Akira Takahashi1, Kazuya Maeda2,3, Kensuke Sasaki1, Shigehiro Doi1, Ayumu Nakashima1, Toshiki Doi1,4, Takao Masaki5. 1. Department of Nephrology, Hiroshima University Hospital, 1-2-3 Kasumi Minami-ward, Hiroshima, 734-8551, Japan. 2. Department of Nephrology, Hiroshima University Hospital, 1-2-3 Kasumi Minami-ward, Hiroshima, 734-8551, Japan. kazu_kazu0725@yahoo.co.jp. 3. Department of Nephrology, Hiroshima Red Cross Hospital and Atomic Bomb Survivors Hospital, 1-9-6 Sendamachi Naka-ward, Hiroshima, 730-8619, Japan. kazu_kazu0725@yahoo.co.jp. 4. Division of Nephrology, Ichiyokai Harada Hospital, Hiroshima, 731-5134, Japan. 5. Department of Nephrology, Hiroshima University Hospital, 1-2-3 Kasumi Minami-ward, Hiroshima, 734-8551, Japan. masakit@hiroshima-u.ac.jp.
Abstract
BACKGROUND: A few previous clinical studies have shown that chloride (Cl) contributes to the progression and development of hypertension or proteinuria. Therefore, we aimed to determine whether hyperchloremia is associated with hypertension or proteinuria in patients with chronic kidney disease (CKD) and to define the relationships between the reduction in serum Cl concentration associated with CKD treatment and improvements in hypertension and/or proteinuria. METHODS: We performed a retrospective observational study of new or referred patients with CKD who had hyperchloremia, moderate proteinuria, renal dysfunction, and hypertension. Patients taking medication for metabolic acidosis or with a history of dialysis were excluded. The participants' systolic and diastolic blood pressure (BP), serum sodium (Na) and Cl concentrations, and urinary protein (UP) concentration were measured at baseline and after 1 month of CKD treatment. RESULTS: Fifty-one patients with CKD were included in the study. Their serum Cl concentration independently correlated with sBP and UP at baseline (P = 0.022 and P = 0.033, respectively). After 1 month's CKD treatment, their serum Na and Cl concentrations, sBP, and UP were significantly lower. The change in sBP during the month (ΔsBP) correlated with the change in serum Cl (ΔCl) (P = 0.012) but not with the change in serum Na. Multivariate analysis showed that ΔsBP was independently associated with ΔCl (P = 0.029). CONCLUSIONS: Hyperchloremia is an independent predictor of hypertension and proteinuria for patients with CKD.
BACKGROUND: A few previous clinical studies have shown that chloride (Cl) contributes to the progression and development of hypertension or proteinuria. Therefore, we aimed to determine whether hyperchloremia is associated with hypertension or proteinuria in patients with chronic kidney disease (CKD) and to define the relationships between the reduction in serum Cl concentration associated with CKD treatment and improvements in hypertension and/or proteinuria. METHODS: We performed a retrospective observational study of new or referred patients with CKD who had hyperchloremia, moderate proteinuria, renal dysfunction, and hypertension. Patients taking medication for metabolic acidosis or with a history of dialysis were excluded. The participants' systolic and diastolic blood pressure (BP), serum sodium (Na) and Cl concentrations, and urinary protein (UP) concentration were measured at baseline and after 1 month of CKD treatment. RESULTS: Fifty-one patients with CKD were included in the study. Their serum Cl concentration independently correlated with sBP and UP at baseline (P = 0.022 and P = 0.033, respectively). After 1 month's CKD treatment, their serum Na and Cl concentrations, sBP, and UP were significantly lower. The change in sBP during the month (ΔsBP) correlated with the change in serum Cl (ΔCl) (P = 0.012) but not with the change in serum Na. Multivariate analysis showed that ΔsBP was independently associated with ΔCl (P = 0.029). CONCLUSIONS: Hyperchloremia is an independent predictor of hypertension and proteinuria for patients with CKD.