particularly if you have diabetes, hypertension, cardiovascular disease, or a family history of kidney disease.
Is chronic kidney disease hereditary?
Some forms of CKD have a strong genetic component. Polycystic kidney disease is inherited, and certain gene variants (such as APOL1) raise risk. Even for non-genetic forms, a family history of kidney disease increases your risk — partly because conditions like diabetes and hypertension that cause CKD also run in families. If kidney disease runs in your family, earlier and more frequent screening is warranted.
Can I take over-the-counter pain relievers with CKD?
NSAIDs (ibuprofen, naproxen, and aspirin at anti-inflammatory doses) should generally be avoided with CKD unless your clinician specifically approves them, as they can worsen kidney function and cause acute kidney injury. Acetaminophen (Tylenol) is generally considered safer for the kidneys but should be used at the lowest effective dose. Always check with your doctor or pharmacist before taking any over-the-counter medication or supplement.
Should I stop my medications if my kidney numbers change?
No — do not stop or change prescribed medications on your own, even if a lab value shifts. Some kidney-protective drugs can cause temporary changes in eGFR or potassium that your clinician expects and monitors. Stopping blood pressure or kidney medicines abruptly can be harmful. Always talk to your prescriber before making any change.
How long can you live with chronic kidney disease?
Life expectancy with CKD depends heavily on the stage at diagnosis, underlying cause, age, and how well comorbid conditions (especially cardiovascular risk factors) are managed. Many people with stage G1-G3 CKD live normal or near-normal lifespans. Even with kidney failure requiring dialysis, people can live for years, and kidney transplant recipients often have life expectancy approaching that of the general population.
What You Can Do Right Now
If you have CKD, the most impactful things you can do are take your medications consistently as prescribed (especially blood pressure and kidney-protective drugs), manage your blood sugar if you have diabetes, follow individualized dietary guidance, stay physically active, avoid nephrotoxic substances, and keep all follow-up appointments so your kidney function can be tracked over time. Ask your clinician whether an SGLT2 inhibitor or other newer kidney-protective medicine is appropriate for you.
If you’re at risk but haven’t been tested, ask your doctor for a kidney function check at your next visit. Two simple tests — blood (eGFR) and urine (albumin) — can detect CKD long before it causes problems. Early detection gives you the widest window of opportunity to slow or stop progression. The kidneys you have are the only ones you’ll get (unless you’re fortunate enough to receive a transplant), and protecting them is worth the effort.
Disclaimer: This article is general educational information about chronic kidney disease, not medical advice, and it does not include medication dosing. CKD diagnosis, staging, and treatment must be individualized by a qualified clinician, and recommendations and drug approvals evolve over time. Do not start, stop, or change any medication or supplement on your own. If you have warning signs such as confusion, an irregular heartbeat, severe shortness of breath, or a sudden drop in urine output, seek emergency care.
Sources
- CDC — Chronic Kidney Disease in the United States: prevalence, risk, and screening (cdc.gov)
- NIDDK / NIH — chronic kidney disease, tests and diagnosis, and kidney failure treatment (niddk.nih.gov)
- National Kidney Foundation & NKF-ASN Task Force — CKD stages and the 2021 race-free eGFR equations (kidney.org)
- KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of CKD — staging and management (kdigo.org)
- NEJM / PubMed — DAPA-CKD, EMPA-KIDNEY, FIDELIO-DKD/FIGARO-DKD (finerenone), and FLOW (semaglutide) trials (pubmed.ncbi.nlm.nih.gov)
- Mayo Clinic — chronic kidney disease symptoms and causes (mayoclinic.org)