This article argues that chronic kidney disease (CKD) should no longer be viewed as inevitably progressive and irreversible. Historically, treatment goals focused on slowing eGFR decline and delaying kidney failure, but newer therapies have shifted the outlook toward preserving kidney function and potentially achieving CKD remission. The authors define remission using objective markers: stable kidney function with a chronic eGFR slope of less than 1 mL/min/1.73 m² per year, or, in earlier CKD, a return to normal eGFR and absence of albuminuria. They emphasize that remission is distinct from cure because disease can return if therapy is stopped or relapse occurs.

The article highlights growing evidence that remission may be achievable in a meaningful proportion of patients, especially when CKD is detected early and treated aggressively with combination therapy. In diabetic kidney disease, RAAS inhibitors, SGLT2 inhibitors, nonsteroidal mineralocorticoid receptor antagonists, and GLP-1 receptor agonists can substantially reduce albuminuria and slow eGFR decline. In IgA nephropathy and other glomerular diseases, newer B-cell-targeted and complement-based therapies are also shifting goals from slowing progression to targeting remission. The authors call for earlier screening with both eGFR and albuminuria, risk-based treatment, clinical decision support, and primary care-led implementation supported by nephrology. Their central message is that CKD care should move from “slowing progression” to “maintaining kidney health.”

Reference: Tangri N, Neuen BL, Cherney DZ, Tuttle KR, Perkovic V. From progression to remission: a new paradigm for success in chronic kidney disease. Kidney Int. 2026 Jan;109(1):17-21. doi: 10.1016/j.kint.2025.10.004.

This article discusses the American Heart Association’s (AHA) cardiovascular-kidney-metabolic (CKM) syndrome framework from a primary care perspective. CKM syndrome connects obesity, diabetes, chronic kidney disease (CKD), hypertension, dyslipidemia, subclinical cardiovascular disease, and clinical cardiovascular disease into one prevention-focused model. The authors note that the framework may help align overlapping guideline recommendations and make care more patient-centered, especially as therapies such as SGLT2 inhibitors, GLP-1 receptor agonists, and RAAS inhibitors can address multiple CKM-related conditions. However, they also caution that primary care clinicians are already overloaded with preventive care, chronic disease management, quality metrics, and competing patient needs, so CKM implementation must avoid becoming another burdensome checklist.

The authors emphasize that CKM syndrome could help elevate CKD detection in primary care by making eGFR and urinary albumin-creatinine ratio testing part of cardiovascular risk assessment, especially for patients with diabetes, hypertension, obesity, or cardiovascular disease. They highlight the AHA PREVENT risk calculator as a practical entry point because it incorporates kidney health measures into cardiovascular risk prediction. To make CKM care work in real practice, the authors argue that health systems will need multidisciplinary support from nephrology, cardiology, endocrinology, pharmacists, and primary care teams, along with electronic decision support, panel management, better performance metrics, and care coordination. They conclude that CKM has strong potential to improve CKD detection and cardiovascular prevention, but only if implementation is practical, supported, and integrated into primary care workflows.

Reference: Rumrill SM, Shlipak MG. The New Cardiovascular-Kidney-Metabolic (CKM) Syndrome: An Opportunity for CKD Detection and Treatment in Primary Care. Am J Kidney Dis. 2025 Apr;85(4):399-402. doi: 10.1053/j.ajkd.2024.09.016.

This review examines hypertension after kidney transplantation, which is common and variably reported depending on how blood pressure is measured and defined. The authors explain that post-transplant hypertension can result from different causes depending on timing after transplantation. In the immediate post-transplant period, contributors may include perioperative volume overload, high-dose steroids, rebound hypertension from abruptly stopped medications, and inadequate pain control. In the early post-transplant period, weight gain, calcineurin inhibitors, steroids, donor kidney factors, and transplant renal artery stenosis may contribute. Later causes can include chronic renal allograft dysfunction, obstructive sleep apnea, and other transplant-related or recipient-related factors.

The article emphasizes that post-transplant hypertension is associated with worse graft, cardiovascular, and patient outcomes, making accurate measurement and individualized management important. Home blood pressure monitoring and ambulatory blood pressure monitoring may help identify masked or white-coat hypertension more reliably than office readings alone. Management should include lifestyle measures, careful medication selection, and treatment of underlying causes such as transplant renal artery stenosis or obstructive sleep apnea. Calcium channel blockers and beta-blockers are commonly used early, while angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers may be considered later when graft function is stable, especially in patients with proteinuria or specific indications. The authors conclude that there is no single preferred antihypertensive strategy for all kidney transplant recipients. Treatment should be tailored to timing, etiology, graft function, comorbidities, and medication risks.

Reference: Tantisattamo E, Molnar MZ, Ho BT, et al. Approach and Management of Hypertension After Kidney Transplantation. Front Med (Lausanne). 2020 Jun 16;7:229. doi: 10.3389/fmed.2020.00229.