World journal of nephrology最新文献

This article comments on Varatharajan et al recent article, highlighting the role of tubulointerstitial damage mechanisms in diabetic nephropathy progression. Evidence suggests a bidirectional interaction between the interstitium, tubular cells, and glomeruli. Renal tubules are highly susceptible to proteinuria, metabolic disorders, and toxins. Since diabetic nephropathy persistently activates inflammatory and fibrotic pathways, epithelial-to-mesenchymal transition mechanisms present promising targets for risk assessment. Periostin, a cellular matrix protein, plays a key role in modulating extracellular interactions. Increased periostin expression in tissue, serum, and urine correlates with type 2 diabetes, making it a valuable biomarker alongside neutrophil gelatinase-associated lipocalin and kidney injury molecule-1. While periostin and neutrophil gelatinase-associated lipocalin reflect distal tubular damage, kidney injury molecule-1 serves as a marker for proximal tubular injury. Combining these biomarkers enhances diagnostic precision.

There is growing evidence suggesting that semaglutide, a glucagon-like peptide-1 receptor agonist (GLP-1RA), is effective in preventing and treating chronic kidney disease (CKD) in patients with type 2 diabetes mellitus (T2D). The Evaluate Renal Function with Semaglutide Once Weekly trial demonstrated that semaglutide significantly reduced the risk of major kidney outcomes, including kidney failure, death from kidney or cardiovascular causes, reduced albuminuria and major cardiovascular events. Emerging evidence also suggests a potential kidney-protective effect of GLP-RAs in people without diabetes. Based on this data, contemporary guidelines now support GLP-1RA use, notably semaglutide, as the fourth pillar of diabetic kidney disease (DKD) management in T2D, alongside existing cardio-kidney protective agents (the other 3 pillars of DKD therapy) sodium glucose co-transporter-2 inhibitors, non-steroidal mineralocorticoid receptor antagonists and renin-angiotensin-aldosterone-system blockers. Semaglutide offers complementary and synchronous benefits through distinct mechanisms, underscoring its role in the comprehensive management of patients with T2D. Furthermore, GLP-1RA use in people with T2D and CKD improves metabolic parameters not achievable with the other DKD therapies. This review summarises the clinical evidence for semaglutide's kidney-protective effects in individuals with and without T2D, and highlights recent trial data supporting its broader metabolic effects in CKD. Together these findings position semaglutide as a key agent in modern CKD management.

Intradialytic hypotension (IDH) is a prevalent and critical complication of haemodialysis associated with significant morbidity, mortality, and reduced quality of life in end-stage renal disease patients. IDH results from multifactorial interactions, including excessive ultrafiltration rates (UFR), rapid osmotic shifts, impaired vascular resistance, and comorbidities such as diabetes and cardiovascular disease. It triggers hypovolemic stress, leading to myocardial stunning, cerebral ischemia, and organ dysfunction. Non-modifiable risk factors, including age and preexisting conditions, exacerbate susceptibility, while modifiable elements such as high interdialytic weight gain and improper dialysis prescriptions worsen outcomes. In this review, we aim to conduct an in-depth analysis of IDH, exploring its clinical relevance, underlying mechanisms, risk factors, and management approaches. Additionally, we advocate for a standardised definition and propose a strategic framework to guide future research efforts. Effective management requires individualised approaches, including optimised UFR, cooled dialysate, and nutritional adjustments, alongside emerging technologies like bio-impedance spectroscopy and artificial intelligence for real-time risk prediction. A multidisciplinary team approach, incorporating nephrologists, nurses, and dietitians, is essential for holistic patient care. Future research and technological advancements hold promise for mitigating IDH's clinical and systemic impact, ultimately improving patient outcomes and survival.

Background: Post-transplant diabetes mellitus (PTDM) adversely affects graft survival and is an independent predictor of adverse cardiovascular events. Observational studies in the general population as well as the post-transplant setting suggest an association between the plasma 25-hydroxyvitamin D [25(OH)D] level and onset of type 2 diabetes mellitus. Literature is very limited in the context of PTDM.

Aim: To study the relationship between vitamin D deficiency at the time of kidney transplant and PTDM in the post-transplant period.

Methods: In this single center study, 72 patients who underwent kidney transplant were included. Blood samples for serum vitamin D level were collected on the day of transplant and analyzed at the end of study. The LIAISON^® 25(OH)D assay was used for quantitative estimation of total 25(OH)D in the serum. PTDM was diagnosed by either fasting plasma glucose (> 126 mg/dL), 2-h post prandial plasma glucose (> 200 mg/dL), or 2-h oral glucose tolerance test after 45 days post-transplant. Hemoglobin A1c was not used to diagnose PTDM. Vitamin D levels were labeled as sufficient (≥ 30.0 ng/mL), insufficient (20.0-29.9 ng/mL), and deficient (< 20.0 ng/mL). Patients were reviewed at 45 days and 1 year post transplant for the occurrence of PTDM.

Results: In our study cohort 72 patients completed the study. Overall, 32 (43.8%) patients developed PTDM during the follow up of 1 year, 44 (61.1%) patients had deficient (< 20 ng/mL) 25(OH)D levels. Twenty-six (81.2%) patients with PTDM had deficient vitamin D levels as compared with 18 (45.0%) patients without PTDM (P = 0.007). This association was also significant when univariable [odds ratio (OR) = 5.3, 95% confidence interval (CI): 1.79-15.67, P = 0.003)] and multivariable (OR = 8.21, 95%CI: 2.19-30.75, P = 0.002) regression analysis was performed. A higher proportion of subjects having PTDM (15.6%) had a positive family history of diabetes mellitus than the controls (2.5%) (P = 0.045). However, this association did not persist in the multivariable regression analysis (OR = 12.6, 95%CI: 0.86-185.4, P = 0.065).

Conclusion: Deficient vitamin D levels (< 20 ng/mL) were significantly associated with PTDM in the post kidney transplant setting. Further studies are needed to see the effect of vitamin D replacement on PTDM.

Background: Chronic kidney disease (CKD) contributes significantly to emergency department (ED) presentations in low- and middle-income countries. These patients frequently have multiple comorbidities and face high in-hospital mortality. However, limited data exist on early predictors of mortality at ED admission. Identifying key clinical and laboratory features associated with adverse outcomes may support timely risk stratification and targeted interventions for acutely ill CKD patients.

Aim: To identify baseline predictors of in-hospital mortality in adult Indian patients with CKD admitted to the ED.

Methods: This retrospective study was conducted from January 2021 to December 2022 at the Acute Care and Emergency Medicine Unit of the Postgraduate Institute of Medical Education and Research, Chandigarh, India. CKD was diagnosed and staged following the Kidney Disease: Improving Global Outcomes guidelines. Data were extracted from medical records using a structured form. All consecutive patients aged ≥ 18 years were included. Independent mortality predictors were identified using multivariate Cox regression analysis.

Results: Among 354 patients (mean age 49 years; 58% males), 60.5% had CKD stage 5, and 41.2% were on maintenance dialysis. Hypertension (74.9%) and diabetes (46.0%) were common comorbidities. Diabetic kidney disease was the primary etiology in 35.6%, while 43.2% had unknown causes. Infection (63.0%) was the most frequent cause for ED admission. In-hospital mortality was 29.1% (n = 103). Independent mortality predictors were Glasgow coma scale (GCS) < 15 [hazard ratio (HR): 1.822, P = 0.017], hyperglycemia (HR: 1.641, P = 0.020), and low albumin (HR: 1.270, P = 0.028). Advanced age, Charlson comorbidity Index, quick Sequential Organ Failure Assessment, and neutrophilia were significant in univariate but not multivariate analysis. CKD stage, dialysis dependency, cardiovascular disease, and neutrophil-lymphocyte ratio were not predictive.

Conclusion: A low GCS, hyperglycemia, and low albumin levels at admission independently predict in-hospital mortality in CKD patients presenting to the ED, warranting early recognition and targeted interventions.

Comorbid type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) pose significant global health challenges, particularly in the Middle East and North Africa region. This review synthesizes current evidence and clinical guidelines to inform dietary management, focusing on macronutrients (carbohydrates, protein, fats), micronutrients (potassium, phosphorus, sodium), and fluid intake. We evaluate culturally adapted strategies for the gulf cooperation council countries, where high rates of T2DM and CKD coincide with dietary practices high in refined carbohydrates and sodium. Key interventions include plant-based protein prioritization, glycemic control through carbohydrate moderation, and heart-healthy fats. Practical considerations for Ramadan fasting and electrolyte management are also discussed.

Renal allograft rejection and its detection are challenging problems for transplant clinicians. Transplant physicians rely on serum creatinine, estimated glomerular filtration rate, proteinuria, donor-specific antibodies, and graft biopsy to detect rejection. The sensitivity and specificity in these blood and urine tests are low, and the invasiveness of graft biopsy has led transplant clinicians to seek alternative diagnostic tools. Cell-free DNA (cfDNA) is a fragment of DNA released from cell death due to necrosis and apoptosis. Donor-derived cfDNA (dd-cfDNA) has been proposed as a potential non-invasive biomarker for detecting rejection. However, one must interpret it cautiously in conditions such as ischemia-reperfusion injury, delayed graft function, BK virus nephropathy, post-kidney biopsy, and dual kidney transplantation, which may cause dd-cfDNA elevation. There is a lack of standardized cutoff values for diagnosing various types of rejections. Low specificity, higher cost, and lack of universal availability are the multiple obstacles to using this tool. There is a need to establish clinical guidelines for its future utility in early rejection detection, graft surveillance, and tailoring of immunosuppression.

The increasing prevalence of pediatric obesity has raised numerous questions about its health implications, particularly regarding renal transplant outcomes. These complications often hinder medical interventions in these children. While kidney transplants are often viewed from an organocentric perspective, the overall health of the patient is critical to the success of the procedure. Current discussions make it clear that childhood obesity poses significant problems not only for graft survival, but also for long-term overall health. Childhood obesity can lead to many metabolic disorders such as diabetes and hypertension. These conditions can significantly affect a child's suitability for a transplant or make the process more difficult. A child's weight can affect the pharmacokinetics of drugs used to prevent organ rejection. Obesity impacts the individual and sets in motion a cascade of effects that can jeopardize transplant success and recovery, so understanding is needed. Research on graft survival rates is both optimistic and concerning. Clinical studies show that obese children often have an increased risk of post-transplant complications, which affects transplant longevity. The likelihood of rejection may increase due to the metabolic status of an obese child. Due to the allocation of healthcare resources for the treatment of obesity-related diseases, availability for the transplant itself may be limited. Many children maintain an adequate quality of life after a kidney transplant, but excessive weight can significantly affect their health and chances of survival. The main target is looking for highly successful strategies to give all children who need a transplant a better future, regardless of their weight.

With notable Reno protective advantages beyond glycemic management, sodium-glucose cotransporter-2 (SGLT2) inhibitors have become a mainstay treatment for type 2 diabetes mellitus and chronic kidney disease (CKD). Although SGLT2 inhibitors' involvement in the course of CKD has been well investigated, new research indicates that they may also have protective benefits in acute kidney injury (AKI), a condition for which there are few pharmacological treatments. The possible ways that SGLT2 inhibitors aid in AKI recovery are examined in this mini-review. These include mitochondrial protection, oxidative stress attenuation, anti-inflammatory effects, intraglomerular pressure decrease, and modulation of tubuloglomerular feedback. Although there is a lack of solid clinical trial data, preclinical models and observational studies suggest that SGLT2 inhibitors may lessen ischemia-reperfusion injury and contrast-induced nephropathy. This review addresses the possibility of incorporating SGLT2 inhibitors into AKI care regimens, critically evaluates the available data, and highlights important research gaps. Robust clinical trials are required to determine the safety, effectiveness, and ideal treatment window of SGLT2 inhibitors in this context, given the burden of AKI-related morbidity and mortality.