Diabetic ketoacidosis (DKA) is an acute and significant life-threatening complication of diabetes. The association of sodium-glucose cotransporter-2 inhibitors (SGLT2i) with euglycemic diabetic ketoacidosis (EDKA) has been well reported. This literature review was conducted to understand the mechanism of EDKA and identify the potential risk factors and precipitants for patients taking SGLT2i. After reviewing the published literature between 2010 and 2020, 32 articles are included in the final review. The underlying mechanism is mainly enhanced lipolysis and ketone body reabsorption. SGLT2i also stimulates pancreatic alpha cells and inhibits beta cells, causing an imbalance in glucagon/insulin levels, further contributing to lipolysis and ketogenesis. Most patients were diagnosed with blood glucose less than 200 mg/dL, blood pH <7.3, increased anion gap, increased blood, or urine ketones. Perioperative fasting, pancreatic etiology, low carbohydrate or ketogenic diet, obesity, and malignancy are identified precipitants in this review. As normoglycemia can conceal the underlying acidosis, physicians should be cognizant of the EDKA diagnosis and initiate prompt treatment. Patient education on risk factors and triggers is recommended to avoid future events.

Marfan syndrome is a rare autosomal dominant disorder of the connective tissue. It results in a mutation in the Fibrillin-1 protein gene. We present a case of Marfan's syndrome in a young adult with life-threatening, sudden onset of chest pain secondary to a non-ST elevation myocardial infarction (NSTEMI) in the setting of an aortic pseudoaneurysm. Taking into consideration potential life-threatening underlying processes, a thorough and detailed methodology must be undertaken when encountering chest pain in a Marfan's syndrome patient. This case highlights the importance of utilizing a multi-disciplinary approach to the complexities of Marfan syndrome.

Background: Sodium-Glucose Co-Transporter-2 Inhibitors (SGLT-2i) association with euglycemic diabetic ketoacidosis (EDKA) has been well reported. The underlying mechanism is mainly enhanced lipolysis and ketone bodies’ reabsorption. They also stimulate the pancreatic alpha cells and inhibit the beta cells, thereby causing an imbalance in glucagon/insulin levels, further contributing to lipolysis and ketogenesis. SGLT-2i were also found to cause EDKA in all types of diabetes, even uncovering undiagnosed Latent Autoimmune Diabetes of the Adult (LADA). Methods: Numerous electronic databases were systematically searched to identify patient-specific risk factors and clinical characteristics of EDKA in patients on SGLT-2i. The patient’s symptoms, clinical profile, laboratory results, and precipitants for EDKA were reviewed. Results: A total of 96 case reports identifying 116 patients with EDKA was fully reviewed. EDKA was twice prevalent in females (66.3%) than males (33.6%); median age was 52.15 ± 13.47, BMI was 29.3 ± 7.0. Among the 116 DKA events in SGLT-2i 92 (79.3%) were associated with Type-2 DM, 15 (12.9%) were Type-1 DM, 8 (6.9%) in LADA. Common symptoms were nausea (48.7%), vomiting (47%), and abdominal pain (28.2%). Canagliflozin was the most common SGLT-2i (40.5%), followed by Empagliflozin (29.3%) and Dapagliflozin (25.9%). The most common precipitant was surgery (17.2%), followed by infection (14.7%), fasting (11.2%), and Keto Diet (9.5%); others being reduced insulin use, alcoholism, and cancer. At presentation, average blood glucose was 196.8 ± 96.5, pH 7.1 ± 0.16, HCO3 8.7 ± 5.7 mmol/L, potassium 4.3 ± 1.03, anion-gap 24.2 ± 6.8 mmol/L, and the average HbA1C was 9.24 ± 2.08. Urine Ketones were positive in 81.89% of patients. 17 patients had pancreatic autoantibodies testing, and 7 were positive (41.2%) for glutamic acid decarboxylase-65 antibodies (anti-GAD-65). As a result, 7 patients were newly diagnosed with LADA who were previously misdiagnosed with type-2 DM. Conclusion: SGLT2i induced EDKA was found to be more predominant in females and type-2 DM. Diabetics should be educated on risk factors and consult physicians before commencing a dietary or exercise change. Physicians should be vigilant in diagnosing EDKA by thoughtful measurement of urine ketones and anti-GAD-65 testing can help diagnose underlying LADA.

Objective: This study aims to assess the prevalence of hyponatremia in ischemic stroke patients. Material and Methods: This study was a descriptive cross-sectional study. This research included all inpatients and outpatients at the Nephrology Institute of Kidney Disease from January 01, 2021, to December 31, 2022. A total of 214 people who had had a stroke were included in the analysis. On an official Proforma, the study's goals, potential harms, and potential rewards were laid out for the participant. Results: The study examined 214 people who had had an ischemic stroke. The average age of the patients was above 35. Patients' ages averaged 70 years. Male patients comprised 64% of the total, with 76 female patients making up 36% of the sample size. The Incidence of hyponatremia in individuals with ischemic stroke was 24%. The prevalence of hyponatremia increased dramatically between the ages of 51 and 75. Patients with hypertension were more likely to have hyponatremia than those without hypertension (31% vs. 12%, p=0.04). Diabetes doubled the Incidence of hyponatremia, which affected both sexes equally. (60 vs. 20 percent) The Incidence of hyponatremia in the context of an ischemic stroke was shown to be doubled in those with a high body mass index (BMI). (35% vs. 19%) Conclusion: There was a significant incidence and frequency of hyponatremia after stroke. The prognosis and mortality rate of stroke patients are already poor, and hyponatremia worsens the situation. Keywords: Inappropriate Antidiuretic Hormone Secretion, Cerebral Salt Wasting Syndrome, Hyponatremia, Stroke, Ischemic, and Hyponatremia.

Objective: To measure the incidence of BK-Virus infection, treatment, and complications among patients who had kidney transplants at the Institute of Kidney Diseases (IKD) in Peshawar, Pakistan. Methodology: The single center experience retrospective study was conducted in IKD Peshawar, Pakistan from January to December 2021. Clinical and analytical data was gathered. Blood samples were tested for BK virus load using quantitative DNA-polymerase chain reaction (PCR). Results: A total of 131 patients were examined. Of the 131 participants, 117 (89.4%) were males and 14 (10.6%) were females, with a mean age of 30.04 5.41. All of the patients received a transplant from a blood relative. After six months, the BK-Virus plasma PCR was found to be positive in eight patients (6.2%) who had had kidney transplantation. Conclusion: Patients who have had a kidney transplant and are on induction treatment or other forms of immune-suppression are at an increased risk of contracting the BK-Virus infection. Immunosuppressive medicines should be reduced to the barest minimum for effective treatment. Keywords: Transplanted Kidneys, BK Virus.