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Nephrologist Perspective in CKD care
What HCPs Really Want to Know in CKD Care: A Nephrologist’s Perspective

Released: December 26, 2025

Jay B. Wish
Jay B. Wish, MD
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Key Takeaways
  • SLGT2 inhibitors should not be discontinued if patients experience an eGFR decline below 20 mL/min/1.73m2 after initiation.
  • CKD should be treated with combination therapy of RAS inhibition plus SLGT2 inhibitor and nonsteroidal MRAs or GLP-1 receptor agonists for select patients per guidelines.
  • HCPs must address the barriers patients face in accessing necessary CKD treatment, including choosing an agent in a class that is both covered by health insurance and has a feasible copay. 

One of the most gratifying aspects of participating in a live symposium about chronic kidney disease (CKD) is hearing the questions healthcare professionals (HCPs) ask when they are applying the latest evidence to their daily practice. During a live event titled “Nephrology at the Helm: Advancing Timely CKD Care Through Cross-Specialty Collaboration,” the questions submitted by HCPs did more than demonstrate their engagement; they reflected a meaningful shift away from reactive care toward proactive, guideline-directed CKD management. As a nephrologist, I find this evolution in practice deeply encouraging. The frequently asked questions addressed in this commentary highlight where uncertainty persists and the need for greater clarity in CKD management that can translate into improved patient outcomes.

SGLT2 and RAS Inhibition in CKD
The first question asked whether sodium-glucose cotransporter-2 (SGLT2) inhibitors were appropriate for patients with CKD who are not “spilling protein.” This was a popular question because the story has changed over time, and most HCPs remember how narrow the original indications were for these agents. SGLT2 inhibitors began as therapies only approved to treat type 2 diabetes, then their indications expanded to include reduced risk of sustained estimated glomerular filtration rate (eGFR) decline, hospitalization, cardiovascular (CV)-related death, and end-stage kidney disease, in patients with CKD regardless of their diabetes status. That said, the practical answer to this question is yes. Furthermore, treatment with these therapies can include those with stage 3 CKD even when albuminuria is not prominent because of the kidney-protective and CV benefits associated with SLGT2 inhibitors.

Another question regarding SGLT2 inhibitors asked: Should HCPs discontinue therapy if patients’ eGFR drops below 20 mL/min/1.73m2 after initiation? The answer is explicit—no, do not stop SLGT2 inhibitor therapy solely because one’s eGFR falls below 20 mL/min/1.73m2 after initiation. Although HCPs should not initiate SGLT2 inhibitors at very low eGFR thresholds in general, continuation can be appropriate even as patients’ CKD progresses. In addition, CV benefits may persist late in CKD progression and into dialysis. The practical takeaway from the symposium is to distinguish initiation vs continuation decisions and not stop a therapy that may be providing ongoing benefit based on a single number alone.

Closely related was a question about the significance of microalbuminuria, including what to do beyond renin–angiotensin system (RAS) inhibition with ACE inhibitors or ARBs. Of note, albuminuria is not merely a lab abnormality; it is central to risk stratification in CKD and is 1 of the 2 core measurements (alongside eGFR) in the Kidney Disease: Improving Global Outcomes (KDIGO) framework. In response to this question, RAS inhibition is a strong first step, but the contemporary approach includes combination treatment with additional “pillars” of therapy, such as SGLT2 inhibitors as well as, in patients with type 2 diabetes, nonsteroidal mineralocorticoid receptor antagonists and GLP-1 receptor agonists, as a part of comprehensive CV–kidney–metabolic care. Of more importance, HCPs must be careful when determining how low albuminuria must get. There is no single, universally agreed upon target that functions as an inflection point in all patients with CKD. Rather, the general principle is that the lower albuminuria is, the better. But treatment should be pushed to tolerance vs meeting a rigid numeric endpoint.

Other common concerns included determining when an ACE inhibitor or ARB is making patients’ CKD worse and when it should be reinitiated after an acute decline. This comprises a mechanism issue, considering RAS inhibition lowers intraglomerular pressure through efferent arteriolar dilation. Therefore, a decline in eGFR (or a rise in creatinine) can be expected after treatment initiation. HCPs should avoid reflex discontinuation when changes are modest and the overall clinical direction is favorable, particularly if patients’ blood pressure improves and albuminuria decreases. This is because we are often trading a short-term hemodynamic change for long-term stabilization. Furthermore, clinically meaningful eGFR declines can occur after hemodynamically active therapies and should prompt evaluation for contributors like volume depletion or renal artery stenosis, not the automatic abandonment of kidney-protective treatment.

Treatment Access and Biomarkers
HCP learners also raised questions regarding the reality of treatment access and role of biomarkers like cystatin C in everyday practice. The prior applies especially to newer, more expensive therapies like SGLT2 inhibitors and GLP-1 receptor agonists. This is a crucial point because the KDIGO guidelines can inadvertently sound like they exist in a world without prior authorizations and copays. HCPs must acknowledge that cost and health insurance coverage can be prohibitive, even when your clinical rationale is clear. The pragmatic approach here includes investigating which agent within a drug class the patient’s insurance will cover and have an affordable copay. In addition, HCPs must recognize that achieving class benefit is often preferable to the idealized scenario of a specific, branded agent that is financially out of reach. This is not settling; it is translating the evidence into something patients can feasibly access.

Finally, regarding cystatin C, it can improve eGFR accuracy in select situations, which is reflected in the KDIGO guidelines for CKD screening. At the same time, CKD risk stratification data in adults are often based on serum creatinine–informed eGFR, whereas cystatin C–based estimates are not routinely used in most practices. For most adults, creatinine-based eGFR should be interpreted alongside urine–albumin-to-creatinine ratio and confirmed over time to establish chronicity. This remains the foundation of CKD screening and risk assessment.

Your Thoughts
If there is a single unifying message across these questions, it is that modern CKD management is both more effective and nuanced today than it was just a few years ago. We now have multiple therapies with additive benefit available, but HCPs must have the confidence to tolerate expected early lab shifts, discipline to confirm chronic abnormalities, and practical skills to choose the right therapy for the right patient. That is the work that is now required and is exactly why these frequently asked questions are worth elevating.

Do you continue SGLT2 inhibitor therapy even if your patients’ eGFR falls below 20 mL/min/1.73m2 after initiation? You can get involved in the conversation by answering the poll question and posting a comment below.

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Do you continue SGLT2 inhibitor therapy even if your patients’ eGFR falls below 20 mL/min/1.73m2 after initiation?

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