TY - JOUR
T1 - Urine ammonium predicts clinical outcomes in hypertensive kidney disease
AU - Raphael, Kalani L.
AU - Carroll, David J.
AU - Murray, Jennifer
AU - Greene, Tom
AU - Beddhu, Srinivasan
N1 - Publisher Copyright:
Copyright © 2017 by the American Society of Nephrology.
PY - 2017/8
Y1 - 2017/8
N2 - Metabolic acidosis is associated with poor outcomes in CKD. Because impaired renal ammoniumexcretion is important in the pathogenesis of acidosis, urine ammonium excretion might be a better and perhaps earlier acid-base indicator of risk than serum bicarbonate, particularly in patients without acidosis. We evaluated the association between baseline ammonium excretion and clinical outcomes in African American Study of Kidney Disease and Hypertension participants (n=1044). Median daily ammonium excretion was 19.5 (95% confidence interval [95% CI], 6.5 to 43.2) mEq. In Cox regression models (adjusted for demographics,measuredGFR, proteinuria, bodymass index, net endogenous acid production, and serum potassium and bicarbonate), hazard ratios of the composite outcome of death or dialysis were 1.46 (95% CI, 1.13 to 1.87) in the low tertile and 1.14 (95% CI, 0.89 to 1.46) in the middle tertile of daily ammonium excretion compared with the high tertile. Among participants without acidosis at baseline, the adjusted hazard ratio for thosewith ammonium excretion <20mEq/dwas 1.36 (95%CI, 1.09 to 1.71) comparedwith those with ammonium excretion ≥20 mEq/d. Additionally, compared with participants in the high ammonium tertile, those in the low ammonium tertile had higher adjusted odds of incident acidosis at 1 year (adjusted odds ratio, 2.56; 95%CI, 1.04 to 6.27). In conclusion, low ammonium excretion is associated with death and renal failure in hypertensive kidney disease, even among those without acidosis. Low ammonium excretion could identify patients with CKD and normal bicarbonate levels who might benefit from alkali before acidosis develops.
AB - Metabolic acidosis is associated with poor outcomes in CKD. Because impaired renal ammoniumexcretion is important in the pathogenesis of acidosis, urine ammonium excretion might be a better and perhaps earlier acid-base indicator of risk than serum bicarbonate, particularly in patients without acidosis. We evaluated the association between baseline ammonium excretion and clinical outcomes in African American Study of Kidney Disease and Hypertension participants (n=1044). Median daily ammonium excretion was 19.5 (95% confidence interval [95% CI], 6.5 to 43.2) mEq. In Cox regression models (adjusted for demographics,measuredGFR, proteinuria, bodymass index, net endogenous acid production, and serum potassium and bicarbonate), hazard ratios of the composite outcome of death or dialysis were 1.46 (95% CI, 1.13 to 1.87) in the low tertile and 1.14 (95% CI, 0.89 to 1.46) in the middle tertile of daily ammonium excretion compared with the high tertile. Among participants without acidosis at baseline, the adjusted hazard ratio for thosewith ammonium excretion <20mEq/dwas 1.36 (95%CI, 1.09 to 1.71) comparedwith those with ammonium excretion ≥20 mEq/d. Additionally, compared with participants in the high ammonium tertile, those in the low ammonium tertile had higher adjusted odds of incident acidosis at 1 year (adjusted odds ratio, 2.56; 95%CI, 1.04 to 6.27). In conclusion, low ammonium excretion is associated with death and renal failure in hypertensive kidney disease, even among those without acidosis. Low ammonium excretion could identify patients with CKD and normal bicarbonate levels who might benefit from alkali before acidosis develops.
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U2 - 10.1681/ASN.2016101151
DO - 10.1681/ASN.2016101151
M3 - Article
C2 - 28385806
AN - SCOPUS:85026528520
SN - 1046-6673
VL - 28
SP - 2483
EP - 2490
JO - Journal of the American Society of Nephrology
JF - Journal of the American Society of Nephrology
IS - 8
ER -