Abstract

Editor, We read with fascination and some excitement, the recent article by Sikaneta et al. [1] reporting on the longitudinal changes during a 1.1-year observation period of eGFR and CKD stages among 1,262 patients, mean age 71.25 years, retrospectively drawn from two large Canadian renal clinics. The authors described CKD stage variability (defined by changes in CKD stages) and reported that CKD stage changed in 40% of the cohort (including 7.4% in whom CKD stage improved) whereas CKD stage remained static in 762 (60.4%) patients [1]. Even though the study did not directly address the issue of medication-induced changes in GFR, the authors had indeed connoted the potential influence of the use of inhibitors of the rennin–angiotensin– aldosterone system as a potential explanation for the improved GFR following dose adjustments in the management of complications such as hyperkalemia [1]. While agreeing with this notion, we would like to conjecture that even more probable is the explanation that drug discontinuation of ACE inhibitors and angiotensin receptor blockers by treating physicians following unexpected rises in serum creatinine during the study would more credibly explain some of the improved eGFR values reported in the study [2–6]. Our experiences at Luther Midelfort Clinic (now Mayo Clinic Health System), Eau Claire, WI, USA, and the recent report from Sheffield, United Kingdom, that demonstrated sustained improvements in eGFR following discontinuation of ACE inhibitors and angiotensin receptor blockers in selected CKD patients are reminiscent of such observations [2–6]. Furthermore, even though the study by Sikaneta et al. [1] observed an increased risk of dialysis as initial CKD stage declined from III through to V, (Table 4), two remarkable points must be noted. First, despite high initial eGFRs of 30–59 ml/min, 17 (10.3%) of 165 patients for whom follow-up data were available still ended up on dialysis after a mean 2.3 years later. This was compared with 141 (29.9%) of 472 CKD IV patients and 192 (74.7%) of 257 CKD V patients [1]. These suggest that even though less eGFR translates into dialysis need, initial eGFR alone does not tell the whole story as to CKD progression to ESRD and the need for dialysis [7]. The above apparent inconsistency is further compounded by a meticulous analysis of Table 3 in the report by Sikaneta et al. [1]. Although 762 patients had remained static, that is to say, they did not experience a change in CKD stage during the observation period, 204 (40%) of the 512 patients from this group who were available for follow-up 2.3 years later still ended up on dialysis [1]. Even more M. A. Onuigbo (&) Department of Nephrology, Mayo Clinic Health System, 1221 Whipple Street, Eau Claire, WI 54702, USA e-mail: onuigbo.macaulay@mayo.edu

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