39 research outputs found
Erratum: A roadmap to parathyroidectomy for kidney transplant candidates (Clinical Kidney Journal (2022) (sfac050) DOI: 10.1093/ckj/sfac050)
No full textThis is an erratum to: Giuseppe Cianciolo, Francesco Tondolo, Simona Barbuto, Andrea Angelini, Francesca Ferrara, Francesca Iacovella, Concettina Raimondi, Gaetano La Manna, Carla Serra, Chiara De Molo, Ottavio Cavicchi, Ottavio Piccin, Pasquale D'Alessio, Loredana De Pasquale, Giovanni Felisati, Paola Ciceri, Andrea Galassi, Mario Cozzolino, A roadmap to parathyroidectomy for kidney transplant candidates. In the originally published version of this manuscript, the images for Figures 2 and 3 were swapped in error. This error has been corrected
Three-dimensional imaging reconstruction and laparoscopic robotic surgery: a winning combination for a complex case of multiple myomectomy
No full textOBJECTIVE: To demonstrate the intraoperative use of three-dimensional (3D) imaging reconstruction for a complex case of multiple myomectomy assigned to robot-assisted laparoscopic surgery. DESIGN: Stepwise demonstration of the technique with narrated video footage. SETTING: University tertiary care hospital. PATIENT(S): A 36-year-old nulliparous infertile woman with multiple uterine myomas (\u3e20) presented with menorrhagia and pelvic discomfort for many months. Because of the huge number of fibroids present, the patient was considered eligible for laparoscopic robotic-assisted myomectomy. INTERVENTION(S): A robotic-assisted laparoscopic myomectomy was performed with the use of intraoperative 3D imaging reconstruction. After opening the retroperitoneum through the adnexal triangle and identifying the ureters, to reduce intraoperative bleeding, bulldog clamps were used to temporarily reduce uterine vascularization. A multiple myomectomy was then performed with the use of tenaculum and Maryland bipolar forceps. During the intervention, the surgeon used the 3D uterine reconstruction to adapt its surgical strategy. Multilayer running closure was achieved using a bidirectional barbed suture ensuring introflexion of the serosa. Patients\u27 consent was obtained for publication of the case; institutional review board approval was not required for this case report as per our institution\u27s policy. MAIN OUTCOME MEASURE(S): Description of a robotic-assisted myomectomy with the intraoperative use of 3D imaging reconstruction. RESULT(S): The total operative time was 105 minutes. A total of 21 fibroids were removed with 150 mL of intraoperative blood loss. The patient was discharged the day after. CONCLUSION(S): The application of 3D imaging technology could overcome one of the limitations of robot-assisted minimally invasive surgery, the lack of haptic feedback, enabling the surgeon to rapidly locate myomas and guide the intraoperative plan to optimize the results. Additional studies evaluating the clinical impact of this technique and its improvement are required
Alkaline Phosphatase : An Old Friend as Treatment Target for Cardiovascular and Mineral Bone Disorders in Chronic Kidney Disease
No full textAlkaline phosphatase (ALP) is an evolutionary conserved enzyme and widely used biomarker in clinical practice. Tissue-nonspecific alkaline phosphatase (TNALP) is one of four human isozymes that are expressed as distinct TNALP isoforms after posttranslational modifications, mainly in bone, liver, and kidney tissues. Beyond the well-known effects on bone mineralization, the bone ALP (BALP) isoforms (B/I, B1, B1x, and B2) are also involved in the pathogenesis of ectopic calcification. This narrative review summarizes the recent clinical investigations and mechanisms that link ALP and BALP to inflammation, metabolic syndrome, vascular calcification, endothelial dysfunction, fibrosis, cardiovascular disease, and mortality. The association between ALP, vitamin K, bone metabolism, and fracture risk in patients with chronic kidney disease (CKD) is also discussed. Recent advances in different pharmacological strategies are highlighted, with the potential to modulate the expression of ALP directly and indirectly in CKD-mineral and bone disorder (CKD-MBD), e.g., epigenetic modulation, phosphate binders, calcimimetics, vitamin D, and other anti-fracture treatments. We conclude that the significant evidence for ALP as a pathogenic factor and risk marker in CKD-MBD supports the inclusion of concrete treatment targets for ALP in clinical guidelines. While a target value below 120 U/L is associated with improved survival, further experimental and clinical research should explore interventional strategies with optimal risk-benefit profiles. The future holds great promise for novel drug therapies modulating ALP.Funding Agencies|ALF grants from Region Ostergotland</p
Molecular weight determination of heparosan- and chondroitin-like capsular polysaccharides: figuring out differences between wild -type and engineered Escherichia coli strains
No full text[Gliflozins: Proteinuria Control and Nephroprotection]
No full text: In recent years, the prevalence of chronic kidney disease (CKD) has significantly increased, with an estimated 843.6 million individuals affected in 2017 [1]. This rise is closely linked to the growing incidence of risk factors such as diabetes mellitus and obesity. Patients with diabetic kidney disease (DKD), one of the most common complications of diabetes, are characterized by high cardiovascular morbidity and mortality. Recent evidence indicates that sodium-glucose cotransporter 2 inhibitors (SGLT2i) play a crucial role in reducing the progression of both DKD and CKD, thanks to its nephroprotective and cardioprotective effects. SGLT2i work by decreasing glomerular hyperfiltration, improving tubulo-glomerular feedback, and reducing blood glucose levels
RAASi, MRA and FGF-23 in CKD progression: the usual suspects?
No full text: Chronic kidney disease (CKD) affects almost 10% of the global population and is a significant health issue. The presence of CKD increases the risk of fatal and non-fatal cardiovascular events, overall mortality, and progression of renal damage leading to kidney failure. Inhibiting the renin-angiotensin-aldosterone system (RAAS) through angiotensin-converting enzyme inhibitor or angiotensin II receptor blockers reduces proteinuria and slows eGFR decline in CKD patients. Several factors can reduce the effect of inhibition RAAS, such as individual variations, drug intolerance, and adverse effects like hyperkalemia. Moreover, the aldosterone breakthrough phenomenon, where aldosterone levels rebound during RAAS therapy, limits treatment efficacy in reducing proteinuria and slowing the progression of CKD and is associated with poor cardiovascular and renal outcomes. Similarly, FGF23 attenuates RAAS blockade effectiveness through, in fact, enhancing the expression of angiotensin-converting enzyme 2 and reducing degradation of angiotensin I to angiotensin 1-9 and angiotensin II to angiotensin 1-7 inducing a reduced efficacy in controlling RAAS-mediated effects and an increase of cardiovascular risk and CKD progression. New therapeutic strategies to reduce the progression of CKD, such as SGLT-2 inhibitors, GLP-1 receptor agonists, and mineralocorticoid receptor antagonists (MRAs), are recommended in CKD patients to reduce the risk of progression and cardiovascular events. Furthermore, these therapies may reduce FGF-23 levels and regulate aldosterone breakthrough. This review aims to clarify the mechanisms underlying CKD progression, with a focus on aldosterone breakthrough, FGF-23, and activins, in order to identify new therapeutic approaches for better management of CKD and its complications
Bone disease in kidney transplant: don't forget about osteomalacia: a case report and literature review
No full textIntroduction
Osteomalacia is an often-overlooked manifestation of post-transplant bone disease that may persist or newly develop in kidney transplant recipients because of pre-existing chronic kidney disease–mineral and bone disorder, ongoing immunosuppression, and alterations in calcium-phosphate metabolism. Severe vitamin D deficiency, hypophosphatemia, and secondary hyperparathyroidism create a metabolic milieu that favors osteoid mineralization defect and leads to debilitating skeletal pain and fragility fractures.
Objective
This case report documents the clinical course, diagnostic work-up, and therapeutic response of a kidney-transplant recipient with severe vitamin D deficiency, with the aim of raising awareness of this condition and outlining practical management strategies.
Case report
A 61-year-old woman underwent living-donor kidney transplantation in 2020. Four months later, she presented with diffuse bone pain, progressive gait impairment, and laboratory evidence of hypercalcemic hyperparathyroidism (PTH 130 pg/mL), severe vitamin D deficiency (25[OH]D 7 ng/mL), and hypophosphatemia (2.8 mg/dL). Very high levels of bone-specific alkaline phosphatase may reflect both bone mineralization defect and high bone turnover. Imaging supported the diagnosis of osteomalacia, revealing bone-marrow edema of both knees, Looser zones, and focal radiotracer uptake on ^99mTc-MDP scintigraphy. The patient started treatment with high-dose cholecalciferol (60,000 IU/day) followed by monthly calcifediol, together with continued cinacalcet and subsequent oral bisphosphonate therapy; this regimen normalized 25(OH)D (42 ng/mL), reduced bone-turnover markers, and enabled the recovery of independent ambulation within 9 months. Follow-up dual-energy X-ray absorptiometry showed lumbar BMD improvement (T-score −3.7 to −2.6) and stabilization of femoral osteopenia at 26 months post-transplant.
Conclusion
Early recognition of osteomalacia after kidney transplantation and aggressive correction of vitamin D deficiency, phosphate wasting, and hyperparathyroidism can result in rapid symptomatic relief and partial reversal of bone loss. Routine monitoring of mineral metabolism and bone turnover markers should therefore be integrated into post-transplant care to prevent delayed diagnosis. Controlled studies are warranted to define optimal supplementation protocols and thresholds in this population
Diagnosis and Therapeutic Management of Bone Disease in Patients with Chronic Kidney Disease or Kidney Transplant Recipients
No full text: Osteoporosis is a chronic skeletal disease characterized by reduced bone mineral density and deteriorated bone microarchitecture, which increases fracture risk. In patients with chronic kidney disease (CKD), osteoporosis management is complicated by disturbances in mineral and bone metabolism (CKD-MBD) that adversely affect bone health. Diagnosis requires a thorough clinical evaluation, including bone mineral density measurement via DEXA, bone microarchitecture assessment with TBS, and analysis of bone turnover biomarkers. Therapeutic management must be personalized and may include anti-resorptive or anabolic therapies, depending on the patient's bone metabolism and renal function. Policlinico Sant'Orsola employs an integrated care model involving nephrologists, endocrinologists, radiologists, and other specialists for optimal osteoporosis management. This multidisciplinary approach addresses the complexities of CKD-MBD comprehensively, improving diagnosis and treatment and, consequently, enhancing patient quality of life through a coordinated and personalized treatment plan
Risk factors for IgA nephropathy recurrence and impact on graft survival in a cohort of kidney transplanted patients
No full textRecurrence of IgA nephropathy (IgAN) after kidney transplant (KT) appears associated with worse graft survival; thus, the identification of risk factors is worthwhile to improve pre-transplant evaluation of KT recipients and to identify the optimal treatment strategy. The aim of this study was to determine incidence, risk factors and impact on renal function and graft survival of IgAN recurrence after KT. We performed a retrospective study including 110 patients with biopsy-proven IgAN, who underwent KT at Policlinico di Sant'Orsola Hospital - University of Bologna from 2005 to 2021. IgAN recurred in 14 patients (12.7%) with a median time-to-recurrence of 59 (16-90) months. We found that a faster progression from IgAN diagnosis to end-stage kidney disease (ESKD), a younger age at ESKD, and a younger age at KT were associated with a higher risk of recurrence. During the first 2 years after KT, 24 h proteinuria was higher in patients with IgAN recurrence than in patients without (0.40 (0.11-1.8) vs 0.22 (0.18-0.37) g/day, p = 0.0003). During the follow-up period, a more rapid decline in eGFR was observed in the Recurrence group (p = 0.023). Additionally, graft survival at 10 years post-kidney transplant was significantly lower in this group (log-rank test p = 0.015). In conclusion, we found that patients with a more aggressive form of IgAN, who reached ESKD before 36 years of age, had an higher risk of recurrence in KT. Moreover we confirmed that recurrent IgAN, especially if clinically relevant, is associated with a worse graft outcome
