The management of high blood pressure (BP) is crucial for improving outcomes in patients with chronic kidney disease (CKD). The updated Kidney Disease: Improving Global Outcomes 2021 BP guideline proposes treating adults with CKD to a target systolic BP (SBP) of <120 mmHg based on the standardized office BP measurement. This suggestion is largely based on the finding of SPRINT (Systolic Blood Pressure Intervention Trial) that targeting an SBP of <120mmHg versus <140mmHg is beneficial for cardiovascular and mortality outcomes, regardless of the patient’s kidney disease status. However, extended follow-up studies of CKD trials showed that intensive versus usual BP control was associated with a lower risk of kidney failure in patients with, but not in those without, proteinuria. Similarly, a recent population-based study in Korea demonstrated that the optimal on-treatment BP for composite cardiorenal and mortality outcomes was left-shifted in adults with CKD, particularly in those with albuminuria, relative to that in patients without CKD. Moreover, in meta-analyses of randomized trials, more intensive versus standard BP control was associated with a lower risk of all-cause mortality in patients with CKD and albuminuria but not in those without CKD. Meanwhile, a 2020 Cochrane review reported that lower BP targets (≤135/85 mmHg), compared with standard targets (≤140/90 mmHg), resulted in a small reduction in cardiovascular events, an increase in other serious adverse events, and no reduction in total serious adverse events. Lowering SBP to <120 mmHg can potentially increase the risk of treatment-related adverse events beyond the cardioprotective benefits, and standardized BP measurement increases the burden on patients and resources. Thus, targeting a BP of <130/80 mmHg with appropriate office BP measurement can be an option in patients with CKD. The presence of albuminuria would need to be additionally considered to determine individualized BP targets.

• Antihypertensive agents
• Blood pressure
• Chronic kidney disease
• Practice guideline

The kidneys play an important role in regulating the acid-base balance. Metabolic acidosis is common in chronic kidney disease (CKD) patients and can lead to poor outcomes, such as bone demineralization, muscle mass loss, and worsening of renal function. Metabolic acidosis is usually approached with evaluating the serum bicarbonate levels but should be assessed by counting blood pH. Current guidelines recommend oral bicarbonate supplementation to maintain the serum bicarbonate levels within the normal range. However, a slow decline in the glomerular filtration rate might occur, even though the serum bicarbonate levels were in the normal range. Because the serum bicarbonate levels decrease when metabolic acidosis advances, other biomarkers are necessary to indicate acid retention for early diagnosis of metabolic acidosis. For this, urine citrate and ammonium excretion may be used to follow the course of CKD patients. Metabolic acidosis can be treated with an increased fruit and vegetable intake and oral alkali supplementation. Previous studies have suggested that administration of oral sodium bicarbonate may preserve kidney function without significant increases in blood pressure and body weight. Veverimer, a non-absorbed, counterion-free, polymeric drug, is emerging to treat metabolic acidosis, but further researches are awaited. Further studies are also needed to clarify the target therapeutic range of serum bicarbonate and the drugs used for metabolic acidosis.

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

Pressure natriuresis refers to the concept that increased renal perfusion pressure leads to a decrease in tubular reabsorption of sodium and an increased sodium excretion. The set point of blood pressure is the point at which pressure natriuresis and extracellular fluid volume are in equilibrium. The term "abnormal pressure natriuresis" usually refers to the expected abnormal effect of a certain level of blood pressure on sodium excretion. Factors that cause abnormal pressure natriuresis are known. Sympathetic nerve system, genetic factors, and dietary factors may affect an increase in renal perfusion pressure. An increase in renal perfusion pressure increases renal interstitial hydrostatic pressure (RIHP). Increased RIHP affects tub- ular reabsorption through alterations in tight junctional permeability to sodium in proximal tubules, redistribution of apical sodium transporters, and/or release of renal autacoids. Renal autocoids such as nitric oxide, prostaglandin E2, kinins, and angiotensin II may also regulate pressure natriuresis by acting directly on renal tubule sodium transport. In addition, inflammation and reactive oxygen species may mediate pressure natriuresis. Recently, the use of new drugs associated with pressure natriuretic mechanisms, such as angiotensin receptor neprilysin inhibitor and sodium glucose co-transporter 2 inhibitors, has been consistently demonstra- ted to reduce mortality and hypertension-related complications. Therefore, the understanding of pressure natriuresis is gaining attention as an antihypertensive strategy. In this review, we provide a basic overview of pressure natriuresis to the target audience of nephrologists.

• Blood pressure
• Hypertension
• Kidney
• Pressure natriuresis
• Sodium excretion

Combination treatment with hypomethylating agents (HMAs) and venetoclax is being used increasingly in elderly patients with acute myeloid leukemia (AML). Venetoclax with HMAs has been reported to be associated with tumor lysis syndrome (TLS) in AML patients with high leukemic burden. We present a case of an elderly AML patient with low leukemic burden who developed TLS while receiving venetoclax and azacitidine (AZA). A 74-year-old man with newly diagnosed AML with NPM1 mutation received combination therapy with venetoclax and AZA in an outpatient clinic. Within 12 hours after starting venetoclax and AZA, the patient was admitted to the emergency room with fever, general weakness, and laboratory findings consistent with TLS. Based on our results, we recommend monitoring at the start of the treatment with venetoclax and HMAs to prevent and control TLS regardless of the leukemic burden and favorable genetic risk.

• Acute myeloid leukemia
• Venetoclax
• Azacitidine
• Tumor lysis syndrome

We report a case of severe hyperphosphatemia in advanced CKD with poor compliance. A 55-year-old male patient with underlying type 2 diabetes mellitus, hypertension, and chronic kidney disease presented emergently with general weakness and altered mental status. The creatinine level was 14 mg/dL (normal range: 0.5-1.3 mg/dL) 2 months prior to consultation, and he was advised initiation of hemodialysis, which he refused. Subsequently, the patient stopped taking all prescribed medications and self-medicated with honey and persimmon vinegar with the false belief it was detoxifying. At the time of admission, he was delirious, and his laboratory results showed blood urea nitrogen level of 183.4 mg/dL (8-23 mg/dL), serum creatinine level of 26.61 mg/dL (0.5-1.3 mg/dL), serum phosphate level of 19.3mg/dL(2.5-5.5mg/dL), total calcium level of 4.3mg/dL(8.4-10.2 mg/dL), vitamin D (25(OH)D) level of 5.71 ng/mL (30-100 ng/mL) and parathyroid hormone level of 401 pg/ml (9-55 pg/mL). Brain computed tomography revealed non-traumatic spontaneous subdural hemorrhage, presumably due to uremic bleeding. Emergent hemodialysis was initiated, and hyperphosphatemia and hypocalcemia were rectified; calcium acetate and cholecalciferol were administered. The patient’s general condition and laboratory results improved following dialysis. Strict dietary restrictions with patient education were implemented. Multifaceted interventions, including dietary counseling, administration of phosphate-lowering drugs, and lifestyle modifications, should be implemented when encountering patients with CKD, considering the extent of the patient’s adherence.

• Hyperphosphatemia
• Chronic kidney disease
• Dietary counseling
• Case report

Adipsia is a rare disorder that occurs due to damage to the osmoreceptor and not feeling thirst despite hyperosmolality. Adipsic hypernatremia can occur when there is damage to the anterior communicating artery that supplies blood to osmoreceptors, and the level of arginine vasopressin secretion varies widely. A 37- year-old woman, suffering from severe headache, was consulted to the nephrology department for hypernatremia and polyuria after clipping of a ruptured aneurysm in the anterior communicating artery. Despite her hypernatremic hyperosmolar state, she denied thirst and did not drink spontaneously. She was diagnosed adipsic hypernatremia by evaluating the osmoregulatory and baroregulatory function tests. Because adipsic hypernatremia is caused by not enough drinking water even for hyperosmolality due to the lack of thirst stimulus, the strategies of treatment are that setting the target body weight when serum osmolality is normal and have the patient drink water until patient reach the target body weight. Adipsic hypernatremia should be considered to be a rare complication of subarachnoid hemorrhage associated with an anterior communicating artery aneurysm.

• Adipsia
• Thirst
• Hypernatremia
• Anterior communicating artery