Takotsubo cardiomyopathy is a reversible cardiomyopathy with a unique morphological feature of the left ventricle characterized by an apical ballooning appearance known for approximately known 25 years. Catecholamine drive plays an essential role in the pathogenesis and pathophysiology of Takotsubo cardiomyopathy; hence, it is also called stress cardiomyopathy. Physical stress could also have an impact and leads to a greater variety of characteristics in Takotsubo cardiomyopathy. Supportive and symptomatic medication remains the mainstay therapy with priority to improving the function of the left ventricle for several days and full recovery in 3-4 weeks. Due to its similarity with myocardial infarction, Takotsubo cardiomyopathy requires careful diagnosis and management for the best possible outcome.

Heart failure (HF) is still a global burden which carries substantial risk of morbidity and mortality. Thus, appropriate approach of diagnosis and layering the prognosis of HF are of great importance. In this paper we discuss and review a novel biomarker, which is called galectin-3 and already approved by Food and Drugs Administration (FDA) as a prediction tool for HF.Galectin-3, which is secreted by macrophages under the influence of mediators like osteopontin, has been known for its significant role in mediating cardiac fibrosis and inflammation. Numerous studies have shown galectin-3 as a novel prognostic biomarker with high predictive value for cardiovascular mortality and re-hospitalization in HF patients. However, there are also other contradictive studies displayed galectin-3 inferiority against other existed HF prognostic biomarkers like NT-proBNP and ST2. Nevertheless, galectin-3 has some advantages such as more stability and resistance against hemodynamic loading and unloading state, and also it could act as an early indicator of cardiac fibrosis, ventricular remodeling, and renal impairment in HF patients.

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Rationale: Renal tubular acidosis (RTA) is a cause of non-anion gap metabolic acidosis (NAGMA) that is infrequently diagnosed and is due to various underlying etiologies that impair the kidney’s ability to retain bicarbonate or excrete acid. Ibuprofen is an over-the-counter non-steroidal anti-inflammatory medication that is used by patients widely for a variety of reasons. Although it is well known that ibuprofen and other non-steroidal anti-inflammatory drugs may have nephrotoxic effects, the role of ibuprofen as a cause of RTA and hypokalemia is not well recognized. Presenting Concerns: A 66-year-old man with chemotherapy-treated lymphoma in remission and ongoing heavy ibuprofen use for chronic pain presented to hospital with a 1-week history of increasing lethargy and otherwise unremarkable review of systems. Investigations showed acute kidney injury, hypokalemia, hyperchloremia, and NAGMA with elevated urinary pH and positive urine anion gap. Diagnoses: The final diagnosis of distal RTA secondary to ibuprofen was made after ruling out gastrointestinal bicarbonate loss and additional secondary causes of RTA, including other medications, autoimmune conditions, and obstructive uropathy. Interventions: The patient was admitted and treated with intravenous sodium bicarbonate for 24 hours with correction of hypokalemia via oral supplementation. His ibuprofen-containing medication was discontinued. Outcomes: His acute kidney injury and electrolyte abnormalities resolved within 48 hours of initiating treatment with concurrent resolution of his lethargy. He was discharged home and advised to stop taking ibuprofen. Lessons Learned: We report a case of patient with hypokalemia and NAGMA secondary to ibuprofen and highlight the importance of monitoring for this side effect in patients taking ibuprofen.