Urine Ammonium and Preclinical Acidosis in CKD

Nephrolithiasis and Elevated Urinary Ammonium: A Matched Comparative Study

“…Due to our study design, we were not able to further investigate this link, though further research may be useful in identifying potential sex-specific cutoffs. Chronic kidney disease has also been found to decrease ammonia excretion thus leading to metabolic acidosis [16][17][18] however we did not detect any differences between the 2 groups in comparing their creatinine or estimated glomerular filtration rate.…”

The Continuum of Acid Stress

“…NH 4 1 ) after metabolism of the amino acid glutamine that also yields a-ketoglutarate. Urine acid excretion as NH 4 1 , along with a-ketoglutarate metabolism to yield HCO 3 2 , constitutes NAE, with regeneration of HCO 3 2 to replace that titrated by accumulated acid (Figure 1). Dietary acid in animals stimulated kidney NH 4…”

“…Acid accumulation that was insufficient to reduce plasma [HCO 3 2 ] below normal, and so not manifest as metabolic acidosis, was greater in animals with reduced than normal GFR (54,57). Likewise, patients with reduced compared with normal eGFR and a high-acid diet had greater acid accumulation despite normal plasma [HCO 3 2 ] (38,58). Higher acid diets directly associated with higher anion gap in individuals with CKD, and the anion gap was higher in those with eGFR 30-59 ml/min per 1.73 m 2 than with eGFR .60 ml/min per 1.73 m 2 , including individuals with plasma [HCO 3 2 ] within normal ranges (59).…”

“…1 excretion in patients with CKD and reduced eGFR, possibly a reflection of suboptimal urine NAE, is associated with adverse kidney outcomes (42,84), and so its measurement might identify patients at risk for eubicarbonatemic acidosis. Although currently not routinely available in clinical laboratories, advances in urine NH 4 1 measurement might identify individuals with low NAE in the setting of reduced eGFR with normal plasma [HCO 3 2 ] that increases risk for acid accumulation. On the other hand, clinicians might identify underlying acid accumulation by assessing compensatory mechanisms that help maintain acid-base status, including urine citrate excretion (85).…”

Metabolic Acidosis and Subclinical Metabolic Acidosis in CKD

“…These compensatory responses to nonvolatile acids suggest that acid-mediated kidney injury might be occurring even in the setting of normal tCO 2 in CKD. This state of nonvolatile acid-mediated organ injury despite having a normal tCO 2 has been referred to as eubicarbonatemic metabolic acidosis, 48 preclinical metabolic acidosis, 49 or subclinical metabolic acidosis. 50,51 In persons with preserved kidney function, subclinical metabolic acidosis might be observed in conditions such as chronic diarrhea or high dietary protein intake.…”