Background: As combination therapy, switching to single-pill combination (SPC) medication after a short period of monotherapy is helpful because reducing pill numbers can improve patients’ adherence to medications. This study was aimed to assess the effect of the single-pill combination (SPC) of olmesartan medoxomil 20 mg and amlodipine besylate 5 mg (OLM 20 mg/AML 5 mg) on blood pressure (BP) reduction in hypertensive patients who did not respond to amlodipine besylate 5mg(AML 5mg) monotherapy for 4 weeks. Methods: This study was a prospective, open-label, multi-center, non-comparative study. Patients whose BP was not got the target BP (≥140 mmHg and if diabetic patients ≥130 mmHg) after 4 weeks treatment with AML 5 mg, were enrolled. AML 5 mg was switched to the SPC (OLM 20 mg/AML 5 mg) treatment for 8 weeks. The primary effectiveness endpoint was the reduction of seated systolic blood pressure (SeSBP) after SPC (OLM 20 mg/AML 5 mg) treatment for 8 weeks. The changes of brachial-ankle pulse wave velocity (baPWV), central BP (CBP), and augmentation index (AIx@75) were evaluated also. Results: Forty-seven patients were enrolled(mean age=52±9 years, 36 men). After the SPC treatment for 8 weeks, SeSBP was reduced from 153±9 mmHg to 131±18 mmHg and seated diastolic BP (SeDBP) from 95±8 mmHg to 81±11 mmHg (p<0.001 and p<0.001, respectively). The reduction of SeSBP/SeDBP were 22 mmHg and 14 mmHg, respectively. The target goal BP achievement rate was 74.5%, and baPWV, CBP, and AIx@75 were improved. Conclusion: SPC (OLM 20 mg/AML 5 mg) treatment for 8 weeks was effective in reducing BP, achieving target BP goal, and also improving arterial stiffness in uncontrolled hypertensive patients with AML 5mg monotherapy.

• Hypertension
• Antihypertensive agents
• Drug combination
• Blood pressure

Background: Most hemodialysis (HD) patients suffer from hypertension and have a heightened cardiovascular risk. While blood pressure (BP) control is essential to end-stage kidney disease (ESKD) patients, overly stringent control can lead to intra- dialytic hypotension (IDH). This study aimed to examine BP variations during and after HD to determine whether these variations correlate with IDH risk. Methods: BP measurements during dialysis were taken from 28 ESKD patients, and ambulatory BP monitoring was applied post-dialysis. Laboratory parameters and risk factors, including diabetes, coronary disease, and LV mass index, were compared between IDH and non-IDH groups using an independent t-test. Results: Of the 28 patients with an average age of 57.4 years, 16 (57.1%) had diabetes, 5 (17.9%) had coronary artery disease, and 1 (3.6%) had cerebrovascular disease. The mean systolic blood pressure (SBP) during and post-HD was 142.26 mmHg and 156.05mmHg, respectively(p=0.0003). Similarly, the mean diastolic blood pressure (DBP) also demonstrated a significant increase, from 74.59 mmHg during HD to 86.82 mmHg post-HD (p<0.0001). Patients with IDH exhibited a more substantial SBP difference (delta SBP, 36.38 vs. 15.07 mmHg, p=0.0033; age-adjusted OR=1.58, p=0.0168) and a lower post-dialysis BUN level (12.75 vs. 18.77 mg/dL, p=0.0015; age-adjusted OR=0.76, p=0.0242). No significant variations were observed in daytime and nocturnal BP between the IDH and non-IDH groups. Conclusion: Hemodialysis patients exhibited a marked increase in post-dialysis BP and lacked a nocturnal BP dip, suggesting augmented cardiovascular risks. This highlights the importance of more stringent BP control after hemodialysis.

• mbulatory blood pressure
• End-stage kidney disease
• Hemodialysis
• Hypertension
• Nocturnal hypertension

Hyponatremia is a common electrolyte disorder requiring careful management to prevent severe complications. Osmotic demyelination syndrome (ODS) is a serious neurological disorder that can develop from rapid correction of hyponatremia. Herein, is a description of the case of a 61-year-old man with multiple risk factors, including alcoholism, hypokalemia, malnutrition, and alcoholic liver cirrhosis, who developed ODS despite adherence to the recommended correction rate for hyponatremia. The patient presented to the emergency department with generalized weakness, gait disturbance, and decreased muscle strength. Initial laboratory investigations revealed severe hyponatremia, hypokalemia, and dehydration. The patient was treated with cautious correction of the hyponatremia below 8 mmol/L per day. However, on the seventh hospital day, he developed tremors, rigidity, and decreased consciousness and was diagnosed with osmotic demyelination syndrome. Despite receiving general supportive care, desmopressin, and dextrose 5% in water to reduce the serum sodium levels, the patient did not show significant improvement and was transferred to a nursing home for long-term conservative care on day 35 of hospitalization. This case report highlights the challenges associated with the diagnosis and management of osmotic demyelination syndrome and the importance of identifying patients at high risk of developing this neurological disorder.

• Alcoholism
• Hypokalemia
• Hyponatremia
• Malnutrition
• Osmotic demyelination syndrome

Hypermagnesemia is a rare but potentially fatal electrolyte disorder often overlooked because of its unfamiliarity. Magnesium is regulated through a balance of bone, intestinal absorption, and renal excretion. Hypermagnesemia typically arises from excessive magnesium intake or reduced renal excretion; however, it also occurs in patients with normal kidney function. Herein, we report two cases of hyper- magnesemia in patients taking magnesium hydroxide for constipation. The first case involved an 82-year-old woman with end-stage renal disease who developed metabolic encephalopathy due to hypermagnesemia, after taking 3,000 mg of magnesium hydroxide daily for constipation. Her magnesium level was 9.9 mg/dL. Her treatment involved discontinuing magnesium hydroxide and continuing hemodialysis, which led to her recovery. In the second case, a 50-year-old woman with a history of cerebral hemorrhage and mental retardation developed hypermagnesemia despite having normal renal function. She was also taking magnesium hydroxide for consti- pation, and her magnesium level was 11.0 mg/dL. She experienced cardiac arrest while preparing for continuous renal replacement therapy (CRRT). After achieving return of spontaneous circulation, CRRT was initiated, and her magnesium level showed a decreasing trend. However, vital signs and lactate levels did not recover, leading to death. These cases highlight the importance of prompt diagnosis and intervention for hypermagnesemia and the need to regularly monitor magnesium levels in individuals receiving magnesium-containing preparations, especially those with impaired kidney function.

• Hypermagnesemia
• Magnesium hydroxide
• Chronic kidney disease
• End stage renal disease

Pseudo-Bartter syndrome is a well-known differential diagnosis that needs to be excluded in cases of normotensive hypokalemic metabolic alkalosis. Pseudo-Bartter syndrome and pseudo-Gitelman syndrome are often collectively referred to as pseudo-Bartter/Gitelman syndrome; however, pseudo-Gitelman syndrome should be considered as a separate entity because Gitelman syndrome is characterized by hypocalciuria and hypomagnesemia, while Bartter syndrome is usually associated with hypercalciuria. Herein, we report the cases of two young adult female patients who presented with severe hypokalemic metabolic alkalosis, hypocalciuria, and hypomagnesemia. Diuretic or laxative abuse and self-induced vomiting were absent, and a chloride deficit and remarkable bicarbonaturia were observed. Initial sequencing studies for SLC12A3, CLCKNB, and KCNJ10 revealed no mutations, and whole-exome sequencing revealed no pathogenic variants. The metabolic alkalosis was saline-responsive in one case, and steroid therapy was necessary in the other to relieve chronic tubulointerstitial nephritis, which was diagnosed with kidney biopsy. A new category of pseudo-Gitelman syndrome should be defined, and various etiologies should be investigated.

• Hypocalciuria
• Hypokalemia
• Metabolic alkalosis
• Pseudo-Gitelman syndrome
• Whole exome sequencing