The incidence and prevalence of end-stage kidney disease (ESKD) in Korea are increasing, and ESKD constitutes a very important medical and social issue. Elderly dialysis patients have the highest risk of early mortality within 3 months after initiating dialysis, and geriatric syndromes such as aging, frailty, functional impairment, and cognitive impairment are crucial for the prognosis of elderly patients. Shared decision-making (SDM) is an approach through which clinicians and patients can achieve informed preferences, thereby yielding better clinical outcomes and quality of life. Through SDM-based, close consultation among patients, families, and healthcare providers, an ESKD Life-Plan for elderly patients should be established. A multidisciplinary approach led by nephrologists can help them to provide proper vascular access for dialysis at the right time, with the right evidence, and to the right patient. Strategies that can improve peritoneal dialysis in elderly patients include assisted peritoneal dialysis, homecare support programs, and automated peritoneal dialysis. In order to enhance the role of kidney transplantation in elderly patients with ESKD, it is necessary to accurately identify patients’ clinical conditions before transplantation and to perform active rehabilitation activities and postoperative management to promote recovery after transplantation. With the aging population and the increase in ESKD in the elderly, clinicians must identify factors affecting the mortality and quality of life of elderly dialysis patients.

• Elderly
• Renal replacement therapy
• Hemodialysis
• Peritoneal dialysis
• Kidney transplantation
• End-Stage Kidney Disease Life-Plan
• Shared decision making

Fabry disease (FD), a rare X-linked lysosomal storage disorder that depletes alpha-galac- tosidase A (α-GalA), is caused by mutations in the GLA gene. Diminished α-GalA enzyme activity results in the accumulation of Gb3 and lyso-Gb3. The pathophysiology of hypertension in FD is complex and unclear. The storage of Gb3 in arterial endothelial cells and smooth muscle cells is known to produce vascular injury by increasing oxidative stress and inflammatory cytokines as a primary pathophysio- logical mechanism. In addition, Fabry nephropathy developed, resulting in a decrease in kidney function and contributing to hypertension. The prevalence of hypertension in patients with FD was between 28.4% and 56%, whereas hypertension in patients with chronic kidney disease ranged between 33% and 79%. A study using 24-hour ambulatory blood pressure monitoring (ABPM) to measure blood pressure (BP) indicated a high prevalence of uncontrolled hyper- tension in FD. Thus, 24-hour ABPM ought to be considered for FD hypertension assessments. Appropriate treatment of hypertension is believed to reduce mortality in patients with FD caused by kidney disease, cardiovascular disease, and cerebrovascular disease because hypertension significantly impacts organ damage. Up to 70% of FD patients have been reported to have kidney involvement, and angiotensin- converting enzyme inhibitors and angiotensin receptor blockers prescribed for proteinuria are recommended as first-line therapy with antihypertensive drugs. In conclusion, hypertension should be controlled appropriately, given the different morbidity and mortality caused by significant organ involvement in FD patients.

• Fabry disease
• Hypertension
• Enzyme replacement therapy
• Angiotensin- converting enzyme inhibitors
• Angiotensin receptor blockers

Metabolic alkalosis is a common acid-base imbalance frequently observed in intensive care unit (ICU) patients and is associated with increased mortality. Post- hypercarbia alkalosis (PHA) is a type of metabolic alkalosis caused by sustained high serum bicarbonate levels following a rapid resolution of hypoventilation in patients with chronic hypercapnia due to prolonged respiratory disturbance. Common causes of chronic hypercapnia include chronic obstructive pulmonary disease (COPD), central nervous system disorders, neuromuscular disorders, and narcotic abuse. Rapid correction of hypercapnia through hyperventilation leads to a swift normalization of pCO2, which lacks renal compensation, consequently causing an increase in plasma HCO3- levels and severe metabolic alkalosis. Most of PHA occurs in the ICU setting requiring mechanical ventilation and can progress severe alkale- mia due to secondary mineralocorticoid excess from volume depletion or decrea- sed HCO3- excretion from decreased glomerular filtration rate and increased proxi- mal tubular reabsorption. PHA is associated with increased ICU stay, ventilator dependency, and mortality. Acetazolamide, a carbonic anhydrase inhibitor, has been utilized for managing PHA by inducing alkaline diuresis and reducing tubular reabsorption of bicarbonate. While acetazolamide effectively improves alkalemia, its impact on hard outcomes may be limited by factors such as patient complexity, co-administered medications, and underlying conditions contributing to alkalosis.

• Metabolic alkalosis
• Hypercapnia
• Hyperventilation
• Chronic obstructive pulmonary disease
• Carbonic anhydrase

Hypertension and potassium imbalance are commonly observed in chronic kidney disease (CKD) patients. The development of hypertension would be related to several mechanisms. Hypertension is related to body mass index, dietary salt intake, and volume overload and is treated with antihypertensives. In CKD patients, managing hypertension can provide important effects that can slow the progression of CKD or reduce complications associated with reduced glomerular filtration rate. The prevalence of hyperkalemia and hypokalemia in CKD patients was similar at 15-20% and 15-18%, respectively, but more attention needs to be paid to treating and preventing hyperkalemia, which is related to a higher mortality rate, than hypo- kalemia. Hyperkalemia is prevalent in CKD due to impaired potassium excretion. Serum potassium level is affected by renin-angiotensin-aldosterone system inhibitors and diuretics and dietary potassium intake and can be managed by potassium restriction dietary, optimized renin-angiotensin-aldosterone system inhibitor, sodium polystyrene sulfonate, patiromer, and hemodialysis. This review discussed strategies to mitigate and care for the risk of hypertension and hyperkalemia in CKD patients.

• Chronic kidney disease
• Hypertension
• Hyperkalemia
• Renin-angiotensin- aldosterone system

Management of metabolic acidosis is crucial for preserving bone, muscle, and renal health, as evidenced by the results of several interventional studies conducted on patients with chronic kidney disease (CKD). Considering the continuity of CKD progression over time, it is reasonable to deduce that a subclinical form of metabolic acidosis may exist prior to the manifestation of overt metabolic acidosis. Covert H+ retention with normal serum bicarbonate level in patients with CKD may result in maladaptive responses that contribute to kidney function deterioration, even in the early stages of the disease. The loss of adaptive compensatory mechanisms of urinary acid excretion may be a key factor in this process. Early modulation of these responses could be an important therapeutic strategy in preventing CKD progression. However, to date, the optimal approach for alkali therapy in subclinical metabolic acidosis in CKD remains uncertain. There is a lack of established guidelines on when to initiate alkali therapy, potential side effects of alkali agents, and the optimal blood bicarbonate levels based on evidence-based practices. Therefore, further research is necessary to address these concerns and establish more robust guidelines for the use of alkali therapy in patients with CKD. Herein, we provide an overview of recent developments on this subject and examine the potential therapeutic approaches that interventional treatments may present for patients with hidden H+ retention, exhibiting normal serum bicarbonate levels - commonly described as subclinical or eubicarbonatemic metabolic acidosis in patients with CKD.

• Metabolic acidosis
• Chronic kidney disease
• Serum bicarbonate
• Total carbon dioxide