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Expert Insights in CKD
Expert Insights in CKD Management: FAQs and What They Reveal About the Evolving Practice

Released: December 23, 2025

Chuck Vega
Chuck Vega, MD, FAAFP
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Key Takeaways
  • Urine–albumin-to-creatinine ratio tests are generally inexpensive, covered by health insurance, and should be used to screen patients with type 2 diabetes or hypertension for CKD.
  • Cystatin C is more accurate in analyzing true kidney function than creatinine when both biomarker tests return inconclusive results.
  • CKD management is transforming into a combination therapy approach with 4 pillars that offer synergistic cardiovascular, kidney, and metabolic benefits.

Chronic kidney disease (CKD) continues to challenge healthcare professionals (HCPs) in the primary care setting because its earliest stages are nearly invisible to detect. As emphasized throughout a live symposium titled “Screen, Spot, Stop! A CKD Gameplan for Primary Care Settings,” 90% of adults with CKD do not know that they have it. Furthermore, patients can remain asymptomatic until their kidney function drops below an estimated glomerular filtration rate (eGFR) of 25 mL/min/1.73 m². This stark reality reframes CKD as a proactive, preventive discipline rather than a reactive one. The HCP learner questions posed during the symposium reflected this shift.

In this commentary, Chuck Vega, MD, FAAFP, answers the 6 questions that rose to the top for their relevance, nuance, and clinical utility. Take home expanded insights and practical direction to help translate the current evidence into everyday decisions for primary care HCPs managing patients with CKD.

Are urine–albumin-to-creatinine ratio (UACR) tests expensive, and does health insurance cover them?
This question underscores 1 of the greatest missed opportunities in CKD detection. Despite UACR being essential for risk stratification, only 25% of patients with type 2 diabetes (T2D) receive this screening annually. In addition, UACR is generally inexpensive and uniformly covered by health insurance when coded appropriately. Cost is rarely the barrier—HCP awareness and clinical workflows are. The more important message is that eGFR alone cannot be used to diagnose CKD or stratify patients’ risk, and relying on creatinine alone leaves far too many patients unidentified until severe disease develops. When HCPs embed UACR into their routine labs for those with T2D or hypertension, CKD progression can be slowed dramatically. 

Is cystatin C useful and when should it be ordered?
Cystatin C has long been the “better test that no one quite knew how to use.” Now, with the removal of race and addition of more consistent test calibration in the 2021 CKD-EPI equations, cystatin C is stepping into its appropriate role. It is most valuable when creatinine-based eGFR is unreliable, whether that be in patients who are muscular, frail, older, and/or taking creatine supplements—all of which can cause inaccurate serum creatinine values. When patients’ eGFR and clinical picture do not match, a cystatin C–based estimate often reveals the true degree of their kidney function. It should not, however, be used in patients with uncontrolled thyroid disease because cystatin C levels are misleading. When used strategically, cystatin C can prevent over- and underdiagnosis while clarifying when referral or therapy escalation is needed.

Should I trust cystatin C more than creatinine?
This question reflects a growing sophistication among HCPs. The answer is simple, trust neither alone. Instead, HCPs must trust the clinical context. Creatinine-based eGFR performs well for most patients, but cystatin C is less influenced by patients’ muscle mass and dietary protein. The KDIGO’s recommendation to use both biomarkers when diagnosis is uncertain results in the meaningful reclassification of approximately 30% of patients. When both tests agree, accuracy is excellent; when they diverge, cystatin C is more accurate in determining true kidney function. Ultimately, the biomarker itself is less important than the pattern over time, which was a lesson repeated throughout the symposium.

Why do labs only flag eGFR once it falls below 60 mL/min/1.73/m2?
This understandably is frustrating for HCPs who are shifting toward earlier CKD detection in their practice. Labs flag eGFRs less than 60 mL/min/1.73 m² because that threshold corresponds to CKD stage 3a, where long-term risk becomes clinically actionable. But it is critical to remember that CKD cannot be diagnosed with a single and abnormal eGFR. HCPs must recheck results after at least 3 months to confirm persistence. More subtle, early disease is often missed unless HCPs are actively screening with both eGFR and UACR, which is recommended by KDIGO for all patients with T2D, hypertension, cardiovascular disease, older age, or prior family history. It was interesting to see how many HCPs in the symposium expressed surprise at the number of patients with a “normal eGFR” who shifted into the high-risk category once their albuminuria was measured.

Can finerenone and GLP-1 receptor agonists be used concomitantly? If so, what should be expected?
One of the most exciting developments in CKD care is the emergence of 4 therapeutic pillars: renin–angiotensin system (RAS) inhibitors, sodium-glucose cotransporter-2 (SGLT2) inhibitors, GLP-1 receptor agonists, and nonsteroidal mineralocorticoid receptor antagonists like finerenone. As discussed in the symposium, GLP-1 receptor agonists improve cardiovascular outcomes, reduce albuminuria, and optimize weight and glycemic control. In turn, finerenone directly reduces inflammation and fibrosis within the heart and kidneys. When layered thoughtfully (ie, RAS inhibitor + SGLT2 inhibitor + GLP-1 receptor agonist + finerenone), patients experience marked improvement in kidney outcomes, heart outcomes, and overall mortality. Hyperkalemia continues to be the primary limiting factor for finerenone, but most patients tolerate it well when potassium remains below 5.0 mmol/L. The take-home message: the 4 therapeutic pillars are synergistic, not redundant, and combination therapy is becoming the new standard of care in CKD management.

When should primary care HCPs refer their patients to nephrology?
Referral remains one of the most challenging—and variable—points in CKD care. I often tell primary care HCPs to refer patients when their eGFR falls below 30 mL/min/1.73m2 or earlier if their eGFR decline is rapid, albuminuria is severe, etiology is unclear, and/or metabolic complications emerge. Many HCPs will wait until patients have CKD stage 4, but nephrology colleagues consistently affirm that CKD stage 3b is not too early for referral, especially if the diagnosis is uncertain or patients are young. Of note, referral is not about handing off care to nephrology but about enhancing it. Early comanagement can improve dialysis preparation, decrease emergent dialysis starts, and improve mortality. Therefore, this remains a powerful myth for my primary care colleagues to dismantle. 

Your Thoughts
A larger theme from the live symposium emerged: CKD management can no longer be passive. Early screening, repeated confirmation, strategic use of biomarkers, and aggressive combination therapy are necessary to redefine expectations for what primary care can achieve. Far from being a slow, inevitable decline, CKD is now a condition that we can interrupt—often dramatically—when detected early and treated comprehensively. My hope is that by elevating these frequently asked questions in this commentary, we can continue shifting CKD from a silent disease to a visible, preventable one via proactive conversations, lab orders, and clinical decision-making.

Do you regularly screen your patients with T2D or hypertension for CKD using both UACR and eGFR equations? You can get involved in the conversation by answering the poll question and posting a comment below.

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Do you regularly screen your patients with T2D or hypertension for CKD using both UACR and eGFR equations?

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