OBJECTIVE: To observe the therapeutic effect of governor vessel moxibustion combined with wenyang yiqi qiwei decoction on erectile dysfunction (ED) with spleen-kidney deficiency and to explore the possible mechanism. METHODS: A total of 130 ED patients with spleen-kidney deficiency were randomized into an observation group (65 cases, 2 cases dropped off) and a control group (65 cases, 3 cases dropped off). The control group was given wenyang yiqi qiwei decoction orally, one dose daily. On the basis of the treatment in the control group, governor vessel moxibustion was applied from Dazhui (GV 14) to Yaoshu (GV 2) in the observation group, 110 min a time, once a day. The treatment of 4 weeks was required in both groups. Before and after treatment, 5-question international index of erectile function (IIEF-5) score, erection quality scale (EQS) score, erectile hardness assessment (EHS) score, TCM syndrome score, serum testosterone (T) level and vascular endothelial function indexes (prostaglandin I2 [PGI2], endothelin-1 [ET-1] and nitric oxide [NO] levels) were observed respectively, and the clinical efficacy was evaluated in both groups. RESULTS: After treatment, the scores of IIEF-5, EQS, EHS and serum levels of T, PGI2, NO were increased compared before treatment (P<0.01), the TCM syndrome scores and serum ET-1 levels were decreased compared before treatment (P<0.01) in the two groups; the scores of IIEF-5, EQS, EHS and serum levels of T, PGI2, NO in the observation group were higher than those in the control group (P<0.01, P<0.05), the TCM syndrome score and serum ET-1 level were lower than those in the control group (P<0.01, P<0.05). The total effective rate was 88.9% (56/63) in the observation group, which was superior to 74.2% (46/62) in the control group (P<0.05). CONCLUSION Governor vessel moxibustion combined with wenyang yiqi qiwei decoction can improve the erectile function and increase the erection hardness and quality in ED patients with spleen-kidney deficiency, its mechanism may relate to improving serum T level and vascular endothelial function.
Humans ; Male ; Administration, Oral ; Drugs, Chinese Herbal/therapeutic use* ; Erectile Dysfunction/therapy* ; Kidney/pathology* ; Kidney Diseases/complications* ; Moxibustion ; Spleen/pathology* ; Splenic Diseases/complications* ; Testosterone/blood* ; Combined Modality Therapy

OBJECTIVE: Small ubiquitin-related modifiers (SUMOs) are a group of post-translational modification proteins extensively expressed in eukaryotes. Abnormal SUMOylation can lead to the development of various diseases. This article summarizes the progress on research of the role of SUMOs in various types of kidney diseases to further increase the understanding of the regulatory functions of SUMOylation in the pathogenesis of kidney diseases. DATA SOURCES: This review was based on articles published in the PubMed databases up to January 2018, using the keywords including "SUMOs," "SUMOylation," and "kidney diseases." STUDY SELECTION: Original articles and critical reviews about SUMOs and kidney disease were selected for this review. A total of 50 studies were in English. RESULTS: SUMO participates in the activation of NF-κB inflammatory signaling pathway, playing a central regulatory role in the inflammation and progression of DN, and the secretion of various chemokines in AKI. SUMO involves in the regulation of TG2 and Nrf2 antioxidant stress, affecting renal tubular injury in AKI. SUMO affects the MAPK/ERK pathway, regulating intracellular signal transduction, modulating the transcription and expression of effector molecules in DN. SUMO contributes to the TGF-β/Smad pathway, leading to fibrosis of the kidney. The conjugate combination of SUMO and p53 regulates cell proliferation and apoptosis, and participates in the regulation of tumorigenesis. In addition, SUMOylation of MITF modulates renal tumors secondary to melanoma, Similarly, SUMOylation of tumor suppressor gene VHL regulates the occurrence of renal cell carcinoma in VHL syndrome. CONCLUSIONS Tissue injury, inflammatory responses, fibrosis, apoptosis, and tumor proliferation in kidney diseases all involve SUMOs. Further research of the substrate SUMOylation and regulatory mechanisms of SUMO in kidney diseases will improve and develop new treatment measures and strategies targeting kidney diseases.
Acute Kidney Injury ; etiology ; Carcinoma, Renal Cell ; etiology ; Diabetic Nephropathies ; etiology ; Fibrosis ; Humans ; Kidney ; pathology ; Kidney Diseases ; etiology ; metabolism ; Kidney Neoplasms ; etiology ; SUMO-1 Protein ; physiology ; Sumoylation

OBJECTIVE: To observe the effect of Quyu Chencuo Formula (, QCF) on renal fibrosis in rats with obstructive nephropathy. METHODS: Twenty-four rats were randomly divided into three groups, 4 for sham operation as the control group, 10 for unilateral ureteral obstruction (UUO) model group, and the rest 10 for QCF treating UUO model group. All rats were sacrificed under 3% pentobarbital (50 mg/kg) anesthesia on the 14th day after surgery, then the right kidney samples of rats were harvested for hematoxylin eosin (HE) staining and Masson staining to observe the renal pathological changes. Immunohistochemistry and Western blotting were used to examine the expression of transforming growth factor β1 (TGF-β1), and real-time polymerase chain reaction (RT-PCR) was employed to examine the expressions of TGF-β1, α-smooth muscle actin (α-SMA) and E-cadherin mRNA. RESULTS: HE and Masson staining showed that the renal interstitial of the rats in the control group had no significant fibrotic lesion; in the model group, there were obvious interstitial fibrosis; for the QCF group, there were epithelial cell necrosis, infiltration of lymphocytes and mononuclear cells, aggravated interstitial fibrosis in varied degrees, but the pathological changes were less in the QCF group than in the model group. The immunohistochemistry and Western blotting results showed that the TGF-β1 expression was increased significantly in the model group, while decreased significantly in the QCF group (P<0.05); RT-PCR showed that the mRNA expression of α-SMA and TGF-β1 increased significantly in the model group, while both were significantly decreased in the QCF group compared with the model group (P<0.05). The mRNA expression of E-cadherin was decreased significantly in the model group, and it was significantly increased in the QCF group as compared with the model group (P<0.05). CONCLUSION QCF may improve renal fibrosis by regulating the expressions of TGF-β1, α-SMA and E-cadherin, and prevent the progress of kidney fibrosis.
Actins ; genetics ; Animals ; Cadherins ; genetics ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Fibrosis ; Kidney ; pathology ; Kidney Diseases ; drug therapy ; metabolism ; pathology ; Male ; RNA, Messenger ; analysis ; Rats ; Rats, Wistar ; Transforming Growth Factor beta1 ; genetics

The expression or dysfunction of long non-coding RNAs (lncRNAs) is closely related to various hereditary diseases, autoimmune diseases, metabolic diseases and tumors. LncRNAs were also recently recognized as functional regulators of fibrosis, which is a secondary process in many of these diseases and a primary pathology in fibrosis diseases. We review the latest findings on lncRNAs in fibrosis diseases of the liver, myocardium, kidney, lung and peritoneum. We also discuss the potential of disease-related lncRNAs as therapeutic targets for the clinical treatment of human fibrosis diseases.
Autoimmune Diseases ; Fibrosis ; Genetic Diseases, Inborn ; Humans ; Kidney ; Liver ; Lung ; Metabolic Diseases ; Myocardium ; Pathology ; Peritoneum ; RNA, Long Noncoding

Biopsy ; Female ; Glomerular Basement Membrane ; metabolism ; Hashimoto Disease ; metabolism ; pathology ; Humans ; Kidney Diseases ; metabolism ; pathology ; Middle Aged ; Proteinuria ; metabolism ; pathology ; Sjogren's Syndrome ; metabolism ; pathology

Background: Diabetes mellitus (DM) has become the leading cause of chronic kidney disease (CKD). Nondiabetic renal diseases (NDRDs) have different clinicopathological features and prognosis from those of diabetic nephropathy. Our study sought to analyze the clinical and pathological features of NDRDs, in different age groups through a cross-sectional study. Methods: All patients with type 2 DM at our center who underwent renal biopsy between March 1997 and March 2017 were screened and divided into three groups by age: Group 1 (youth group), 18-44 years old; Group 2 (middle-aged group), 45-59 years old; and Group 3 (elderly group), ≥60 years old. We analyzed the clinicopathological data and risk factors by univariate and multivariate logistic regression for NDRD of the patients to identify the features of NDRD in different age groups. Results: We included 982 patients in the final analysis. Patients with NDRD accounted for 64.4% of all patients. IgA nephropathy (IgAN) was the most common pathological pattern in young patients with NDRD, accounting for 26.3%. In the middle-aged group, the two most common pathological patterns were IgAN and membranous nephropathy. Membranous nephropathy was the most common pathological pattern in elderly patients with NDRD, accounting for 29.3%. Consistent with pathological features, glomerular hematuria is a risk factor for NDRD in Group 1 (odds ratio [OR], 26.514; 95% confidence interval [CI], 2.503-280.910; P = 0.006). On the other hand, rapidly increasing proteinuria or nephrotic syndrome is a risk factor for NDRD in Group 2 (OR, 5.921; 95% CI, 2.061-17.013; P = 0.001) and Group 3 (OR, 90.409; 95% CI, 6.198-1318.826; P = 0.001). Conclusions This single-center study showed that the proportion and composition of NDRD differ among different age groups. Consistent with pathological features, some clinical indices such as hematuria and proteinuria showed different features among different age groups.
Adult ; Age Factors ; Aged ; Cross-Sectional Studies ; Diabetic Nephropathies ; pathology ; Female ; Glomerulonephritis, IGA ; pathology ; Humans ; Kidney Diseases ; pathology ; Logistic Models ; Male ; Middle Aged

Biomarkers ; urine ; Cross-Sectional Studies ; Diabetes Mellitus, Type 2 ; pathology ; urine ; Enzyme-Linked Immunosorbent Assay ; Hepatitis A Virus Cellular Receptor 1 ; metabolism ; Humans ; Intracellular Signaling Peptides and Proteins ; urine ; Kidney Diseases ; pathology ; urine ; Lipocalin-2 ; urine ; Membrane Proteins ; urine ; Sialoglycoproteins ; urine ; Tissue Inhibitor of Metalloproteinase-2 ; urine

Renal anemia, mainly caused by the deficiencies of erythropoietin (EPO) and iron metabolism disorder, is one of the most common complications of chronic kidney disease. Hypoxia-inducible factor (HIF) is a class of transcription factors responsible for maintaining homeostasis during oxygen deprivation. In normoxia, HIF is degraded by prolyl hydroxylase (PHD). While under hypoxic conditions, the hydroxylation activity of PHD is inhibited, and the cellular concentration of HIF is elevated, resulting in an increase in endogenous EPO production and iron absorption. Therefore, this regulating pathway, also termed as the HIF-PHD axis, has become a promising therapeutic target of treating renal anemia. Several innovative drugs acting as selective HIF-PHD inhibitors have been successfully developed in the past years, and some of them are undergoing clinical trials. In this review, we will introduce the definition and regulatory mechanism of HIF-PHD axis, as well as current insights into its physiologic and therapeutic role in renal anemia.
Anemia ; enzymology ; pathology ; Humans ; Hypoxia ; pathology ; Hypoxia-Inducible Factor 1 ; metabolism ; Kidney Diseases ; enzymology ; pathology ; Oxygen ; Prolyl Hydroxylases ; metabolism

Transforming growth factor-β (TGF-β) is a driving force of renal fibrosis, which may lead to chronic kidney diseases and even end stage renal diseases. By activating canonical and non-canonical signaling pathways, TGF-β promotes the synthesis of extracellular matrix while preventing their degradation. In the injured kidney, TGF-β induces apoptosis, proliferation and fibrotic response of renal cells including epithelial cells, endothelial cells, podocytes, fibroblasts, pericytes and macrophages, and it also promotes transdifferentiation, activation and proliferation of myofibroblasts. Additionally, TGF-β exerts profibrotic effects by interplaying with other signaling pathways like BMP-7, Wnt/β-catenin and MAP kinase. Smad3 is the central pathological gene in renal fibrosis, and epigenetic regulation of TGF-β/Smad3 is a hot topic in kidney field. Although direct targeting TGF-β may cause side effects including tumorigenesis and immune diseases, the therapeutic strategies targeting the balance of downstream Smad3 and Smad7 may prevent or delay the progression of fibrotic kidney disease.
Epigenesis, Genetic ; Fibrosis ; Humans ; Kidney Diseases ; pathology ; Signal Transduction ; Smad3 Protein ; metabolism ; Smad7 Protein ; metabolism ; Transforming Growth Factor beta ; metabolism

Congenital renal arteriovenous fistula complicated with multiple renal arteries malformation is rare and hard to diagnose at early stage. Blood loss and complications after embolization are both severe. Some cases can be diagnosed by ultrasound, enhanced CT scan or digital subtraction angiography (DSA). Cystoscopy and ureteroscopy can identify the location of bleeding, exclude tumors, and discharge ureteral obstruction. A case of congenital renal arteriovenous fistula complicated with multiple renal arteries malformation was reported to investigate the pathogenesis, clinical characteristics, diagnosis and treatment of congenital renal arteriovenous fistula with multiple renal arteries malformation. A 36-year-old female patient with congenital renal arteriovenous fistula with multiple renal arteries malformation was hospitalized in the Department of Urology of Peking University People's Hospital. Five days before admission, the patient experienced whole course painless gross hematuria for 5 days with many blood clots. The patient's blood pressure was 90/70 mmHg, and hemoglobin was 60 g/L. The urinary CT scan showed a right hydronephrosis associated with dilatation of the upper ureter which was obstructed by space occupying lesion of the lower ureter. Many clots in the bladder could also be found in the CT scan. Cystoscopy showed many blood clots in the bladder and confirmed that the bleeding was fromthe right ureteral orifice. Ureteroscopy confirmed that the bleeding was from the right renal pelvis and many blood clots in the right ureter, and found no tumor in the right ureter and renal pelvis. We cleared the blood clots in the right ureter and inserted a ureteral stent.We thought that renal vascular malformation of the right kidney might lead to the hematuria from right renal pelvis. DSA showed a double renal arteries malformation in the right kidney. The diagnosis of "renal arteriovenous fistula" was considered with renal arteriovenous fistula in the right kidney. Selective arteriography revealed the presence of tortuous, coiled, dilated, and multichannelled vessels in the middle of the right kidney. With stainless steel coils, we embolized the vessels which supplied the fistula. Four days after the procedure, gross hematuria disappeared. Five days after the procedure, the patient's anemia improvedand the patient was discharged in good condition. Four months after the procedure, gross hematuria did not recur. The Doppler showed that the right kidney was normal and the renal dynamic showed that the right kidney function was normal. So DSA is the golden standard for diagnosis of congenital renal arteriovenous fistula complicated with multiple renal arteries malformation. Confirming the number of renal arteries by abdominal aorta angiography is necessary to avoid missed diagnosis. Renal arterial embolization is safe and effective.
Adult ; Arteriovenous Fistula/therapy* ; Embolization, Therapeutic ; Female ; Humans ; Kidney ; Kidney Diseases/therapy* ; Renal Artery/pathology* ; Ureteral Diseases