End-stage renal disease (ESRD) represents the final stage of chronic kidney disease and is characterized by progressive loss of renal function, metabolic instability, inflammation, and increased risk of protein-energy wasting. Although kidney transplantation improves survival, the early post-transplant period remains clinically complex due to surgical stress, immunosuppressive therapy, and fluctuating renal function. These factors significantly increase energy expenditure, promote protein catabolism, and predispose patients to electrolyte abnormalities, underscoring the critical role of evidence-based medical nutrition therapy (MNT). Current standards of care recommend comprehensive nutrition assessment by a registered dietitian (RD) within the first 90 days post-transplant and routine monitoring of anthropometrics, intake adequacy, and biochemical markers. For metabolically stable post-transplant patients, energy needs are estimated at 25–35 kcal/kg/day, with higher targets of 30–35 kcal/kg/day in the early post-operative period. Protein recommendations increase to 1.2–2.0 g/kg/day initially to counter negative nitrogen balance and support wound healing. Sodium intake is generally limited to <2.3 g/day for blood pressure and volume control, while potassium and phosphorus are adjusted based on laboratory trends. If oral intake is inadequate beyond several days, enteral nutrition (EN) is recommended when gastrointestinal function permits, with parenteral nutrition (PN) reserved for cases where oral and EN routes cannot meet needs. This case report illustrates the application of evidence-based MNT standards in a post–kidney transplant patient during inpatient rehabilitation and highlights the integral role of RD-led care in supporting metabolic stabilization and clinical recovery.

Acute pancreatitis (AP) is an inflammatory condition characterized by premature pancreatic enzyme activation leading to autodigestion, local tissue injury, and systemic inflammation. AP commonly causes abdominal pain, nausea, vomiting, and ileus, which can decrease oral intake and increase the risk of malnutrition. In clinical practice, patients with AP often present with comorbid conditions that further complicate feeding tolerance. Historically, bowel rest and delayed feeding were standard management strategies. However, growing evidence demonstrates that early nutrition intervention improves outcomes, including reduced infectious complications, shorter hospital length of stay, and preservation of gut mucosal integrity. Medical nutrition therapy in AP requires careful assessment of feeding tolerance, disease severity, and metabolic demands. Current evidence-based guidelines recommend early oral feeding in mild pancreatitis and initiation of enteral nutrition within 24–48 hours in moderate to severe cases, with parenteral nutrition reserved for patients unable to tolerate enteral intake or meet requirements. Recommended diet progression involves advancement to low-fat or regular diets as tolerated rather than routine use of restrictive liquid diets. Key interventions include early diet advancement, appropriate diet or formula selection based on tolerance, provision of approximately 25–35 kcal/kg/day and 1.2–1.5 g/kg/day protein, and close monitoring of fluid status and biochemical markers, with adjustments individualized to clinical status. This case report reviews current nutrition guidelines for AP and highlights the importance of implementing evidence-based nutrition strategies in a patient with complex clinical presentations and increased nutrition risk.

Non-occlusive mesenteric ischemia (NOMI) is a rare but highly fatal form of acute mesenteric ischemia, which is defined by a sudden interruption of blood supply to the intestines. NOMI occurs most commonly in critically ill, mechanically ventilated patients with hemodynamic instability presenting with low cardiac output and vasoconstriction. Mortality remains high due to diagnostic delays, rapid progression to bowel necrosis, and multisystem organ failure. While nutrition therapy is not a primary treatment for NOMI, it becomes essential following diagnosis due to repeated surgical interventions, sepsis, and increased metabolic demand, and the frequent interruption of feeding caused by hemodynamic instability. In critically ill patients, particularly with obesity, medical nutrition therapy (MNT) must balance the risks of underfeeding with the potential risks of enteral nutrition (EN) intolerance and bowel ischemia. Current evidence supports early nutrition intervention, prioritizing EN when hemodynamically stable, while initiating parenteral nutrition (PN) when EN is contraindicated or not feasible. Guidelines recommend hypocaloric, high protein feeding in obese critically ill patients to preserve lean mass and reduce the risks of complications of overfeeding. This case report highlights complexities of implementing evidence-based nutrition support in NOMI, and emphasizes the importance of individualized nutrition strategies, close monitoring, and interdisciplinary coordination to preserve nutritional status and support clinical outcomes.

Prebiotic sodas are marketed as healthy alternatives to traditional soda, but these claims have not yet been substantiated by research. This study evaluated the effects of fasted consumption of the prebiotic sodas Olipop and Poppi, compared with Diet Coke and Coca-Cola Original, on blood glucose, insulin, glucagon-like-peptide-1 (GLP-1), satiety, gastrointestinal symptoms, and beverage preference. A single-blind, repeated-measures design was employed with 10 participants. Participants completed four randomly assigned trials with a one-week washout period between each. During each visit, blood samples and satiety questionnaires were collected at baseline and throughout a two-hour trial. Beverage preference was assessed post-consumption, and gastrointestinal symptoms were evaluated using a follow-up questionnaire 24h post-intervention. The results from this study are expected to be completed by mid-April (by SRS).

The overall goal of our study is to understand how excess adiposity in women with and without
confounding cardiometabolic risk factors influences breast cancer cell growth and oxidative stress
signaling. I have already collected preliminary data indicating that activity of the antioxidant response
gene, NRF2, and expression of NRF2 targets are decreased in serum from obese subject, regardless of
phenotype. We investigated the functional consequences of these responses
by measuring and quantifying differences in reactive oxygen species (ROS) production. We also
investigated if these changes could lead to changes in breast cancer cell growth. To
investigate this, MCF7 breast cancer cells was grown in 6 distinct treatment groups reflecting varied
human metabolic health: CON (healthy control), NWO (normal weight obese), MUO (metabolically
unhealthy obese), and MHO (metabolically healthy obese), alongside the standard fetal bovine serum-
containing media a negative control. Reactive oxygen species production was assessed using a reagent
that fluoresces when it becomes oxidized by ROS. We expect cells grown in serum from obese subjects
will have higher levels of ROS production and increased invasive capacity. However, the results have yet
to be processed as of Mar 6. This research could demonstrate how total systemic metabolic health
influences oxidative stress responses and invasive potential, linking gene expression to real functional
outcomes. These insights could heavily inform medical assessments.