Introduction: Butterfly pea (Clitoria ternatea) is a vine that has various colors such as pink, light blue, white, and purple. This plant is commonly used as a food coloring and ornamental plants. Butterfly pea has pharmacological potential, among others, as high antioxidants. The antioxidants of the butterfly pea show much higher activity than other flowers. Antioxidants are substances that can prevent the occurrence of Acute Kidney Injury (AKI), which is currently increasing in incidence and mortality due to AKI reaching 23.9% in adults and 13.8% in children. Aim of study: This article aims to discuss the potential of butterfly pea extract (Clitoria ternatea) as a preventative for Acute Kidney Injury (AKI). Method: The research method used is the literature search technique on 20 articles from the Google Scholar database. Results and Discussion: The results of the literature search show that the butterfly pea (Clitoria ternatea) has antioxidant compounds that have the potential to prevent the occurrence of acute kidney injury (AKI). Butterfly pea extract has the potential to reduce levels of urea, serum creatinine, reduce levels of malondialdehyde (MDA) and increase levels of glutathione, catalase, and superoxide dismutase (SOD). The antioxidant activity of flavonoids and tannins in butterfly pea extract was found to have a nephroprotective effect against exposure to toxic substances. Conclusion: The conclusion from this literature search is that the antioxidant content contained in butterfly pea extract can be a good alternative as a nephroprotector to prevent AKI.

Globally, it is estimated that around 422 million adults had diabetes in 2014. Diabetics then have a higher risk of developing other diseases, such as: stroke and heart attack. Circadian rhythm disorders such as sleep disorders are one of the factors causing type 2 diabetes mellitus. This study isintended to increase knowledge and as a basis for further research on the effect of circadian misalignment in type 2 diabetes mellitus and to determine the effect of sleep disorders on type 2 diabetes. This research is a literature review with a database of articles on Google Scholar, PubMed, and Science Direct from 2016 to 2021 from national journals, and international journals indexed by Scopus and ISSN. Circadian misalignment discussed in this study is that sleep disorders affect the incidence of type 2diabetes mellitus. Lack of or little sleep will affect type 2 diabetes mellitus. This effect is mediated by a number of hormones such as melatonin, cortisol, leptin, and ghrelin. There is an effect of circadian misalignment on the incidence of type 2 diabetes mellitus.

Introduction: Hypokalemia is common disorder characterized by low plasma potassium levels (<3.5 mEq / L). Hypokalemia can be caused by genetic disorders. Bartter syndrome and Gitelman syndrome are rare genetic disorders that cause damage to the tubular kidneys. The cause of hypokalemia must be determined by analyzing the diagnosis algorithm of hypokalemia. Case Illustration: A 27-year-old woman was brought to the emergency room with complaints of weakness in both legs since 1 day ago. Obtained a history of chronic hypokalemia since 5 years ago. No history of thyroid disease, and never taking diuretic drugs. The patient is calm. Vital signs: BP: 110/60, regular pulse 88x/minute, temperature: 36.7°C, respiratory rate 14x/minute, oxygen saturation 99% in room air. ECG showed Normal sinus rhythm with normal T wave. Laboratory findings showed severe hypokalemia with plasma potassium 1.7 mEq/L, increased urine potassium (71.1 mmol/24 hours), increased urine sodium 306 mmol/24 hours, and increased urine chloride (342 mmol/24 hours), plasma magnesium levels were normal (1.91 mg/dL). KCl infusion was given to correct electrolyte imbalance condition. Discussion: : Several examinations must be performed to confirm the cause of hypokalemia condition. The diagnosis of this patient was suspected to lead to Bartter syndrome and Gitelman syndrome, because there was an increase in urinary potassium excretion, normotensive conditions, no suspicion of metabolic acidosis, and no symptoms of nausea and vomiting and no history of diuretic drugs usage. Keywords: Hypokalemia, Bartter syndrome, Gitelman syndrome

Introduction: Hypokalemia is common disorder characterized by low plasma potassium levels (<3.5 mEq / L). Hypokalemia can be caused by genetic disorders. Bartter syndrome and Gitelman syndrome are rare genetic disorders that cause damage to the tubular kidneys. The cause of hypokalemia must be determined by analyzing the diagnosis algorithm of hypokalemia.Case Illustration: A 27-year-old woman was brought to the emergency room with complaints of weakness in both legs since 1 day ago. Obtained a history of chronic hypokalemia since 5 years ago. No history of thyroid disease, and never taking diuretic drugs. The patient is calm. Vital signs: BP: 110/60, regular pulse 88x/minute, temperature: 36.7°C, respiratory rate 14x/minute, oxygen saturation 99% in room air. ECG showed Normal sinus rhythm with normal T wave. Laboratory findings showed severe hypokalemia with plasma potassium 1.7 mEq/L, increased urine potassium (71.1 mmol/24 hours), increased urine sodium 306 mmol/24 hours, and increased urine chloride (342 mmol/24 hours), plasma magnesium levels were normal (1.91 mg/dL). KCl infusion was given to correct electrolyte imbalance condition.Discussion: : Several examinations must be performed to confirm the cause of hypokalemia condition. The diagnosis of this patient was suspected to lead to Bartter syndrome and Gitelman syndrome, because there was an increase in urinary potassium excretion, normotensive conditions, no suspicion of metabolic acidosis, and no symptoms of nausea and vomiting and no history of diuretic drugs usage. Keywords:  Hypokalemia, Bartter syndrome, Gitelman syndrome