ABSTRACT: Post-bariatric surgery patients face higher risk of micronutrient malabsorption and often receive intravenous iron like Ferric carboxymaltose (FCM).  Recent studies associate FCM with severe (serum phosphate levels < 1 mg/dL) and prolonged hypophosphatemia caused by elevated Fibroblast Growth Factor 23 (FGF23) levels, which reduces phosphate reabsorption in the kidneys via α-Klotho co-receptor. FCM, in particular, can therefore lead to notable and sustained FGF23-mediated hypophos-phatemia. We present a case of prolonged and severe hypophosphatemia secondary to fibroblast growth factor 23 (FGF23)-mediated phosphaturia following ferric carboxymaltose (FCM) administration in a post-bariatric surgery patient. This case underscores the complex interplay between intravenous iron therapy, phosphate metabolism, and altered absorption physiology following bariatric surgery. It highlights the need for clinicians to monitor phosphate levels after FCM administration, particularly in high-risk patients such as those with malabsorption.

ABSTRACT: Background: Rapid identification of patients at risk of contrast-associated acute kidney injury (AKI) is essential in acute settings such as acute myocardial infarction and ischemic stroke. Point-of-care (POC) creatinine testing provides immediate assessment of kidney function; however, its reliability for clinical risk stratification relative to standard laboratory measurements remains uncertain. This study evaluated the agreement between laboratory- and POC creatinine-based risk stratification and their association with subsequent AKI after contrast angiography.
Methods: In this prospective observational study, 295 adults undergoing contrast-enhanced angiography for acute myocardial infarction or acute ischemic stroke were enrolled. Serum creatinine was measured using both standard laboratory methods and a POC device before contrast administration. Estimated glomerular filtration rate (eGFR) was calculated using the CKD-EPI 2021 equation, and predicted risk of post-contrast AKI was assessed using the Mehran risk score. AKI was defined according to KDIGO criteria (≥1.5-fold increase from baseline or ≥26.5 µmol/L increase within 7 days). Agreement between laboratory- and POC-derived risk categories was evaluated using weighted Cohen’s kappa.
Results: The median age was 64 years (interquartile range 57–70), and 66.8% of participants were male. Based on laboratory measurements obtained in the hospital central laboratory, categories were low in 8.8%, moderate in 37.3%, high in 25.4%, and very high in 28.5% of patients. Among patients with available follow-up creatinine measurements (n = 127), CA-AKI occurred in 11.0% (14/127). Agreement between laboratory- and POC-based risk classifications was near-perfect (κ = 0.97, 95% CI 0.95–0.98). The correlation between laboratory and POC creatinine values was moderate (r = 0.63, p < 0.001).
Conclusion: POC creatinine–based Mehran risk stratification shows excellent diagnostic agreement with laboratory-based assessment for identifying patients at risk of post-contrast AKI. POC testing may facilitate rapid bedside risk assessment in patients undergoing angiography for acute myocardial infarction or ischemic stroke without compromising risk classification reliability.

ABSTRACT: Focal segmental glomerulosclerosis (FSGS) is a common pathological lesion in kidney biopsies with diverse etiologies, including genetic mutations.
We report a case of a 39-year-old man presenting with proteinuria of 2 g/day, normal kidney function, and no nephrotic syndrome. A kidney biopsy revealed findings consistent with FSGS (not otherwise specified )NOS( type), and whole-exome sequencing (WES) identified two heterozygous variants in the CRB2 gene: c.3219C>G (likely pathogenic) and c.1864G>A (variant of uncertain significance). The patient was managed conservatively with renin-angiotensin-aldosterone system (RAAS) inhibitor and Sodium-Glucose cotransporter 2 (SGLT2) inhibitor, resulting in sustained proteinuria reduction and preservation of kidney function over a three-year follow-up. This report highlights a possible novel presentation of CRB2 mutation-associated FSGS without steroid resistance or nephrotic syndrome, that was successfully managed without immunosuppression.