World Journal of Nephrology最新文献

Kidney disease (KD) is characterized by the presence of elevated oxidative stress, and this is postulated as contributing to the high cardiovascular morbidity and mortality in these individuals. Chronic KD (CKD) is related to high grade inflammatory condition and pro-oxidative state that aggravates the progression of the disease by damaging primary podocytes. Liposoluble vitamins (vitamin A and E) are potent dietary antioxidants that have also anti-inflammatory and antiapoptotic functions. Vitamin deficits in CKD patients are a common issue, and multiple causes are related to them: Anorexia, dietary restrictions, food cooking methods, dialysis losses, gastrointestinal malabsorption, etc. The potential benefit of retinoic acid (RA) and α-tocopherol have been described in animal models and in some human clinical trials. This review provides an overview of RA and α tocopherol in KD.

The development of maintenance hemodialysis (HD) for end stage kidney disease patients is a success story that continues to save many lives. Nevertheless, intermittent renal replacement therapy is also a source of recurrent stress for patients. Conventional thrice weekly short HD is an imperfect treatment that only partially corrects uremic abnormalities, increases cardiovascular risk, and exacerbates disease burden. Altering cycles of fluid loading associated with cardiac stretching (interdialytic phase) and then fluid unloading (intradialytic phase) likely contribute to cardiac and vascular damage. This unphysiologic treatment profile combined with cyclic disturbances including osmotic and electrolytic shifts may contribute to morbidity in dialysis patients and augment the health burden of treatment. As such, HD patients are exposed to multiple stressors including cardiocirculatory, inflammatory, biologic, hypoxemic, and nutritional. This cascade of events can be termed the dialysis stress storm and sickness syndrome. Mitigating cardiovascular risk and morbidity associated with conventional intermittent HD appears to be a priority for improving patient experience and reducing disease burden. In this in-depth review, we summarize the hidden effects of intermittent HD therapy, and call for action to improve delivered HD and develop treatment schedules that are better tolerated and associated with fewer adverse effects.

Virus-related cancers in humans are widely recognized, but in the case of renal cancer, the link with the world of viruses is not clearly established in humans, despite being known in animal biology. In the present review, we aimed to explore the literature on renal cell carcinoma (RCC) for a possible role of viruses in human RCC tumorigenesis and immune homeostasis, hypothesizing the contribution of viruses to the immunogenicity of this tumor. A scientific literature search was conducted using the PubMed, Web of Science, and Google Scholar databases with the keywords "virus" or "viruses" or "viral infection" matched with ("AND") "renal cell carcinoma" or "kidney cancer" or "renal cancer" or "renal carcinoma" or "renal tumor" or "RCC". The retrieved findings evidenced two main aspects testifying to the relationship between RCC and viruses: The presence of viruses within the tumor, especially in non-clear cell RCC cases, and RCC occurrence in cases with pre-existing chronic viral infections. Some retrieved translational and clinical data suggest the possible contribution of viruses, particularly Epstein-Barr virus, to the marked immunogenicity of sarcomatoid RCC. In addition, it was revealed the possible role of endogenous retrovirus reactivation in RCC oncogenesis, introducing new fascinating hypotheses about this tumor's immunogenicity and likeliness of response to immune checkpoint inhibitors.

People exposed to liver ischaemia reperfusion (IR) injury often develop acute kidney injury and the combination is associated with significant morbidity and mortality. Molecular mediators released by the liver in response to IR injury are the likely cause of acute kidney injury (AKI) in this setting, but the mediators have not yet been identified. Identifying the mechanism of injury will allow the identification of therapeutic targets which may modulate both liver IR injury and AKI following liver IR injury.

Background: Unilateral small-sized kidney is a radiological term referring to both the congenital and acquired causes of reduced kidney volume. However, the hypoplastic kidney may have peculiar clinical and radiological characterizations.

Aim: To evaluate the clinical presentations, complications, and management approaches of the radiologically diagnosed unilateral hypoplastic kidney.

Methods: A retrospective review of the records of patients with a radiological diagnosis of unilateral hypoplastic kidney between July 2015 and June 2020 was done at Assiut Urology and Nephrology Hospital, Assiut University, Egypt.

Results: A total of 33 cases were diagnosed to have unilateral hypoplastic kidney with a mean (range) age of 39.5 ± 11.2 (19-73) years. The main clinical presentation was loin pain (51.5%), stone passer (9.1%), anuria (12.1%), accidental discovery (15.2%), or manifestations of urinary tract infections (12.1%). Computed tomography was the most useful tool for radiological diagnosis. However, radioisotope scanning could be requested for verification of surgical interventions and nephrectomy decisions. Urolithiasis occurred in 23 (69.7%) cases and pyuria was detected in 22 (66.7%) cases where the infection was documented by culture and sensitivity test in 19 cases. While the non-complicated cases were managed by assurance only (12.1%), nephrectomy (15.2%) was performed for persistent complications. However, symptomatic (27.3%) and endoscopic (45.6%) approaches were used for the management of correctable complications.

Conclusion: Unilateral hypoplastic kidney in adults has various complications that range from urinary tract infections to death from septicemia. Diagnosis is mainly radiological and management is usually conservative or minimally invasive.

Background: Hema-Plus, a recombinant human erythropoietin (rHuEPO) or epoetin alfa has shown effectiveness in correction of anemia in Thai population in clinical practice. This study was aimed to demonstrate efficacy and safety under the evidence-based approach.

Aim: To evaluate the efficacy and safety of rHuEPO (Hema-Plus) for treatment of anemia over 12 wk in Thai patients with Stage V chronic kidney disease (CKD) on peritoneal dialysis (PD).

Methods: This study was an open-label, multi-center study to enroll 30 CKD patients identified to start PD with hemoglobin (Hb) less than 9.5 g/dL, serum ferritin more than 100 ng/mL, serum transferrin saturation more than or equal to 20% and who had not previously received epoetin. Patients with conditions that could increase the risk of adverse effects from study participation or interfere with study outcomes, were using concomitant androgens or had secondary hyperparathyroidism were excluded. All eligible patients started Hema-Plus by SC injection at 4000 IU once or twice weekly (week 0) and with follow-up at weeks 2, 4, 8, and 12. Dosage adjustment could be done to achieve Hb level of 11-12 g/dL. Primary end point was mean change in Hb level from baseline to end of treatment (week 12). Safety was assessed throughout the study. Quality of life (QoL) was assessed using KDQOL-36.

Results: All 30 enrolled patients completed the study. Mean (standard deviation) Hb at baseline (week 0) to the end of 12 wk was significantly increased from 7.39 (1.29) g/dL to 11.15 (1.73) g/dL (paired t-test, P value < 0.001). Overall change of Hb means from baseline over the other 4 visits was statistically significantly increased (repeated measure ANOVA, P value < 0.001). Ten out of 39 adverse events (AEs) were serious. Two serious AEs were probably related to study medication by investigators' assessment. At week 12, the QoL scores in all domains were significantly increased from baseline.

Conclusion: Hema-Plus administered for 12 wk for treatment of anemia in patients on PD effectively increased Hb levels with acceptable safety profile.

Background: Lemierre's syndrome is a disease that causes anaerobic sepsis, internal jugular vein thrombosis, and septic embolism in the lungs and other organs after acute oropharyngeal infection. It was named after André-Alfred Lemierre in 1936.

Case summary: Here, we have reported a case of Lemierre's syndrome in a 56-year-old female patient who presented with a sore throat. The patient had septic shock, had not voided, and had severe hyperglycemia at the time of her visit. Imaging tests revealed bilateral pneumonia, pleural effusion, pulmonary embolism, and renal vein thrombosis. The patient was admitted to the intensive care unit and placed on mechanical ventilation due to acute respiratory distress syndrome. Continuous renal replacement therapy was administered to treat renal failure with anuria. Klebsiella pneumoniae was cultured from blood and sputum samples. After reviewing various results, the patient was ultimately diagnosed with Lemierre's syndrome. The patient was treated with appropriate antibiotics and thrombolytic agents. She was discharged from the hospital after recovery.

Conclusion: Lemierre's syndrome is associated with a high mortality rate. Therefore, clinicians should be familiar with the signs and symptoms of this disease as well as the preemptive examinations, procedures, and treatments.

Nephrotic syndrome (NS) is relatively common in children, with most of its histological types being minimal changed disease. Its etiology has long been attributed to lymphocyte (especially T-cell) dysfunction, while T-cell-mediated vascular hyperpermeability increases protein permeability in glomerular capillaries, leading to proteinuria and hypoproteinemia. Based on this etiology, steroids and immunosuppressive drugs that are effective against this disease have also been considered to correct T-cell dysfunction. However, in recent years, this has been questioned. The primary cause of NS has been considered damage to glomerular epithelial cells and podocyte-related proteins. Therefore, we first describe the changes in expression of molecules involved in NS etiology, and then describe the mechanism by which abnormal expression of these molecules induces proteinuria. Finally, we consider the mechanism by which infection causes the recurrence of NS.