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Hypertension is a known cause and promoting factor for chronic kidney disease (CKD). A high urinary sodium-to-potassium ratio (U-Na/K) is thought to be one of the causes of treatment-resistant hypertension. The Japan Society of Hypertension recommends a U-Na/K ratio below 4 as a feasible target and below 2 as an ideal goal for healthy people. Japanese people consume an excess of salt. Elderly citizens do not like a change in taste resulting from salt reduction, and therefore, excessive salt reduction reduces their appetite. They particularly desire salty and/or refreshing fruits.
The characteristics of salt and potassium intake in patients with CKD in our hospital, as well as their impacts on the life prognosis of kidney diseases, are not known[Author1] . The sodium and potassium consumption of patients with CKD in our area and its effect on the progression of CKD to end-stage renal disease [Author2] and mortality risk are unclear. To find an answer to these questions and to reconsider future dietary guidance, we investigated the relationship between clinical data and prognosis of CKD-linked outpatients at our hospital.
Our study included outpatients referred to Niigata Rinko Hospital from the nearby clinics between March 1, 2009 and September 30, 2025 for their urinary-exam abnormality or elevated serum creatinine levels. Niigata Rinko Hospital is a medical care center in the east area of Niigata City, Niigata Prefecture, Japan. Prognostic investigations were conducted on a total of 235 patients with CKD who had a medical examination during the time period noted above. Of these, 197 cases were analyzed for urine storage tests. The study protocol was approved by the Ethics Committee of Niigata Rinko Hospital (approval no. 143).
Baseline clinical and laboratory variables included age, sex, body mass index (BMI), estimated glomerular filtration rate (eGFR), creatinine clearance (Ccr), diabetes, urea nitrogen excretion, sodium excretion, potassium excretion, and blood biochemistry (hemoglobin, Na, K, Cl, Ca, P, and intact parathyroid hormone). Left ventricular mass index (LVMi) was determined through an echocardiogram. Dietary protein intake was calculated using the equation given by Maroni et al. using a 24-h urine sample: protein intake = 6.25 × urinary nitrogen excretion (g/24 h) + weight (kg) × 0.031 (g/kg/day).
Salt and potassium intake were also determined from the 24-h urine sample. The cases were divided into two groups based on the U-Na/K: samples with U-Na/K <4 were termed as the target achievement group (A group), and those with U-Na/K ≥4 were the target non-achievement group (non-A group).
Mean age, proportion of males/females, median[A1] eGFR, and Ccr of the 197 patients with CKDs were 71.3 ± 1.0 (range: 19–96) years, 79 female patients (40.1%), 41.1 ± 1.4 mL/min/1.73 m2 (range: 10.5–108.0), and 58.2 ± 2.2 mL/min/1.73 m2 (range: 5.0–171.5), respectively. Causes of CKD based on medical history, urine findings, and kidney size on echo were as follows: nephrosclerosis in 92 patients (46.7%), diabetic nephropathy in 24 (12.2%), chronic glomerulonephritis in 45 (22.8%), polycystic kidney disease in 4 (2.0%), and others including normal in 32 (16.2%). The eGFR of approximately two-thirds of patients was less than 45 (n = 128).
With regard to U-Na/K, 107 patients were categorized in group A, and 90 in group non-A. Urinary potassium excretion was significantly lower, and systolic blood pressure, serum creatinine level, urine protein amount, LVMi, sodium excretion, and BNP [Author2] value were significantly higher in the non-A group (p < 0.05). No significant differences were observed in the age, BMI, diastolic blood pressure, serum Hb, eGFR, Ccr, urine output, and HbA1c value.
The cumulative survival curve demonstrated a significant difference between the two groups divided by U-Na/K, and this trend was also observed in the group with an eGFR of less than 45 (p < 0.05).
Potassium intake in CKD did not have a negative effect on renal or life prognosis in our area.
