CKD is defined by abnormal kidney structure or function lasting for at least 3 months. CKD is very prevalent, both in the US and worldwide, affecting 15% to 20% of adults globally—more than 800 million people in the world.¹ As many as 37 million Americans meet criteria for CKD.² 

CKD is important because it is associated with a very high risk of cardiovascular disease (CVD) and heart failure. A patient with CKD is already at risk for developing kidney failure. Kidney failure, in general, is defined by the requirement for dialysis or kidney transplant to survive.

One of the challenges associated with CKD is that it is often asymptomatic in the early stages. People can feel completely normal and be asymptomatic when their glomerular filtration rate (GFR) is approximately 50 to 60 mL/min/1.73 m². If patients have albuminuria levels of 200 mg/g, they likely do not have any symptoms related to kidney disease itself, often contributing to underdiagnosis. The patient may not be aware that they have CKD and may not have even been tested for it.

CKD prevalence has been increasing annually both worldwide and in the US due to the increased prevalence of other risk factors, including obesity. Because of this, CKD needs to be detected and managed much earlier. Fortunately, new interventions that target the early stages of CKD have been discovered over the last 10 years, aiding in the prevention of progression to more advanced kidney disease.

CKD is defined by abnormal kidney structure (eg, polycystic kidney disease) or function, assessed via renal ultrasound, for at least 3 months with health implications. CKD is most commonly defined based on 2 measures: urine albumin-to-creatinine ratio (uACR) and estimated GFR (eGFR), measured via a blood test.³ When a patient receives a diagnosis of CKD, it is important to consider the cause. Is it due to diabetes? Is it due to hypertension? Is it due to a genetic disease? uACR and eGFR are used to establish the severity of CKD and guide the type of intervention needed.⁴

It is important to determine whether patients have been taking nephrotoxic medications for years that may have caused kidney disease. Nonsteroidal anti-inflammatory drugs, lithium, and other medications can cause chronic kidney damage.

Healthcare professionals (HCPs) should look for signs and symptoms of urinary tract abnormalities. Does this patient have benign prostatic hypertrophy? Do they have nocturia? Are they urinating a lot at night? Have they had kidney stones that may have caused kidney damage? It is important to obtain a detailed medical history because hypertension, diabetes, or other medical problems may have predisposed them to kidney disease.

Patients’ social and environmental history will also provide insight. Have they been exposed to certain types of heavy metals in the type of work they do?

HCPs also need to assess whether patients have a systemic disease. Symptoms and signs of systemic diseases that may affect the kidney and put a patient at higher risk for kidney disease are conditions such as diabetes, lupus, amyloidosis, and HIV. Many types of kidney disease can be genetic, the most prevalent being polycystic kidney disease, but there are many types that can be genetic in nature, such as Fabry disease and Alport syndrome. Some are autosomal dominant, and some are autosomal recessive, so family history is crucial.⁵ 

Once medical history has been obtained, the HCP will perform a urinalysis and look for blood in the urine under a microscope. The GFR, uACR, and other serologic measures, when necessary, will be determined. An ultrasound may reveal an obstruction, kidney stones, chronic changes, or atrophy. In some cases, a kidney biopsy is needed to define exactly what the disease is, especially when interstitial or glomerular disease is suspected. Genetic testing should be incorporated more frequently into testing for patients with kidney disease, as genetic variants that increase susceptibility to kidney disease are being increasingly recognized.⁴

Which patients should be screened? There is some debate in the literature as to whether everyone should be screened. The KDIGO 2024 recommendations include prioritizing screening for those at high risk for CKD like people with diabetes, hypertension, CVD, and obesity. People with genetic causes or a family history and individuals experiencing any symptoms that may be related to the kidney should also be screened.

How are patients screened for kidney disease? eGFR and uACR. The most common method used to determine the eGFR is the CKD-EPI, an equation that does not incorporate race. Measuring urine albumin and urine creatinine is important for staging the disease and assessing prognosis. The guideline emphasizes the use of cystatin C. Creatinine is affected by muscle mass and may impact the GFR. Cystatin C has other determinants independent of kidney function, but when used together, the result often provides the most accurate estimate of GFR.

Patients in whom the eGFR may not be accurate are those who are hospitalized, those in intensive care units, and those who have lost a lot of muscle mass. Their creatinine is very low, and their eGFR will be falsely too high. In these patients, the addition of cystatin C should help estimate kidney function. Kidney disease should always be confirmed with repeat testing 3 months later because kidney function can change within 1 week.⁴ Over short periods, this is called acute kidney injury (AKI), so CKD should be distinguished from AKI or acute kidney disease (AKD).

It is important to distinguish between AKD and CKD and to establish chronicity. Initially, the GFR or ACR is measured, and a GFR less than 60 mL/min/1.73 m² or an ACR greater than or equal to 30 mg/g means that the patient meets initial criteria for abnormal kidney function. These tests should be repeated in 3 months to determine whether the values persist. If the GFR remains less than 60 mL/min/1.73 m² or the ACR remains greater than 30 mg/g at that time, the criteria for CKD are met. If they do not persist, the patient may have either AKD or AKI based on the timing of the resolution of the abnormalities.⁴

This heat map is important for showing how to stage CKD. CKD is staged based on GFR criteria as G1, G2, G3a, G3b, G4, or G5, but the ACR is also measured, which is represented in the second column. As demonstrated in this slide, a patient who falls within either of the 2 green boxes does not meet criteria for CKD. Every other box meets criteria for CKD either by GFR (less than 60 mL/min/1.73 m²) or ACR (greater than or equal to 30 mg/g). As the GFR becomes lower, the colors change from yellow to orange to pink to red, meaning more severe kidney disease and higher risk for disease progression and CVD. The GFR and ACR are independent of each other. Therefore, high levels of albuminuria with preserved GFR are associated with a high risk for progression. A low GFR, even without high levels of albuminuria, also indicate high risk. In all of these stages, HCPs should consider initiating treatment, with the treatments becoming more aggressive depending on the level of albuminuria and GFR. Patients at highest risk are those with very low GFRs and high levels of albuminuria.⁴

Listen to this brief audio clip about the GFR and ACR categories.

The evaluation framework is based on CGA, which is cause, GFR category, and albuminuria category. When assessing cause, it is crucial to know the GFR and albuminuria to stage the disease and inform initial treatment. Again, the diagnostic threshold for kidney disease is a GFR less than 60 mL/min/1.73 m² or a uACR greater than or equal to 30 mg/g. The addition of cystatin C for estimating GFR can improve accuracy where creatinine alone may not be sufficient, as in patients who have lost muscle mass or undergone an amputation. Focus on chronicity: a CKD diagnosis requires at least 3 months of abnormal kidney structure or function.

In patients who are at high risk for CVD and kidney disease, HCPs need to determine the risk of developing the hard cardiovascular or kidney outcomes. Validated prediction tools can be used to estimate these risks. One such tool is the kidney failure risk equation (KFRE), which primarily incorporates the level of albuminuria, GFR, age, and sex and estimates the risk of kidney failure over 2 to 5 years. Cardiovascular prediction tools have also been developed for patients with kidney disease. One such example is the PREVENT tool from the American Heart Association, which incorporates albuminuria and eGFR into the risk equation. Incorporating these parameters into validated equations more accurately estimates an individual’s risk of developing various cardiovascular outcomes in the presence of CKD.⁴ This helps inform patients and gives them an idea of their risk of developing CVD and progressing to kidney failure over the next 10 years.

CKD treatment should be personalized, and lifestyle interventions must be introduced. Many are consistent with recommendations in the general population, but some are unique to patients with kidney disease. From a dietary standpoint, plant-based foods are healthier. Red meat and high-protein foods are not good for the kidney and will promote hyperfiltration and kidney disease progression. Ultra-processed foods should be limited in patients with kidney disease. In general, lowering sodium intake to approximately less than 2 g per day should be recommended, especially in people with hypertension. High protein intake should be avoided in people with stage G3 to G5 disease. The general recommendation is 0.8 g/kg/body weight/day in adults with CKD stage 3 to 5, but this is partly dependent on each patient’s condition.

As in the general population, 150 minutes per week of moderate-intensity activity based on patient tolerance should be encouraged. If the patient is very deconditioned, exercise should be introduced slowly. Focus on achieving and maintaining a healthy body mass index, which is important for determining the risk of CVD and progression of kidney disease. Smoking cessation is strongly recommended for reducing cardiovascular risk, cancer risk, and progression of kidney disease.⁴

For approximately 3 decades, renin-angiotensin-aldosterone system (RAAS) inhibitors have been particularly helpful for all stages of CKD, especially in patients with albuminuria. RAAS inhibitors are used to treat blood pressure, but they also reduce albuminuria, slow the progression of kidney disease, and may help prevent CVD based on multiple clinical trials on diabetic and nondiabetic CKD. The higher the level of albuminuria, the more beneficial these medicines are.⁴

Other considerations during treatment include patient characteristics such as frailty or comorbid conditions. Previous KDIGO guidelines recommended a targeted systolic blood pressure (SBP) of less than 120 mm Hg, when tolerated, for cardiovascular protection. This recommendation was based primarily on the CKD subgroup of the Systolic Blood Pressure Intervention Trial (SPRINT) that assumes standardized measures of blood pressure are used (ie, in the clinic, blood pressure is measured 2 or 3 times and then averaged).⁶ However, some guidelines recommend a targeted SBP of less than 130 mm Hg to reduce cardiovascular outcomes.⁷

Previous guidelines have reported individual glycated hemoglobin (A1C) targets, which depend on the individual, of between 6.5% and 8% in patients with CKD and diabetes. Patients who are at increased risk for hypoglycemia are allowed a slightly higher A1C. In general, the target is approximately 7% for patients with CKD,⁸ but it is understood that some patients with diabetes are frail, and harm should not be caused by making their blood sugar levels too low. Each of these recommendations, as well as the associated benefits and risks, should be discussed with patients to promote shared decision-making.

The KDIGO 2024 treatment strategy summarizes some things I previously mentioned. A healthy diet is critical, and physical activity is very important for cardiovascular health. Tobacco cessation is necessary, and patients should maintain a healthy body mass index.

Some first-line agents include sodium-glucose cotransporter-2 (SGLT2) inhibitors, which have been shown to reduce the progression of kidney disease and risk of CVD. In patients without diabetes, primarily those with albuminuria, the target SBP is less than 120 mm Hg (assuming standardized blood pressure measurements), and a RAAS inhibitor is helpful. As shown on the right side of the graph, statin-based therapy is recommended for patients with CKD over age 50. Statins are recommended because they have been shown to reduce the risk of atherosclerotic disease (ASCVD).

Glucagon-like peptide 1 (GLP-1) receptor agonists are helpful for diabetes control and may exert kidney-protective effects, particularly in patients who may be overweight. Nonsteroidal mineralocorticoid receptor antagonists (MRAs) can be added to SGLT2 and RAAS inhibitors in patients with diabetes and kidney disease who have albuminuria greater than 30 mg/g, as these agents slow the progression of kidney disease and may reduce the risk of CVD. Patients with kidney disease have a high prevalence of hypertension and frequently require several agents. Dihydropyridine calcium channel blockers are good for blood pressure control. Patients with kidney disease are at risk for volume retention, so they often need diuretics for blood pressure control. In a patient with ASCVD, an antiplatelet agent is often prescribed, and as kidney function progresses, acidosis, bone and mineral metabolism, and potassium abnormalities are managed. Steroidal MRAs are particularly helpful if patients have resistant hypertension, but with MRAs, both steroidal and nonsteroidal, potassium levels should be monitored, particularly when RAAS inhibitors are prescribed. If a patient cannot tolerate a statin, other medicines can be used for ASCVD prevention, including PCSK9 inhibitors and ezetimibe.⁴

When patients are taking several medications (eg, RAAS inhibitor, SGLT2 inhibitor, nonsteroidal MRA), it is not uncommon to observe initial dips in the GFR, as these are hemodynamically active medications, but in the longer term, these agents slow the progression of kidney disease. It is important to let patients know that although blood tests may show worsening kidney function, increased creatinine, and/or a decreased eGFR, this response is normal and not necessarily bad. GFR reductions of 10% to 15% can be anticipated following initiation. A GFR reduction greater than 30% of baseline may exceed the expected variability and suggest another underlying cause.⁴ Did the patient experience volume depletion? Did they take another medicine that caused the GFR to drop? In these cases (ie, declines of 30%, 50%, or 100%), the medicine may need to be withheld. The HCP should reassess the patient and perhaps start with a lower dose.

For example, a patient is started on an angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB), and serum creatinine and potassium are monitored for 2 to 4 weeks after starting or changing the dose. If the potassium level does not increase, and if there is less than a 30% decrease in eGFR, one can conclude that the medication was well tolerated, and blood pressure is under control.

In the presence of hyperkalemia, the level of severity should be assessed. Dietary indiscretion could be the culprit. However, if the diet cannot be modified, diuretics should be considered. If the patient’s sodium bicarbonate level is low, it may be beneficial to add some. Potassium binders could be introduced. New potassium binders from the last 5 years can help keep the potassium level in range.

If the eGFR drops by more than 30%, other possible causes of this decline should be assessed. Most importantly, follow laboratory measures like potassium and eGFR after RAAS inhibitors are started.⁴

Although many medicines benefit patients with kidney disease, HCPs must be very careful because these patients are frequently on more medications than the general population. There are concerns for drug interactions and medication adherence. At all points throughout transitions of care, medications should be thoroughly reviewed. Adherence, need, and any drug interactions should be assessed. Regardless of who the patient is being seen by (ie, endocrinologist, cardiologist), at each visit, the HCP should know exactly what medications the patient is taking and confirm they are on an appropriate regimen. In general, over-the-counter medicines and dietary and herbal remedies should be limited, as some have side effects on the kidney and may be harmful. Others have not been evaluated, so these should also be avoided. Kidney function should be assessed using established equations like the CKD-EPI, which will help estimate the GFR and dose medications appropriately.⁴

Is each medication necessary? Is any other medication required? Is this medicine the preferred one for this indication? Is the dosage correct? Review the medication list for interactions and ensure proper monitoring. Is this patient taking all of their medications? When in doubt, ask the patient to bring in all of their prescriptions. Communicate with the pharmacy to ensure the patient is picking up their medicines. Most importantly, ensure that all HCPs are on the same page and communicating effectively.

Listen to this brief audio clip about medication review.

Patients with CKD can have symptoms that are part of other conditions associated with CKD, but sometimes the symptoms are related to the CKD itself. Therefore, symptom identification and assessment is important for highlighting changes, redirecting toward patient-centered care, and possibly holding discussions about supportive care. The new guideline emphasizes shared decision-making and effective communication between HCPs and patients.⁴

Some symptoms that patients with kidney disease experience may include fatigue (present with advanced CKD), which could also be related to anemia. Patients with shortness of breath may be retaining fluid or have CVD. Some patients have poor mobility for various reasons. Bone and joint pain could be part of a systemic disease (ie, autoimmune disease). As kidney disease progresses, patients may report decreased appetite or itching due to phosphorus retention. Patients may report sexual dysfunction or poor sleep, all of which are symptoms of kidney disease. HCPs need to be aware of these symptoms to effectively communicate with patients and provide the best care possible.⁴

The new guideline emphasizes shared decision-making, a collaborative process between the patient and their HCP. Engaging and empowering the patient are important in shared decision-making. The patient needs to be given information about all treatment options as well as alternatives. The risk of disease progression, risk of CVD, and potential side effects should be explained. Questions to ask may include: “How many medications are you taking?” “Are you willing to take another that is going to help reduce your risk of CVD?” It is crucial to listen to your patient’s preferences and incorporate them into the treatment plan.⁹

When is shared decision-making needed? This question is relevant to most patients with kidney disease. It is needed when there are options and the results of the intervention may have health, financial, or quality of life implications. Shared decision-making is also needed when discussing daily management and lifestyle choices for chronic conditions. The process for shared decision-making is as follows. The HCP shares with the patient information about testing or treatment options, the probability of harm, the probability of benefits, and any possible alternatives. The patient then explores and shares their preferences regarding the above, assessing what is important to them and communicating it in their own words. This ensures that the patient understands the risks and benefits. Then the patient and HCP make a mutual decision as to what is best for that particular patient.¹⁰

Listen to this brief audio clip about shared decision-making.

Advanced care planning should always be considered in patients with kidney disease. These plans depend on the stage of CKD and involve interventions to examine. As kidney disease progresses, patients and their HCPs should think about transplant, dialysis, and/or conservative care if the patient is close to developing stage 5 CKD. With advanced care planning, it is always good to incorporate the patient and their family members so that everyone is on the same page.⁴

This figure helps to define some primary outcomes of kidney disease. Green represents patients in the earlier stages of CKD; those with a low eGFR and without high albuminuria. Kidney failure risk is less than 3% to 5% in 5 years. These patients are often taken care of by primary care providers (PCPs). Patients at risk for CVD need to be identified early so that the risk can be mitigated. Appropriate medications are necessary.

Patients with stage 3 CKD have an eGFR of 30 to 60 mL/min/1.73 m² and might be starting to experience some complications from kidney disease (eg, altered bone and mineral metabolism, anemia). Their kidney failure risk, on average, may be slightly higher over 5 years (3%-5%). The goal is to prevent progression to CKD stage 4 or stage 5.

At stage 4 CKD, the risk of kidney failure may be greater than 10% in 2 years, and HCPs may want to start introducing new concepts regarding the risk of kidney failure and appropriate options. The patient should be educated as to what may happen.

At stage 5 CKD, kidney failure is a major concern. Discussions with a kidney replacement preparation team may be warranted. HCPs should determine whether their patient is a candidate for kidney transplant or dialysis and what type of dialysis (ie, hemodialysis, peritoneal dialysis) is appropriate. Would this patient favor conservative care? These are all considerations as patients reach advanced stages of CKD, and incorporating the patient and their family is important when making these decisions.⁴

Key treatment considerations include a regular review of medicines and assurance of adherence to the prescribed therapy. Drug interactions and ongoing indications for therapy should be constantly evaluated. Monitor the eGFR throughout the disease. When hemodynamic medications such as RAAS inhibitors are initiated, evaluate kidney function and potassium a couple of weeks later. Determine whether the dose can be increased (eg, if the potassium is stable and the eGFR did not drop more than anticipated). If there is an eGFR decline greater than 30%, further evaluation is required, as this may indicate volume depletion or renal artery stenosis. Do the medications need to be withheld and the patient reassessed? Combination therapy should be avoided, as should the use of direct renin inhibitors with ACE inhibitors or ARBs, because there is a risk of hypotension, hyperkalemia, and AKI. However, ACE inhibitors or ARBs can be used together with MRAs, particularly in patients with diabetes and proteinuria. There may be added benefits, but potassium and any changes in kidney function should be closely monitored when used together.⁴

Multidisciplinary teams are critical when caring for patients with CKD. As mentioned earlier, CKD is a complex disease with multiple different causes and often multiple comorbid conditions. Working as a team helps improve adherence to guidelines through collaborative care. Patients also feel empowered and know they can depend on their cardiologist and nephrologist.⁴

Multidisciplinary teams generally include some combination of the following: a nephrologist to manage the kidney disease; a cardiologist to mitigate cardiovascular risk; a PCP to facilitate early detection, coordinate amongst specialists, and ensure adherence to lifestyle and medication plans; a dietitian to support new dietary lifestyle modifications, create meal plans, and promote dietary sodium and protein restrictions; and a pharmacist to optimize medication regimens and avoid adverse interactions between medications.⁴

Listen to this brief audio clip about multidisciplinary teams.

Implementation challenges are barriers to multidisciplinary teams and having patients incorporate all recommendations. These include a lack of time, tools, and resources. Clinicians often have limited time to adopt new CKD-specific workflows and tools. Workforce shortages, especially in underserved areas, may also present a challenge. There is much stress on medical providers to help care for a patient with multiple comorbid conditions. There is also a lack of awareness or slow adoption of new guidelines. HCPs may not be aware of all the new guidelines, how to incorporate them into practice, and/or how to easily incorporate them into practice. Sometimes there are delayed referrals and limited patient engagement. Patients often do not want to see many practitioners; they want one person to take care of everything. Patients are also often referred very late to nephrology care, making it challenging to incorporate multidisciplinary teams and screen for CKD early.²

How do HCPs overcome barriers to CKD management? Multidisciplinary education is important. All of the clinical practice guidelines for patients with CKD essentially recommend implementing self-management programs, multidisciplinary care models that incorporate multiple members of the healthcare team, and implementing strategies that decrease risks.²

Here are some solutions to implementation challenges. Streamline education for HCPs. Implement clear, concise, targeted training on the updated KDIGO recommendations, emphasizing tools such as the CKD-EPI equation and incorporating cystatin C for risk education. Enhance public awareness of CKD. Campaign to educate the general population as to who is at risk—for example, people with diabetes, hypertension, and CVD—and how lifestyle interventions may reduce the progression of kidney disease as well as the incidence of CVD.⁴

Provide expert guidance in easily digestible formats. Create easily accessible resources and quick references for HCPs so both clinicians and patients understand and can apply KDIGO recommendations. Use validated clinician prediction tools, which may include the KFRE or equations that estimate the risk of CVD, so that risks can be discussed with patients via shared decision-making.⁴

Listen to this brief audio clip about solutions to implementation challenges.

This 58-year-old male has a history of type 2 diabetes and hypertension and presents to the clinic for a routine evaluation. He denies any symptoms, such as fatigue, swelling, or decreased appetite. His eGFR is 55 mL/min/1.73 m², uACR is 180 mg/g, A1C is 7.8%, and blood pressure is 138/88 mm Hg on lisinopril and amlodipine.

His eGFR is below 60; if less than 3 months, it would be consistent with CKD. His uACR is 180 mg/g; if this value was consistent when repeated, he would meet criteria for CKD. His A1C is slightly high, and his SBP is slightly higher than the target of either 120 or 130 mm Hg.

In summary, this patient has CKD stage 3a, with an eGFR of 45 to 59 mL/min/1.73 m², moderately increased albuminuria, with a uACR between 30 and 300 mg/g. This patient has a significant risk of CKD progression and cardiovascular complications. The 2024 guideline recommends adding an SGLT2 inhibitor, such as empagliflozin, for patients with CKD in the presence of diabetes. This medicine will reduce the risk of CVD as well as progression of kidney disease in this type of patient. SGLT2 inhibitors are thought to be safe and effective when used alongside an ACE inhibitor or ARB.

There is no benefit to discontinuing lisinopril and switching to losartan. The HCP should reassess eGFR and uACR in 3 months to confirm chronicity, but this patient is meeting many criteria where the addition of an SGLT2 inhibitor would have benefits for both kidney disease and cardiovascular protection.

With the rising global burden of CKD, it is crucial to stay ahead with proactive strategies. Here are some key takeaways and next steps to guide effective management. To improve patient outcomes and overall kidney health, focus on early detection, optimizing treatment, and slowing disease progression. Aim for personalized, guideline-concordant care that optimizes kidney and cardiovascular health.¹¹

Next steps include integrating the KDIGO 2024 recommendations into daily practice. Foster team-based care to improve patient outcomes. Early nephrology referrals are important if there are any questions about the cause of CKD, particularly as patients progress through the more advanced stages. Utilize shared decision-making with patients and empower them through education. Patients should understand why they are on each medication, potential side effects, and why the benefits outweigh the risks.¹¹