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.

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 19.3 mg/dL (2.5-5.5 mg/dL), total calcium level of 4.3 mg/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.

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 ris

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 tubular 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 demonstrated 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.

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.

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 <120 mmHg versus <140 mmHg 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.

A 44-year-old man with chronic alcoholism presented with seizure and loss of consciousness. He was diagnosed with alcoholic hepatic encephalopathy, and his neurologic symptoms recovered after lactulose enema treatment. His initial serum sodium level was 141 mEq/L. However, his mental state became confused after treatment with lactulose enema for five days, and his serum sodium level increased to 178 mEq/L. After five days of gradual correction of serum sodium level from 178 mEq/L to 140 mEq/L, the patient’s mental state recovered, but motor weakness in both limbs remained. Therefore, magnetic resonance imaging of the brain was performed. T2-weighted brain images showed bilateral symmetrical hyperintensities in the central pons, basal ganglia, thalami, hippocampi and unci, which were consistent with central pontine and extrapontine myelinolysis. We report a rare case of osmotic demyelination syndrome that occurred as a result of a rapid increase from a normal sodium level to hypernatremia caused by lactulose enema administered to treat alcoholic hepatic encephalopathy.

Hypokalemic periodic paralysis (hypoPP) is a disorder characterized by episodic, short-lived, and hypo-reflexive skeletal muscle weakness. HypoPP is a rare disease caused by genetic mutations related to expression of sodium or calcium ion channels. Most mutations are associated with autosomal dominant inheritance, but some are found in patients with no relevant family history. A 28-year-old man who visited the emergency room for paralytic attack was assessed in this study.He exhibited motor weakness in four limbs. There was no previous medical history or family history. The initial electrocardiogram showed a flat T wave and QT prolongation. His blood test was delayed, and sudden hypotension and bradycardia were observed. The blood test showed severe hypokalemia. After correcting hypokalemia, his muscle paralysis recovered without any neurological deficits. The patient’s thyroid function and long exercise test results were normal. However, because of the history of high carbohydrate diet and exercise, hypoPP was suspected. Hence, next-generation sequencing (NGS) was performed, and a mutation of Arg669His was noted in the SCN4A gene. Although hypoPP is a rare disease, it can be suspected in patients with hypokalemic paralysis, and iden tification of this condition is important for preventing further attacks and improving patient outcomes. Diagnosing hypoPP through targeted NGS is a cost-effective and useful method.

Urate is produced in the liver by the degradation of purines from the diet and nucleotide turnover and excreted by the kidney and gut. The kidney is the major route of urate removal and has a pivotal role in the regulation of urate homeostasis. Approximately 10% of the glomerular filtered urate is excreted in the urine, and the remainder is reabsorbed by the proximal tubule. However, the transport of urate in the proximal tubule is bidirectional: reabsorption and secretion. Thus, an increase in reabsorption or a decrease in secretion may induce hyperuricemia.In contrast, a decrease in reabsorption or an increase in secretion may result in hyperuricosuria. In the proximal tubule, urate reabsorption is mainly mediated by apical URAT1 (SLC22A12) and basolateral GLUT9 (SLC2A9) transporter. OAT4 (SLC22A11) also acts in urate reabsorption in the apical membrane, and its polymorphism is associated with the risk of hyperuricemia. Renal hypouricemia is caused by SLC22A12 or SLC2A9 loss-of-function mutations, and it may be complicated by exercise-induced acute kidney injury. URAT1 and GLUT9 are also drug targets for uricosuric agents. Sodium-glucose cotransporter inhibitors may induce hyperuricosuria by inhibiting GLUT9b located in the apical plasma membrane. Urate secretion is mediated by basolateral OAT1 (SLC22A6) and OAT3 (SLC22A8) and apical ATP-binding cassette super-family G member 2 (>ABCG2), NPT1 (SLC17A1), and NPT4 (SLC17A3) transporter in the proximal tubule. NPT1 and NPT4 may be key players in renal urate secretion in humans, and deletion of SLC22A6 and SLC22A8 in mice leads to decreased urate excretion. Dysfunctional variants of >ABCG2 inhibit urate secretion from the gut and kidney and may cause gout. In summary, the net result of urate transport in the proximal tubule is determined by the dominance of transporters between reabsorption (URAT1, OAT4, and GLUT9) and secretion (ABCG2, NPT1, NPT4, OAT1, and OAT3).

The worldwide coronavirus disease 2019 (COVID-19) pandemic is still in progress, but much remains unknown about the disease. In this article, we review the association of hypertension or the renin-angiotensin system (RAS) with COVID-19 and the correlation between electrolyte disorders and disease severity. Underlying hypertension is likely to be associated with severe or critical COVID-19, but the relationship is not clear owing to confounding factors. Angiotensin-converting enzyme 2 (ACE2) plays an important role in the non-classical RAS pathway and binds to a receptor binding domain of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The RAS blockade is known to increase ACE2 levels, but controversy remains regarding the effect of RAS blockade therapy in the course of COVID-19. Some reports have indicated a protective effect of RAS blockade on COVID-19, whereas others have reported an association of RAS blockade therapy with the occurrence of severe complications such as acute kidney injury and admission to the intensive care unit. Electrolyte disorders are not uncommon in patients with COVID-19, and severe COVID-19 has frequently shown hypokalemia, hyponatremia, and hypocalcemia. Electrolyte imbalances are caused by alteration of RAS, gastrointestinal loss, effects of proinflammatory cytokines, and renal tubular dysfunction by the invasion of SARS-CoV-2.