Niigata Japan - A Japanese registry has identified a blind spot in the routine care of patients with chronic kidney disease (CKD). Serum bicarbonate levels are rarely measured, leaving metabolic acidosis largely undetected and hence, undertreated.
Metabolic acidosis is a common complication of CKD and is associated with muscle loss, bone disease, insulin resistance, accelerated kidney decline, and increased mortality. Clinical guidelines recommend treatment when the serum bicarbonate level falls below 22 mEq/L. However, real-world data from Asia have been limited.
To address this, Mai Tanaka and colleagues extracted nationwide data from more than 21 university hospitals through the Japan Chronic Kidney Disease Database Extension (JCKDDBEx) and evaluated bicarbonate measurement, diagnosis, and treatment patterns in adults with CKD stages 3a–4 between 2014 and 2021 as seen in Figure 1.
The key finding was that serum bicarbonate was rarely tested in routine CKD care. "The annual measurement rate of serum bicarbonate levels in Japanese patients with CKD stages 3a to 4 was consistently below 10%, suggesting that metabolic acidosis itself may be underassessed," says the lead author of the study, Mai Tanaka.
Because testing was so infrequent, the prevalence of metabolic acidosis appeared very low in the overall CKD population, reflecting limited measurement rather than the actual absence of the disease. However, when the analysis focused on patients who actually had bicarbonate measured, a very different picture emerged. Nearly half of the population met the criteria for metabolic acidosis, and its prevalence increased with more advanced CKD.
The study showed that even among cases with serum bicarbonate levels below 22 mEq/L, the gap between diagnosis and treatment was concerning; the diagnosis and treatment rates were only 8.6% and 7.5%, respectively. Tanaka added, "the rate of serum bicarbonate measurement was low in CKD patients, suggesting that more attention to metabolic acidosis is needed in routine CKD care."
A large real-world analysis across the American and Canadian cohorts led by Abramowitz and Whitlock revealed that metabolic acidosis remains undiagnosed in many CKD cases. Fewer than 20% patients received sodium bicarbonate therapy, and may cases remained unrecognized in administrative records. Furthermore, acid retention accelerates kidney damage through pathways that promote tubulointerstitial injury and fibrosis; dietary acid load further complicates the picture. Together, these findings suggest that the gap observed in Japan reflects a broader global pattern.
Clinical guidelines, including those issued by the Japanese Society of Nephrology, recommend monitoring metabolic complications of CKD and correcting acidosis when present to maintain serum bicarbonate at or above 22 mEq/L. Yet, routine implementation appears inconsistent in standard CKD management workflows, as shown by Tanaka's study. Serum bicarbonate measurement is inexpensive and widely available. The barrier appears to be awareness and routine care.
Nonetheless, this is a clear opportunity to conduct a systemic assessment of bicarbonate in CKD patients that could substantially improve the detection of metabolic acidosis. Earlier recognition may enable a timely initiation of alkali therapy or dietary interventions, both of which seem promising for slowing kidney function decline.
For clinicians and health systems, the findings highlight an actionable quality improvement target: incorporating bicarbonate testing into standard CKD monitoring panels. As CKD prevalence rises globally, particularly in aging populations, closing this assessment gap by ensuring that metabolic complications are routinely evaluated may represent a practical and scalable strategy to improve outcomes.
The study's message is straightforward but powerful, metabolic acidosis in CKD may be hidden in plain sight, not because it is uncommon, but because it is not consistently measured.
