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Background: Atypical hemolytic uremic syndrome (HUS) is a rare form of thrombotic microangiopathy (TMA) characterized by complement dysregulation. Cocaine use has been reported to be a potential trigger of TMA; however, the underlying mechanisms remain poorly elucidated. Proposed hypotheses include direct endothelial injury, activation of the complement cascade, and the unmasking of whether HUS is genetic or acquired. Case Report: We report the case of a 47-year-old man who presented with hypertensive emergency and acute kidney injury following intranasal cocaine use. The laboratory findings were consistent with microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and markedly elevated lactate dehydrogenase (LDH) levels. Renal biopsy (RB) revealed classic features of TMA, including glomerular capillary thrombosis, fibrinoid necrosis, and acute tubular injury. Complement studies demonstrated reduced levels of Factor I, indicative of complement dysregulation. The patient was treated with therapeutic plasma exchange and four weekly doses of eculizumab, resulting in hematologic remission and significant improvement in renal function, without the need for dialysis. Genetic testing for known atypical HUS-associated mutations was negative; therefore, maintenance therapy with eculizumab was discontinued without clinical relapses. Discussion: This case underscores cocaine as a rare but important precipitating factor for atypical HUS in predisposed individuals. Early diagnosis, RB, and complement evaluation were essential in determining the etiology and guiding targeted therapy. Complement inhibition with eculizumab was effective in halting disease progression and preventing long-term renal damage. Conclusions: This case highlights the relevance of considering cocaine use as a potential trigger of complement-mediated TMA. Early identification of aHUS features and prompt initiation of complement inhibition therapy may be critical to preventing irreversible kidney injury.

Background and Objectives: Sodium glucose cotransporter-2 (SGLT-2) inhibitors have emerged as integral therapeutic tools in the management of patients with cardiovascular–kidney–metabolic (CKM) syndrome. In addition to their well-documented effects on lowering glucose levels and cardiovascular- and reno-protective actions, SGLT-2 inhibitors, through a reduction in body weight (BW), generate changes in the body composition and volume status that have not been clearly studied. Materials and Methods: This retrospective, observational longitudinal cohort, single-center study analyzed and compared body composition and fluid status measured by bioelectrical impedance analysis (BIA) from weeks 0 to 12 after the initiation of the cardiac rehabilitation (CR) program for coronary artery disease and heart failure in 59 patients who started treatment with SGLT-2 inhibitors (SGLT-2iG) and 112 patients without SGLT-2 inhibitors (non-SGLT-2iG). Results: Changes between the baseline and week 12 in the SGLT-2iG and non-SGLT-2iG were −0.3 L (p = 0.003) and −0.03 L (p = 0.82) in extracellular water (ECW) (p = 0.05), −0.39 L (p < 0.001) and −0.14 L (p = 0.33) in intracellular water (ICW) (p = 0.12), −0.69 (p < 0.001) and −0.16 (p = 0.52) in total body water (TBW) (p = 0.08), and −0.01 (p = 0.37) and −0.001 (p = 0.25) in the ECW/TBW ratio, respectively. After 3 months of exercise therapy in the CR program, patients in the SGLT-2iG showed a greater decrease than the non-SGLT-2iG in weight (−1.34 kg, p < 0.001 vs. −0.99, p = 0.02), body mass index (BMI) (−0.45 kg/m2, p < 0.001 vs. −0.38, p = 0.004), arm circumference (−0.57 cm, p = 0.008 vs. −0.12 cm, p = 0.21), waist circumference (−1.5 cm, p = 0.04 vs. −0.11 cm, p = 0.83), systolic blood pressure (SBP) (−8.9 mmHg, p = 0.049 vs. −4.19, p = 0.08), and diastolic blood pressure (DBP) (−5.15, p = 0.03 vs. −2.85, p = 0.01). The bioelectrical impedance analysis (BIA) revealed a significant decrease in body fat mass (BFM) and visceral fat area, without a loss of lean body mass (LBM) or skeletal muscle mass in the SGLT-2iG. Conclusions: SGLT-2 inhibitors exert beneficial effects on body compartments and volume status. Although they induce modest weight loss, this appears to be mainly directed at ECW, BFM, and visceral fat, without a loss of LBM nor skeletal muscle mass, which could contribute to the observed CKM benefits.

Background: Uremic tumoral calcinosis (UTC) is a rare yet severe complication of chronic kidney disease (CKD), predominantly occurring in patients undergoing renal replacement therapy (RRT). It is characterized by extensive soft tissue calcifications, frequently associated with chronic hyperphosphatemia and disruptions to calcium–phosphorus metabolism. Case report: This report describes a 34-year-old woman with end-stage renal disease (ESRD) secondary to lupus nephritis, undergoing continuous ambulatory peritoneal dialysis (CAPD). She presented with a progressively enlarging calcified mass in the proximal phalanx of the third finger on her right hand, accompanied by functional impairment. Laboratory findings revealed persistent hyperphosphatemia (8.8 mg/dL), elevated parathyroid hormone levels (901 pg/mL), and low vitamin D levels (9 ng/mL), indicating significant disturbances to mineral metabolism. Imaging studies, including X-ray and whole-body 18F-Choline positron emission tomography/computed tomography (PET/CT), confirmed the presence of localized calcifications in the soft tissue of the proximal phalanx of the third finger on her right hand and parathyroid hyperplasia, respectively. Initial management included the optimization of phosphate binders and calcimimetic therapy, with the subsequent intensification of dialysis therapy. Transitioning to automated peritoneal dialysis (APD) with high-volume exchanges resulted in a notable improvement in biochemical parameters and the eventual remission of the calcified mass. Conclusion: This case underscores the importance of comprehensive management in dialysis patients, including dietary phosphate restriction, the appropriate use of non-calcium-based binders, and tailored dialysis regimens to prevent and treat CKD-related mineral and bone disorders. It also highlights the utility of imaging modalities such as PET/CT in diagnosing UTC and monitoring response to therapy. Further research is needed to elucidate the pathophysiology of UTC and optimize its management in dialysis patients.