Fatal complication from Foley’s catheter: a case report

Renal artery stenosis is the major cause of renovascular hypertension, can be found isolated or have association with syndromes or autoimmune conditions. It can be due to atherosclerotic deposition in vessels, autoimmune etiology or fibromuscular dysplasia, the latter is the commonest cause, however, needs biopsy for diagnosis and exclusion of other possible causes. Patients can have diverse presentation, disease may be discovered as incidental finding, with hypertensive crises, Nephropathy or cardiac manifestations. We report a case of 7 years female patient presented with severe respiratory distress, hypertension, Grade 1 BL pitting edema, hepatomegaly, basal crackles in chest and gallop. He had no history of any diagnosed medical condition prior. However, symptoms were evident for last 2 months with Headache, fatigue, cough, exertional dyspnea, edema and decreased urine output. She had no history of arthralgia, frothy urine, hematuria or any skin rashes. Evaluation for Hypertension revealed small sized right kidney with decreased perfusion in segmental arteries. Echocardiography showed Biventricular dilation, dysfunction with Ejection fraction of 40%. She initially managed with iv labetalol infusion later started enalapril and amlodipine then referred to specialty where percutaneous transangioplasty planned abut deferred by pediatrics nephrology as patient responded with medical management and it is considered for resistant hypertension or persistent high renin and aldosterone. The case concluded with diagnosis of Reno cardiac type-iv syndrome, as manifestations are concordant with chronic kidney disease – right SSK due to hypoperfusion that resulted in renovascular hypertension and Cardiac failure.

The impact of intra-abdominal pressure on urine output in postoperative cardiac surgery patients: Insights from continuous monitoring.

ABSTRACTPresented here is an extremely rare case of bilateral ureteral obstruction due to Candida albicans fungus balls, which led to acute kidney dysfunction and candidemia. An 83‐year‐old man was brought to our hospital after falling due to poor physical condition. He had been receiving abiraterone acetate for 1 month for metastatic castration‐resistant prostate cancer, while past medical history included type II diabetes, cardiovascular disease, and dementia. Blood test results revealed severe liver dysfunction, though whole‐body computed tomography (CT) findings showed no abnormalities. Based on the recent therapy course, the patient was diagnosed with drug‐induced liver damage caused by abiraterone acetate, and steroid pulse therapy and antibiotic administration were started. On Day 11 after starting that treatment, decreased urine output and renal dysfunction were noted. CT scanning revealed bilateral hydronephrosis and slightly dense masses at the origin of ureteral obstruction on both sides. Subsequently, C. albicans was detected in blood and urine samples, thus fungus balls were determined as the cause of bilateral hydronephrosis. Temporary hemodialysis was required, though clinical symptoms and biochemical findings gradually improved following insertion of bilateral ureteral stents and administration of antifungal therapy, and the patient was discharged 72 days after admission.

Acute kidney injury (AKI) affects thousands of hospitalized patients annually, yet early detection remains challenging as serum creatinine elevation lags behind clinical deterioration. Decreased urine output (UO) represents a key diagnostic criterion of AKI, sometimes manifesting hours before biochemical changes; however, current manual monitoring methods are labor-intensive and prone to error. Here, we developed and validated a simple, cost-effective automated urine flow meter using non-contact optical sensors, a peristaltic pump, and microcontroller-based automation for precise, real-time monitoring of urine output in clinical settings, named P-meter. Three successive prototypes (V1, V2, V3) were validated against gold-standard gravimetric measurements over 285 h of testing during animal experiments that required bladder catheterization. Iterative refinement addressed miniaturization challenges, fluid dynamics optimization, and sensor positioning to achieve progressively improved accuracy. The optimized V3 prototype demonstrated further enhanced volumetric precision, stability, and flow accuracy with near-unity linearity vs. reference method (R2 = 0.9889), minimal bias (mean error −0.1 mL), and 94.18% agreement within confidence limits (n = 86), outperforming the initial V1 prototype (R2 = 0.9971, mean error −1.69 mL, n = 207) and intermediate V2 design (R2 = 0.9941, mean error 3.63 mL, n = 390), primarily in terms of reduced bias and improved agreement. The P-meter offers accurate urine output monitoring at a lower cost than commercial systems, facilitating its use in early AKI detection and thereby improving patient outcomes.

Congenital nephrogenic diabetes insipidus (CNDI) is characterized by resistance of the distal nephrons and collecting ducts to arginine vasopressin (AVP). High doses of 1-deamino-8-D-arginine vasopressin (DDAVP), a V2-receptor-selective agonist, are effective in some cases. The present study aimed to demonstrate the use, efficacy, and safety of DDAVP and the characteristics of patients who responded to this treatment. The present, retrospective, multicentric, observational survey of patients with CNDI receiving DDAVP was based on a previous, nationwide survey conducted by the Japanese Society for Pediatric Endocrinology (JSPE) and collected data on the use (formulation, dosage, and treatment duration), efficacy (change in urine output and height SDS), and safety of DDAVP. In the initial survey, 43 of 123 JSPE council members (35.0%) observed the patients. The secondary survey of 13 patients found DDAVP to be effective in five patients (38.5%), as evidenced by a 12.6-31.6% decrease in urine output. The maximum urine osmolality on a water deprivation test and urine osmolality after vasopressin injection were lower in patients who were unresponsive to DDAVP than in those who were responsive to the drug (106 vs. 206 mOsm/H2O/kg, 140 vs. 525 mOsm/H2O/kg). The AVPR2 variants identified in the DDAVP-responsive group were p.Ala37Pro, p.Leu44Phe, p.Arg104Cys, and p.Tyr128Ser. DDAVP was effective against CNDI with residual V2R function. The water deprivation test with vasopressin injection and genetic testing may be useful for predicting responsiveness to DDAVP.

Abstract Background Pathogenesis of Scrub typhus (ST), a tick-borne acute zoonotic disease caused by the bacterium Orientia tsutsugamushi, involves infection of vascular endothelial cells, triggering a potent cytokine host response that causes organ damage. Methods Prospective study in a tertiary care hospital in North-west India in 30 cases of Scrub typhus. Measurements of cytokines IL-17A, INF-γ, TNF-α, IL-10, IL-6, IL-4, and IL-2 were carried out at admission in all 30 patients and a control group of 10 healthy persons using BDTM Cytometric Bead Array, BD Biosciences, San Diego, California, USA. Results Mean age of the entire cohort was 36 years, and the male-female ratio was 2:1. The most common symptoms were dyspnea 87%, altered sensorium 23%, abdominal pain 20%, decreased urine output 10% and myalgia in 10%. On clinical examination, eschar was present in 40%. Investigations revealed anemia in 80% cases, leukocytosis in 46.6%, thrombocytopenia in 90%, jaundice in 53.3% and elevated serum transaminase levels in 84% cases. Of all complications, acute respiratory distress syndrome occurred in 90% patients, acute kidney injury in 37% patients, acute meningoencephalitis syndrome in 30%, and myocarditis in 23%. The mean APACHE 2 score of the entire cohort was 12 . Multi-organ dysfunction syndrome (MODS) was seen in 67% of cases, and the overall mortality rate was 20%. On Fisher's Exact Correlation analysis, presentation with meningoencephalitis, myocarditis, systemic acidosis, and a high APACHE 2 score correlated with mortality. The serum levels of cytokines were elevated in all patients compared to the healthy control group (Table 1), but did not significantly differ between survivors and non-survivors. Furthermore, the elevated levels of TNF-α (p=0.004) and IL-10 (p=0.029) strongly correlated with multi-organ dysfunction syndrome (MODS). Conclusion In Scrub Typhus, the strong correlation of serum levels of TNF-α and IL-10 with multi-organ dysfunction syndrome (MODS) suggests their involvement in disease progression. The high prevalence of acute respiratory distress syndrome and MODS, alongside a mortality rate of 20%, highlights the critical nature of scrub typhus and the necessity for early recognition of complicated disease and intervention. Disclosures All Authors: No reported disclosures

ABSTRACTPhytobezoars are the most common and well known type of bezoars yet one of the uncommon causes of mechanical obstruction of the small intestine. The reported prevalence rate of phytobezoars is estimated to be 0.4% despite being the 5th most common cause of acute small bowel obstruction. A previously healthy five‐year‐old girl presented to the Emergency Medicine Department with a 5‐day history of nonprojectile, nonbile stained vomiting, abdominal pain, and decreased urine output. Physical examinations revealed severe dehydration symptoms, and laboratory tests indicated abnormal electrolyte levels and metabolic alkalosis. The patient experienced a seizure, received medical interventions, and was diagnosed with mechanical intestinal obstruction due to a phytobezoar. After stabilization, she underwent surgical removal of the phytobezoar without complications and followed postoperative advice successfully. In cases without significant complications, surgical or aggressive medical treatment for bezoars may be unnecessary. Coca‐Cola, alone or combined with endoscopic methods, is effective in dissolving gastric phytobezoars, with success rates exceeding 90%. Conservative management involves proteolytic enzymes, cellulase, carbonated beverages, and endoscopic fragmentation. Clinicians should stay vigilant, as small bowel obstruction can occur up to 6 weeks later. Prokinetic agents and dietary guidelines help minimize bezoar formation. Surgical intervention, unlikely to address the root cause and potentially worsening motility issues, requires careful consideration. Phytobezoars are a significant consideration in pediatric small bowel obstruction cases. Conducting a thorough dietary history, focusing on fiber‐rich foods, is crucial. Radiographic and endoscopic studies aid in locating the phytobezoar. Timely surgical intervention is essential to prevent complications associated with small bowel obstruction.

This clinical decision-making (CDM) case is intended for emergency medicine residents of all levels, medical students, and fellows preparing for standardized oral board exams. Fever in a neonate (infant <28 days old) is a medical emergency due to the high risk of serious bacterial infections (SBIs) like meningitis, sepsis, or urinary tract infections (UTIs).1-3 Compared with older infants and children, neonates have immature immune responses, reduced ability to localize infection, and limited physiologic reserve, which contribute to rapid clinical deterioration and increased morbidity and mortality when invasive infection is present.1,3Importantly, clinical presentation in this age group is often subtle and nonspecific. Neonates with life-threatening infections may appear well or only mildly ill on initial examination, with symptoms such as poor feeding, irritability, or decreased urine output serving as early but easily overlooked warning signs.1,4 As a result, reliance on appearance or focal examination findings alone is insufficient to safely exclude SBI in febrile neonates.Current evidence supports a standardized approach to the evaluation of neonatal fever. This includes a complete sepsis workup-consisting of blood, urine, and cerebrospinal fluid studies-along with early administration of empiric, age-appropriate intravenous antibiotics and hospital admission for close monitoring.1-3This clinical decision-making case is designed to reinforce these foundational principles within the context of an emergency department presentation. It emphasizes early recognition of neonatal fever as a high-risk condition, systematic diagnostic reasoning, timely initiation of empiric therapy, and appropriate disposition to a higher level of care. Learners are challenged to clearly articulate their clinical reasoning and management decisions in a high-stakes environment that mirrors real-world emergency medicine practice. By the end of this CDM case, learners will be able to: 1) demonstrate familiarity with the CDM case format, 2) recognize the critical importance of fever in a neonate and initiate a thorough evaluation, 3) develop an appropriate differential diagnosis and understand the workup for febrile neonates, 4) identify and justify the appropriate diagnostic studies and interpret their findings in the context of a neonate with fever, 5) justify a treatment plan and understand the critical disposition of a neonate with fever. The case will be presented as a CDM case with questions posed by the examiner. Learners will be asked to list the history, physical exam findings, differential diagnosis, diagnostic studies, treatments, and final diagnosis in response to the examiner's prompts. Learners' performance will be evaluated using standardized oral board scoring guidelines. Efficacy will be assessed through feedback from both learners and faculty, focusing on knowledge acquisition and application in a high-stakes environment. Pre- and post-case surveys or performance scoring may be used for evaluation. Preliminary assessments from learners demonstrated improved confidence in managing febrile neonates after completing the case, with a focus on early recognition and appropriate escalation of care. Neonatal fever is a high-risk scenario requiring prompt, appropriate management. This case reinforced the importance of early sepsis recognition, comprehensive evaluation, and timely treatment. Learners benefited from exposure to the CDM Case format aiding in their exam preparation. Neonatal fever, sepsis, meningitis, pediatric emergency management, antibiotic management, ABEM Certifying Exam, clinical decision-making case.

Pregnancy related acute kidney injury is an infrequent complication associated with postpartum haemorrhage, sepsis, preeclamsia and less commonly with thrombotic microangiopathy. Hereby, we are presenting a case of a young female who underwent cesarean section and developed acute kidney injury in postpartum period decreased urine output. She was diagnosed with thrombotic microangiopathy. She was managed with collaborative intervention and discharged with complete recovery.

Abstract Introduction Penile vasculopathy leading to erectile dysfunction can be an early indicator of systemic disease. Despite rising popularity of penile implants, these devices are not well understood by non-urologists. Traditionally, reservoirs are placed on the right side in the retropubic space, near where a transplant renal vein anastomosis would be located. Renal vein thrombosis is a surgical emergency occurring in 1% of renal transplant recipients. Doppler Ultrasound is diagnostic; showing an enlarged kidney with absent venous flow, a thrombus-filled renal vein, and prolonged plateauing of flow on power doppler due to reversal of arterial flow in diastole. Objective We present a case of management of transplant renal vein thrombosis secondary to refilling of the IPP reservoir post-operatively. This is a 69-year-old male who presented for simultaneous liver-kidney transplant (SLK). The patient’s past medical history is relevant for end stage liver disease due to nonalcoholic steatohepatitis with hepatocellular carcinoma (T2), CKD stage 5, diabetes and erectile dysfunction. He had undergone placement of a penile prosthesis in 2015 with reservoir placement in the left retropubic space. In a post-operative discussion, the patient reported occasional auto-inflation of his IPP when lying supine. The transplant kidney was placed in the left iliac fossa in the area of the patient’s IPP reservoir. On POD1, the patient deflated the penile prosthesis. On POD2, he developed hematuria associated with decreased urine output, and rising creatinine. A transplant renal ultrasound showed renal vein thrombosis. He was taken to the operating room for emergent renal vein thrombectomy. It was at this time that the inflated reservoir was noted to be abutting the renal vein anastomosis. Methods Urology was consulted intraoperatively due to renal vein thrombosis with suspicion for the IPP reservoir as the cause. We discussed with the patient’s wife removal of the reservoir vs. repositioning of the reservoir. The transplant team did not feel comfortable with significant dissection around the transplant. All parties agreed to remove the reservoir only and pass the tubing into the scrotum to facilitate replacement of the reservoir at a future date. The reservoir capsule was dissected free and the reservoir was removed. The prosthesis was drained and the reservoir tubing was clipped with hemolok and metal clips before being passed back into the scrotum. The capsule was closed to ensure the prosthesis remained in a separate compartment to decrease infection risk. Copious antibiotic irrigation was used throughout the procedure. Results Following renal vein thrombectomy and reservoir explant the patient and the renal allograft function improved. He was discharged home on POD5 following his renal vein thrombectomy. Conclusions We present a case of transplant renal vein thrombosis in a patient with a penile prosthesis. This is a rare complication that can be hard to predict for non-urologists. Future considerations could include involving urologists in pre-transplant care of these patients, in order to assess the reservoir position and whether it presents a risk for renal vasculature. Repositioning or explant of the reservoir are viable strategies to manage this complication and require discussion with the patient or their partner. Disclosure No

Background: Sepsis is a common problem in paediatric critical care units. It has different clinical spectra like systemic inflammatory response syndrome (SIRS), sepsis, severe sepsis, septic shock and multi-organ failure. As per previously reported studies, sepsis accounts for 80% of under-five mortality worldwide. Septic shock is a fatal complication of sepsis. Thus, early identification and treatment is key in management of sepsis.Objectives: To identify early predictors of poor outcome of septic shock patients in the paediatric intensive care unit (PICU)Method: This was a retrospective observational study in the critical care ICU of a tertiary care hospital in Western India. Patients fulfilling inclusion criteria were included in study. Demographic factors and clinical factors were noted. Relevant investigations were sent and patients were managed as per hospital protocols.Results: There was a total of 51 cases of septic shock with different aetiology admitted in our hospital. There were 29 (56.9%) males and 22 (43.1%) females. Mean age of study participants was 3.25+3.77 years. Most of them had septic shock due to respiratory diseases (pneumonia 29.4%). Out of 51 cases 34 (66.7%) died and 17 (33.3%) survived. There was no significant difference between age distribution and gender distribution among deaths and survivals (p&gt;0.05). Incomplete immunization, altered sensorium and decreased urine output had a significant effect on outcome (death) of study participants (p&lt;0.05). Among laboratory findings, decreased platelet count, hyperkalaemia and oxygen saturation on room air had a significant role in disease outcome (p&lt;0.05).Conclusions: Incomplete immunization, oxygen saturation on room air, altered sensorium, decreased urine output, decreased platelet count and hyperkalaemia had significant effects on disease outcome.

A 32-year-old male presented with a history of decreased urine output following an alleged history of deliberate self-harm by consuming glufosinate ammonium 13.5% w/w SL herbicide (Synkill®) two days earlier. General physical examination revealed pulse 86 beats/minute, blood pressure 140/90 mmHg, and respiratory rate 20/minute. Laboratory investigations revealed elevated serum creatinine (5.96 mg/dl), creatinine phosphokinase (340 i.u./L), and elevated serum hepatic transaminases. On day 6 of hospitalization, he developed right-sided lower motor neuron facial palsy and was started on oral prednisolone. The following day, the weakness progressed, and bilateral lower motor neuron facial palsy developed. During the next few days, a descending type of flaccid paralysis developed, including involvement of respiratory muscles, requiring assisted mechanical ventilatory support. Magnetic resonance imaging (MRI) of the brain showed a normal study. The electroneuromyography test showed prolonged latency with reduced amplitude and conduction velocity. The sensorium of the patient also worsened with a Glasgow Coma Scale (GCS) of E1VTM1 by day 11 of hospital stay. A computed tomography scan of the brain done after a fall in GCS showed no abnormality of the brain parenchyma. The blood and urine samples sent for toxicological analysis revealed the presence of glufosinate in urine alone. The patient was discharged against medical advice from the hospital. Our patients highlights a very rare manifestation of glufosinate ammonium herbicide poisoning.

Tuberculosis-triggered IgA nephropathy (TB-IgAN) is a rare but important renal manifestation that often goes unrecognised due to its non-specific presentation. We report the case of a woman in her 30s who presented with progressive oedema, decreased urine output, frothy urine, intermittent dark-coloured urine and a short history of productive cough. She was diagnosed with pulmonary Mycobacterium tuberculosis (MTB) and biopsy-confirmed IgAN, revealing TB-IgAN as the cause of her rapidly progressive kidney disease. This case highlights the importance of evaluating haematuria and proteinuria in patients with TB, as early identification of TB-related renal involvement (TB-IgAN in this case) can significantly alter the management of IgAN. Although a kidney biopsy is challenging in the context of active MTB, it remains essential for accurate diagnosis. MTB can manifest with atypical features and trigger immune-mediated renal complications such as IgAN, warranting a high index of suspicion in compatible clinical settings.

Second Episode of Rhabdomyolysis: A Case Report.

A 16-year-old male presented with severe shortness of breath, fever with chills, and decreased urine output for four days. On examination, oxygen saturation was 84% on room air, blood pressure 140/90 mmHg, and heart rate 114/min. Respiratory system examination revealed bilateral coarse crepitations. Laboratory investigations showed markedly elevated blood urea (256 mg/dL) and creatinine (13.56 mg/dL) with metabolic acidosis (pH 7.27, bicarbonate 12.2mmol/L). Ultrasonography demonstrated bilateral swollen kidneys, and NCCT KUB confirmed acute pyelonephritis. The patient was managed with intravenous broad-spectrum antibiotics and haemodialysis in view of severe uraemia, acidosis, and volume overload. Over the following week, renal function and urine output improved significantly, and dialysis was discontinued. Subsequent evaluation revealed an HbA1c of 8.0%, indicating previously undiagnosed diabetes mellitus as an underlying predisposing factor. The patient was discharged on the 8th day in stable condition. This case underscores that acute pyelonephritis with acute kidney injury can be the first manifestation of undiagnosed diabetes mellitus, even in adolescents, and highlights the importance of early recognition, prompt antibiotic therapy, and renal support for favourable outcomes.

Various autoimmune diseases frequently cause both acute and chronic kidney injuries through complex mechanisms involving autoantibodies and cellular immune responses that result in tissue damage. Intercalated cells (ICs), specialized renal tubular epithelial cells responsible for proton secretion, are strategically positioned at the epithelial-immune interface, making them ideal sensors of stress signals and potential triggers of immune responses. This study investigates the molecular mechanisms by which ICs interact with immune cells to maintain renal immune homeostasis and contribute to the development of autoimmune kidney disease. We depleted Foxp3+ regulatory T cells (Tregs) by injecting diphtheria toxin (DT) into male and female Foxp3-DTR mice. Two weeks after depletion, we observed autoimmune inflammation marked by increased renal immune infiltration, including neutrophils, macrophages, and subsets of T and B cells, along with the formation of ectopic lymphoid-like structures and enhanced antigen presentation. We found higher levels of renal autoantibodies in urine and serum, with antibodies depositing in glomeruli and tubules. Our analysis identified several renal antigens targeted by autoantibodies, suggesting their potential role in antibody-mediated renal injury. Kidney damage included smaller glomeruli, proximal tubular injury, an increased urine albumin/creatinine ratio, and decreased urine output. Disruption of immune tolerance led to the upregulation of inflammasome-related genes and IL-33 in ICs, which acts as a key alarmin signaling damage and promoting activation and expansion of Tregs. Our findings uncover a novel IC-Treg interaction mediated by the IL-33 pathway, revealing immune-regulating mechanisms that support renal immune tolerance. Although Tregs were initially depleted, a significant rebound in their numbers and function occurred. Understanding the cellular and molecular mechanisms behind autoimmune renal injury is crucial for developing targeted therapies and identifying appropriate biomarkers.

Background: Acute gastroenteritis ranks among the major problems of morbidity in children all over the world, and the most severe complication of this situation is severe dehydration. The early detection of predictable clinical factors is necessary to start management in time, particularly in resource-constrained environments. Objectives: The shortcoming procedure aims to identify clinical predictors of severe dehydration in children who present with acute gastroenteritis. Methods: This was a cross-sectional study of the clinical population of 100 children (aged 6 months to 12 years) with acute gastroenteritis who were presented to a tertiary care hospital. The patients were assessed with the detailed history and systematic clinical examination. The severity of dehydration was categorized as per the world health organization (WHO) criteria. Demographic factors, frequency of diarrhea and vomiting, and the significant clinical manifestations, such as sunken eyes, dryness of the mucous membranes, time of capillary refill, skin turgor, heart-rate, mental status, peripheral pulses, and urine output, were measured on structured proforma. The statistical analysis was done to identify relationships between clinical predictors and severe dehydration. Results: Out of 100 children, Dehydration was severe in 38% of them. Markedly poor skin turgor, prolonged capillary refill time (&gt;2 seconds) was also found to be significantly related to severe dehydration, as well as, sunken eyes (92.1%), dry mucous membranes (86.8%), tachycardia (71%), and lethargy (55.2%). Children who had 8 or more episodes/day diarrhea and 5 or more diarrhea episodes/day vomiting also exhibited the increased risk of severe dehydration. Another good predictor was decreased urine output which was reported in 81.5% of children who were severely dehydrated. Conclusion: Significant clinical features of severe dehydration such as sunken eyes, delayed capillary refill, dry mucous membranes, and poor skin turgor are good predictors of severe dehydration in pediatric acute gastroenteritis. It is possible to use these available bedside cues to contribute to fast triage and prompt action, especially in resource-limited settings. Keywords: Acute gastroenteritis, Severe dehydration, Pediatrics, Clinical predictors, Capillary refill time, Diarrhea.

Abstract Disclosure: T. Jain: None. K. Zulqadar: None. S. Ifthikhar: None. R. Sharma: None. N. Jaafar: None. S. Israr: None. A. Khan: None. Background: Insulin therapy for diabetes management can occasionally trigger rare complications like insulin edema, leading to rapid fluid retention and volume overload. We present a case where insulin initiation unmasked heart failure with preserved ejection fraction (HFpEF), highlighting the need for vigilance in managing insulin in at-risk patients. Case Presentation: A 63-year-old male with a history of atrial fibrillation (AF), hypertension and type 1 diabetes mellitus presented to emergency department (ED) with progressive shortness of breath, orthopnea, leg swelling and 42 lb weight gain in 11 days. On exam, he had jugular venous distension and anasarca. The patient was diagnosed with uncontrolled diabetes, with an HbA1c of 17%, and was initiated on a basal-bolus insulin regimen 11 days prior to presentation. In the ED, labs revealed normal troponin levels, an elevated pro- brain natriuretic peptide at 1462 pg /mL and EKG revealed AF with rapid ventricular response, Q waves in II, III, AVF and poor R wave progression. He was admitted for acute decompensated HF. A transthoracic echocardiogram demonstrated mild concentric left ventricular hypertrophy with an ejection fraction of 55% with no wall motion abnormalities, and indetermined diastolic function. Thyroid, liver and renal function testing was normal with no proteinuria. The patient reported a notable decrease in urine output since starting insulin therapy. Previously, he experienced polyuria, voiding large volumes every 2-3 hours. His symptoms were attributed to new-onset HFpEF following insulin therapy, which led to reduced polyuria but exacerbated fluid retention, worsening his heart failure symptoms. He received intravenous diuretics, resulting in symptom resolution and was discharged with a titratable diuretic regimen. Conclusion: This case highlights a rare complication of insulin therapy—rapid fluid retention leading to HF symptoms, even in patients without a prior HF diagnosis. Insulin edema is rare complication of insulin use that can cause variety of manifestations ranging from lower extremity edema to anasarca and heart failure1. Clinicians should be vigilant about this potential complication when starting insulin in patients with predisposing conditions. 1.Chelliah A, Burge MR. Insulin Edema in the Twenty-first Century: Review of the Existing Literature. Journal of Investigative Medicine. 2004;52(2):104-108. doi:10.1177/108155890405200218 Presentation: Sunday, July 13, 2025

Abstract Background and Aims Recently, a new drug called Tusi, a phonetic translation of 2C or 2C-B, has emerged in Latin America and Europe. It is composed of a low proportion of various substances such as ketamine, 3,4-methylenedioxymethamphetamine (MDMA), methamphetamines, and opioids. It is also known as pink cocaine, as it is usually found in pink powder form, though it rarely contains actualcocaine. Its primary effect is hallucinogenic and is mediated by its activity on serotonin receptors. The effects appear within 1–3 hours and can last up to 8 hours. It may cause fever, hypertension, tachycardia, nausea, rhabdomyolysis, seizures, and behavioral effects. Its metabolism occurs in the liver, and it is excreted through the kidneys, remaining detectable in urine for up to 3–4 days after consumption. Case 1 A 22-year-old male from Colombia presented to the emergency department after a street fight following alcohol consumption. He was discharged with a normal physical examination. 48 hours later, he returned with abdominal pain, vomiting, and decreased urine output. Laboratory tests revealed a creatinine level of 4.06 mg/dL and creatine kinase (CK) of 1778 U/L. An abdominal CT scan ruled out obstructive uropathy and bleeding. Urine toxicology was positive for cannabis, benzodiazepines, and methylenedioxymethamphetamine. He was admitted to the Nephrology department and started on intravenous fluids, showing improvement in renal function and a decrease in CK levels (peaking at 4593 U/L). Upon further questioning, he confirmed using Tusi on the same day as the altercation. He was discharged with a creatinine level of 1 mg/dL. Case 2 A 42-year-old male from Ecuador was brought to the emergency department with muscle weakness that prevented him from moving. He mentioned being at a bar where people nearby were snorting Tusi. Ten hours later, he developed vomiting and decreased urine output. Upon arrival at the emergency department, a loss of strength in the lower limbs was confirmed. Laboratory results revealed a creatinine level of 4.17 mg/dL and CK of 55,000 U/L. Urine toxicology was negative. After receiving intravenous fluids, he remained oliguric and was admitted to the ICU. Forty-eight hours later, his CK reached 179,500 U/L and his creatinine increased to 9.6 mg/dL. Blood ethanol level was 0.2 g/L. Upon discharge from the ICU, he was transferred to the Nephrology department with ongoing renal dysfunction and oliguria, with a peak creatinine of 11.6 mg/dL, at which point he began hemodialysis. After 7 days, he showed improvement in urine output and a decrease in creatinine, reaching 1.9 mg/dL at discharge. Samples were sent to the National Institute of Toxicology and Forensic Sciences in Madrid. In Case 1, the sample was obtained on the 4th day after consumption, testing positive only for cannabis. In Case 2, the sample was collected on the 5th day after consumption, and it was negative for drugs. MDMA has been associated with acute renal failure (ARF), primarily attributed to non-traumatic rhabdomyolysis and the direct toxic effect of the drug on myocytes. Dehydration worsens the nephrotoxicity of myoglobinuria. In the case of methamphetamines, rhabdomyolysis is common, and dehydration and alcohol consumption contribute to renal damage. Conclusion Tusi is a growing drug combination in Spain that can cause ARF secondary to rhabdomyolysis, and its effects are exacerbated by simultaneous alcohol consumption. The detection of this drug is complex: the mixtures vary in their compounds and concentrations, which limits its detection. There is a delay in obtaining toxicology samples due to the lack of awareness of this drug's existence.