Chronic kidney disease is estimated to affect approximately 10 to 15% of the Chinese population. Renal fibrosis is characterized by progressive extracellular matrix deposition in the kidney parenchyma with eventual tissue scarring and inevitable deterioration of renal function. Vascular rarefaction, glomerulosclerosis, interstitial inflammation, and fibrogenesis are associated with or contribute to renal fibrosis. Recent studies have revealed that glial cell-derived neurotrophic factor (GDNF) is involved in kidney morphogenesis and amelioration of renal injury. Ideal therapies targeting the pathogenesis of renal fibrosis should have the potential to inhibit glomerular and tubulointerstitial fibrosis by targeting multiple pathological events. GDNF plays a unique role in both renal development and improvement of renal fibrosis, and GDNF kidney receptors and signaling pathways can ameliorate renal apoptosis and inflammation. Our work contributes to the establishment of GDNF as an emerging therapy that can increase the effectiveness of currently used interventions to improve renal fibrosis. This literature review focuses on the important role of GDNF in renal development and its relationship with renal fibrosis.

Chronic kidney disease is estimated to affect approximately 10 to 15% of the Chinese population. Renal fibrosis is characterized by progressive extracellular matrix deposition in the kidney parenchyma with eventual tissue scarring and inevitable deterioration of renal function. Vascular rarefaction, glomerulosclerosis, interstitial inflammation, and fibrogenesis are associated with or contribute to renal fibrosis. Recent studies have revealed that glial cell-derived neurotrophic factor (GDNF) is involved in kidney morphogenesis and amelioration of renal injury. Ideal therapies targeting the pathogenesis of renal fibrosis should have the potential to inhibit glomerular and tubulointerstitial fibrosis by targeting multiple pathological events. GDNF plays a unique role in both renal development and improvement of renal fibrosis, and GDNF kidney receptors and signaling pathways can ameliorate renal apoptosis and inflammation. Our work contributes to the establishment of GDNF as an emerging therapy that can increase the effectiveness of currently used interventions to improve renal fibrosis. This literature review focuses on the important role of GDNF in renal development and its relationship with renal fibrosis.

Chronic kidney disease is estimated to affect approximately 10 to 15% of the Chinese population. Renal fibrosis is characterized by progressive extracellular matrix deposition in the kidney parenchyma with eventual tissue scarring and inevitable deterioration of renal function. Vascular rarefaction, glomerulosclerosis, interstitial inflammation, and fibrogenesis are associated with or contribute to renal fibrosis. Recent studies have revealed that glial cell-derived neurotrophic factor (GDNF) is involved in kidney morphogenesis and amelioration of renal injury. Ideal therapies targeting the pathogenesis of renal fibrosis should have the potential to inhibit glomerular and tubulointerstitial fibrosis by targeting multiple pathological events. GDNF plays a unique role in both renal development and improvement of renal fibrosis, and GDNF kidney receptors and signaling pathways can ameliorate renal apoptosis and inflammation. Our work contributes to the establishment of GDNF as an emerging therapy that can increase the effectiveness of currently used interventions to improve renal fibrosis. This literature review focuses on the important role of GDNF in renal development and its relationship with renal fibrosis.

Chronic kidney disease is estimated to affect approximately 10 to 15% of the Chinese population. Renal fibrosis is characterized by progressive extracellular matrix deposition in the kidney parenchyma with eventual tissue scarring and inevitable deterioration of renal function. Vascular rarefaction, glomerulosclerosis, interstitial inflammation, and fibrogenesis are associated with or contribute to renal fibrosis. Recent studies have revealed that glial cell-derived neurotrophic factor (GDNF) is involved in kidney morphogenesis and amelioration of renal injury. Ideal therapies targeting the pathogenesis of renal fibrosis should have the potential to inhibit glomerular and tubulointerstitial fibrosis by targeting multiple pathological events. GDNF plays a unique role in both renal development and improvement of renal fibrosis, and GDNF kidney receptors and signaling pathways can ameliorate renal apoptosis and inflammation. Our work contributes to the establishment of GDNF as an emerging therapy that can increase the effectiveness of currently used interventions to improve renal fibrosis. This literature review focuses on the important role of GDNF in renal development and its relationship with renal fibrosis.

Chronic kidney disease is estimated to affect approximately 10 to 15% of the Chinese population. Renal fibrosis is characterized by progressive extracellular matrix deposition in the kidney parenchyma with eventual tissue scarring and inevitable deterioration of renal function. Vascular rarefaction, glomerulosclerosis, interstitial inflammation, and fibrogenesis are associated with or contribute to renal fibrosis. Recent studies have revealed that glial cell-derived neurotrophic factor (GDNF) is involved in kidney morphogenesis and amelioration of renal injury. Ideal therapies targeting the pathogenesis of renal fibrosis should have the potential to inhibit glomerular and tubulointerstitial fibrosis by targeting multiple pathological events. GDNF plays a unique role in both renal development and improvement of renal fibrosis, and GDNF kidney receptors and signaling pathways can ameliorate renal apoptosis and inflammation. Our work contributes to the establishment of GDNF as an emerging therapy that can increase the effectiveness of currently used interventions to improve renal fibrosis. This literature review focuses on the important role of GDNF in renal development and its relationship with renal fibrosis.

Background/Aims: Roxadustat, an oral medication for treating renal anemia, is a hypoxia-inducible factor prolyl hydroxylase inhibitor used for regulating iron metabolism and promoting erythropoiesis. To investigate the efficacy and safety of roxadustat in patients undergoing peritoneal dialysis (PD) with erythropoietin hyporesponsiveness. Methods: Single-center, retrospective study, 81 PD patients (with erythropoietin hyporesponsiveness) were divided into the roxadustat group (n = 61) and erythropoiesis-stimulating agents (ESAs) group (n = 20). Hemoglobin (Hb), total cholesterol, intact parathyroid hormone (iPTH), brain natriuretic peptide (BNP), related indicators of cardiac function and high-sensitivity C-reactive protein (hs-CRP) were collected. Additionally, adverse events were also recorded. The follow-up period was 16 weeks. Results: The two groups exhibited similar baseline demographic and clinical characteristics. At baseline, the roxadustat group had a mean Hb level of 89.8 ± 18.9 g/L, while the ESAs group had a mean Hb level of 95.2 ± 16.0 g/L. By week 16, the Hb levels had increased to 118 ± 19.8 g/L (p < 0.05) in the roxadustat group and 101 ± 19.3 g/L (p > 0.05) in the ESAs group. The efficacy of roxadustat in improving anemia was not influenced by baseline levels of hs-CRP and iPTH. Cholesterol was decreased in the roxadustat group without statin use. An increase in left ventricular ejection fraction and stabilization of BNP were observed in the roxadustat group. Conclusions For PD patients with erythropoietin hyporesponsiveness, roxadustat can significantly improve renal anemia. The efficacy of roxadustat in improving renal anemia was not affected by baseline levels of hs-CRP0 and iPTH.

The incidence of chronic kidney disease (CKD) is increasing worldwide and the current prevalence rate is 13.4%. There are > 120 million CKD patients in China and this number is expected to increase. One of the main abnormalities in patients with CKD and kidney impairment is decreased synthesis of erythropoietin (EPO), which causes anemia and affects iron metabolism. The probability of developing is higher in anemia patients with CKD than in the general population, and the incidence increases as kidney function decreases. Deficient EPO production by the kidney is the most important cause of renal anemia. Notably, anemia in patients with CKD has multiple causes, such as bleeding caused by platelet dysfunction, iron deficiency due to digestive and absorption disorders of the gastrointestinal tract, and shorter red blood cell life. Anemia is also a leading cause of hospitalization in patients with CKD. A new oral medication to treat renal anemia, the hypoxia-inducible factor prolyl hydroxylase inhibitor called roxadustat (FG-4592), regulates iron metabolism and promotes erythropoiesis. This drug has a therapeutic effect on patients with CKD. Roxadustat showed advantages over EPO in clinical experiments. This review summarizes the mechanisms of action, clinical applications, effectiveness, and safety of roxadustat.

Discordant lymphoma (DL) is the coexistence of two or more distinct subtypes in separate anatomic sites. There are limited reports on DL cases especially involving more than two subtypes in more than two sites. We report a 76-year-old man who presented with constitutional symptoms, flank mass and painless lymphadenopathies for six months. Laboratory tests revealed moderate anaemia, markedly elevated serum IgM (13400 mg/dL), IgM Lambda paraproteinemia and Lambda light chain paraproteinuria with unmeasurable serum lactate dehydrogenase due to hyperviscous sample. CT scan showed multiple subcutaneous masses over chest wall and retroperitoneum, with lytic bone lesions, and hepatosplenomegaly. Further biopsy findings with morphological, immunohistochemical and molecular analysis of the tissue sections revealed diffuse large B-Cell lymphoma in the chest wall mass, follicular lymphoma in the inguinal lymph node and lymphoplasmacytic lymphoma in the bone marrow. This case highlights the rare DL. The importance of histopathological evaluation of lymphoma despite the availability of PET-CT scans for disease staging is undeniable.

Previous research has investigated whether hyperuricemia serves as an independent risk factor for cardiovascular and renal diseases. Hyperuricemia is defined as an abnormally high level of uric acid (UA; i.e., serum urate level > 6.8 mg/dL). Hyperuricemia has been considered a complication of chronic kidney disease (CKD). However, it seems to play a pathogenic role in the progression of renal diseases. There has been increasing focus on the link between hyperuricemia and CKD. The results of randomized controlled trials have implied independent associations between hyperuricemia and the progression of cardiovascular and renal morbidities. These associations may be mediated by renin-angiotensin system activation, nitric oxide synthase inhibition, and macrovascular/microvascular disease development. There remains controversy regarding the use of serum UA level as an indirect index of renal vascular disease. This literature review focuses on the role of asymptomatic hyperuricemia in the progression of CKD, as well as the association between hyperuricemia and cardiovascular disease. It also provides a general overview of the physiological metabolism of UA.

Objective: Acorus calamus (AC) L. (Araceae) is an annual semi-aquatic and aromatic plant found in Europe, North America and Asia. Its rhizomes are often used by Native Americans, Americans, and Chinese as well as by other cultures. Ethnobotanical studies and documents have shown their use in various disease treatments, such as insomnia, mental disorders, diabetes mellitus, epilepsy, inflamma-tion, asthma, neuropathic pain, and diarrhea. In this study, the antidepressant activity of methanolic and hydroalcoholic extracts of the AC rhizome part in mice was investigated. Methods: Three doses of methanolic extract of AC rhizome (MEACR) (25, 50 and 100 mg/kg b.wt), three doses of hydroalcoholic extract of AC rhizome (HAACR) (100, 200 and 400 mg/kg b.wt), and standards (imipramine, 15 mg/kg b.wt and fluoxetine, 20 mg/kg b.wt) was daily oral administration to the mice for consecutive 14 days. The extract effect on the immobility time was monitored by a tail suspension test (TST) and a forced swimming test (FST). Monoamine oxidase (MAO) levels were also analyzed using standard methods. Results: The optimum antidepressant activity was viewed at 100 mg/kg b.wt of MEACR extract and 400 mg/kg b.wt of HAACR extract with 23.82％ and 20.59％ immobility period reduction, respectively. Besides, the extracts weakened the FST-induced elevation of MAO activity significantly and returned to near-normal levels of neurotransmitters in the brain. 100 mg/kg b.wt or above of MEACR extract significantly prevented the MAO-A and MAO-B activities in mice brain at a dose-dependent fashion. But, just 400 mg/kg b.wt of HAACR extract prevented the activity of MAO-A and MAO-B. Fluoxetine and imipramine showed a tendency to prevent the activity of MAO-A and MAO-B. Conclusion: This study suggests that AC rhizome extract mediated antidepressant activity by modulating the central neurochemical and hypothalamic-pituitary-adrenal (HPA) axis in response to FST and TST-induced stress. Therefore, AC rhizome extract can be used as a valuable plant supplement to treat depressive disorders.