scholarly journals Moxibustion Alleviates Injury in a Rat Focal Segmental Glomerulosclerosis Model

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Yi Li ◽  
Yuxia Sun ◽  
Chunling Zhang ◽  
Ke Wang ◽  
Peicheng Shen ◽  
...  
Keyword(s):  
Focal Segmental Glomerulosclerosis ◽  
Rat Model ◽  
Interstitial Fibrosis ◽  
Similar Efficacy ◽  
Glomerular Sclerosis ◽  
Control Group ◽  
Therapeutic Effects ◽  
Repeated Injection ◽  
Moxibustion Group ◽  
Segmental Glomerulosclerosis

Objectives. To evaluate the therapeutic effects of moxibustion at Shenshu (BL-23) and Geshu (BL-17) acupoints in a focal segmental glomerulosclerosis (FSGS) model in rats. Methods. A FSGS rat model was established by single nephrectomy and repeated injection of doxorubicin. The FSGS rats were randomly divided into the model group, losartan (positive control) group, Shenshu moxibustion group, and Geshu moxibustion group. Molecular indicators of kidney function and renal pathological changes were monitored. Results. Urinary protein, serum creatinine, urea nitrogen, and serum uric acid were significantly reduced after 12-week intervention with losartan, Shenshu, or Geshu moxibustion. Renal α-SMA, FN, and TGF-β were also decreased, while podocin and nephrin protein and mRNA were increased. The pathological damage in renal tissue was obviously alleviated by all three treatments, which suggests that moxibustion may have similar efficacy to losartan in the treatment of FSGS. Conclusion. Moxibustion alleviates podocyte injury and inhibits renal interstitial fibrosis in the FSGS rat model, thereby minimizing the progression of glomerular sclerosis and improving renal function.

scholarly journals Assessment of Toxicity and Therapeutic Effects of Goose Bone in a Rat Model

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Md. Yousuf Ali ◽  
Alamgir Kabir ◽  
Shahad Saif Khandker ◽  
Tareq Hossan ◽  
Md. Salman Shakil ◽  
...  
Keyword(s):  
Rat Model ◽  
Biochemical Parameters ◽  
Hematological Parameters ◽  
Atherogenic Index ◽  
Control Group ◽  
Histopathological Study ◽  
Therapeutic Effects ◽  
Related Disorder ◽  
Serum Biochemical ◽  
Hematological And Biochemical Parameters

Goose bone is traditionally used in the treatment of many ailments including in bone fracture. The aim of the present study was to evaluate the subacute toxicity of goose bone in a rat model by investigating some hematological and biochemical parameters in rats. Subsequently, a histopathological study was performed to confirm the presence of pathological lesions in the rat’s vital organs including the liver, kidney, heart, brain, pancreas, lung, spleen, and stomach. Adult Wistar rats were divided into four groups (n = 8) and were orally administrated with three doses (30, 60, and 120 mg/kg) of goose bone once daily for 21 days as compared to control animals (received only drinking water). Goose bone did not cause any significant changes on body weight, relative organ weight, and percentage water content at any of the administered doses. There were also no significant alterations in hematological parameters seen. All three doses administered significantly reduced the triglyceride levels as well as the atherogenic index of plasma (AIP). Animals treated with 120 mg/kg doses had significantly reduced alkaline phosphatase (ALP) activity as compared to the control group. There was no significant alteration on other serum biochemical parameters seen. Additionally, histopathological findings confirmed that there was no inflammatory, necrotic, or other toxicological feature seen for all three doses. It is concluded that goose bone is nontoxic and is safe for consumption besides having the potential to be investigated for the treatment of high triglycerides or liver-related disorder.

scholarly journals Lithium Nephrotoxicity

2000 ◽  
Vol 11 (8) ◽  
pp. 1439-1448 ◽  
Author(s):  
GLEN S. MARKOWITZ ◽  
JAI RADHAKRISHNAN ◽  
NEERAJA KAMBHAM ◽  
ANTHONY M. VALERI ◽  
WILLIAM H. HINES ◽  
...  
Keyword(s):  
Serum Creatinine ◽  
Focal Segmental Glomerulosclerosis ◽  
Interstitial Fibrosis ◽  
Renal Cysts ◽  
Significant Degree ◽  
Fisher Exact Test ◽  
Tubular Atrophy ◽  
Segmental Glomerulosclerosis ◽  
Tubulointerstitial Nephropathy ◽  
Collecting Tubules

Abstract. This study examines the clinical features, pathologic findings, and outcome of 24 patients with biopsy-proven lithium toxicity. The patient population was 50% male, 87.5% Caucasian, and had a mean age of 42.5 yr (range, 26 to 57). Mean duration of lithium therapy for bipolar disorder was 13.6 yr (range, 2 to 25). All patients were biopsied for renal insufficiency (mean serum creatinine 2.8 mg/dl; range, 1.3 to 8.0), with associated proteinuria >1.0 g/d in 41.7%. Nephrotic proteinuria (>3.0 g/d) was present in 25%. Other features included nephrogenic diabetes insipidus in 87% and hypertension in 33.3%. Renal biopsy revealed a chronic tubulointerstitial nephropathy in 100%, with associated cortical and medullary tubular cysts (62.5%) or dilatation (33.3%). All of the renal cysts stained for epithelial membrane antigen, while 51.4% stained with lectin Arachis hypogaea, and only 3.8% stained with Tetragonolobus purpureas, indicating they originated from distal and collecting tubules. The degree of tubular atrophy and interstitial fibrosis was graded as severe in 58.3%, moderate in 37.5%, and mild in 4.2% of cases. There was a surprisingly high prevalence of focal segmental glomerulosclerosis (50%) and global glomerulosclerosis (100%), sometimes of equivalent severity to the chronic tubulointerstitial disease. The significant degree of foot process effacement (mean 34%, five of 14 cases with >50%) suggests a potential direct glomerular toxicity. Focal segmental glomerulosclerosis correlated with proteinuria >1.0 g/d (P= 0.0014, Fisher exact test). Despite discontinuation of lithium, seven of nine patients with initial serum creatinine values >2.5 mg/dl progressed to end-stage renal disease (ESRD). Only three patients, all with initial serum creatinine <2.1 mg/dl, had subsequent improvement in renal function. By Kaplan-Meier survival analysis, the only significant predictor of progression to ESRD was serum creatinine >2.5 mg/dl at biopsy (P= 0.008). In conclusion, lithium nephrotoxicity primarily targets distal and collecting tubules, with a higher incidence of proteinuria and associated glomerular pathology than recognized previously. Renal dysfunction is often irreversible despite lithium withdrawal, and early detection is essential to prevent progression to ESRD.

scholarly journals Case Report: Glucocorticoids Combined With Immunosuppressant in the Treatment of Acromegaly Complicated With Focal Segmental Glomerulosclerosis

2021 ◽  
Vol 7 ◽  
Author(s):  
Ruiqiang Wang ◽  
Yunqi Wu ◽  
Dongyue An ◽  
Pupu Ma ◽  
Yuanyuan Guo ◽  
...  
Keyword(s):  
Focal Segmental Glomerulosclerosis ◽  
Experimental Studies ◽  
Urinary Protein ◽  
Glomerular Sclerosis ◽  
Not Otherwise Specified ◽  
Segmental Glomerulosclerosis ◽  
Body Tissues ◽  
Progression Of Kidney Disease ◽  
Factor Type ◽  
Excessive Secretion

Background: Acromegaly is a chronic disease caused by excessive secretion of growth hormone (GH), which circulates and stimulates the liver and body tissues to produce insulin-like growth factor type 1 (IGF-1). Experimental studies have shown that excessive secretion of GH is related to glomerular sclerosis, and elevated IGF-1 levels may be involved in the occurrence of glomerular hypertrophy. But relevant clinical cases are rare. Here, we reported a case of acromegaly complicated with focal segmental glomerulosclerosis (FSGS).Case Presentation: A 49-year-old man was admitted to our hospital because of acromegaly for more than 10 years and proteinuria for more than 3 years. Acromegaly was confirmed by contrast-enhanced magnetic resonance imaging, minimally invasive surgery and pathology. The results of renal biopsy showed FSGS-NOS (not otherwise specified) with ischemic renal injury and mesangial IgA deposition. One month after transnasal transsphenoidal space occupying resection, GH and urinary protein decreased significantly, and nephropathy was partially relieved. In the next 4 months, GH stabilized at the normal level, while urinary protein gradually increased. When the urinary protein increased to 4.2 g/d, the dosage of glucocorticoids increased to 20 mg/d, and tacrolimus 1 mg/d were added, and the urinary protein decreased again. However, when the urinary protein decreased to 0.43 g/d, the patient stopped taking glucocorticoids and tacrolimus, and the urinary protein increased to 2.85 g/d after 8 months, but the GH was still in the normal range.Conclusion: In this case, GH is partially involved in the formation of FSGS. Not only does surgery reduce the effects of GH, but low doses of glucocorticoids and immunosuppressant are effective in slowing the progression of kidney disease, at least in reducing urinary protein.

scholarly journals Sex and kidney ACE2 expression in primary focal segmental glomerulosclerosis: A NEPTUNE study

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252758
Author(s):  
Nicholas A. Maksimowski ◽  
James W. Scholey ◽  
Vanessa R. Williams ◽  
Keyword(s):  
Kidney Disease ◽  
Focal Segmental Glomerulosclerosis ◽  
Current Knowledge ◽  
Interstitial Fibrosis ◽  
Linear Regression Analysis ◽  
Renin Angiotensin System ◽  
Multiple Linear Regression Analysis ◽  
Tubular Atrophy ◽  
Kidney Fibrosis ◽  
Segmental Glomerulosclerosis

Background Angiotensin-converting enzyme 2 (ACE2) has been implicated in the pathogenesis of experimental kidney disease. ACE2 is on the X chromosome, and in mice, deletion of ACE2 leads to the development of focal segmental glomerulosclerosis (FSGS). The relationship between sex and renal ACE2 expression in humans with kidney disease is a gap in current knowledge. Methods We studied renal tubulointerstitial microarray data and clinical variables from subjects with FSGS enrolled in the Nephrotic Syndrome Study Network (NEPTUNE) study. We compared relationships between ACE2 expression and age, estimated glomerular filtration rate (eGFR), urinary albumin to creatinine ratio (UACR), interstitial fibrosis, tubular atrophy, and genes implicated in inflammation and fibrosis in male and female subjects. Results ACE2 mRNA expression was lower in the tubulointerstitium of males compared to females (P = 0.0026). Multiple linear regression analysis showed that ACE2 expression was related to sex and eGFR but not to age or treatment with renin angiotensin system blockade. ACE2 expression is also related to interstitial fibrosis, and tubular atrophy, in males but not in females. Genes involved in inflammation (CCL2 and TNF) correlated with ACE2 expression in males (TNF: r = -0.65, P < 0.0001; CCL2: r = -0.60, P < 0.0001) but not in females. TGFB1, a gene implicated in fibrosis correlated with ACE2 in both sexes. Conclusions Sex is an important determinant of ACE2 expression in the tubulointerstitium of the kidney in FSGS. Sex also influences the relationships between ACE2, kidney fibrosis, and expression of genes involved in kidney inflammation.

scholarly journals An Experimental Study: Benefits of Digoxin on Hepatotoxicity Induced by Methotrexate Treatment

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Banu Taskin ◽  
Mümin Alper Erdoğan ◽  
Gürkan Yiğittürk ◽  
Sibel Alper ◽  
Oytun Erbaş
Keyword(s):  
Rat Model ◽  
Liver Tissue ◽  
Liver Toxicity ◽  
Male Rats ◽  
Control Group ◽  
Therapeutic Effects ◽  
Tissue Samples ◽  
Liver Model ◽  
Tnf Α ◽  
Group 2

Purpose. The aim of the study is to examine the possible therapeutic effects of a known cardiac glycoside, digoxin, on a rat model of MTX-induced hepatotoxicity. Methods. The study was conducted on twenty-four male rats. While eighteen rats received a single dose of 20 mg/kg MTX to obtain an injured liver model, six rats constituted the control group. Also, the eighteen liver toxicity model created rats were equally divided into two groups, one of which received digoxin 0.1 mg/kg/day digoxin (Group 1) and the other group (Group 2) was given saline (% 0.9NaCl) with a dose of 1 ml/kg/day for ten days. Following the trial, the rats were sacrificed to harvest blood and liver tissue samples to determine blood and tissue MDA, serum ALT, plasma TNF-α, TGF-β, IL-6, IL-1-Beta, and PTX3 levels. Results. MTX’s structural and functional hepatotoxicity was observable and evidenced by relatively worse histopathological scores and increased biochemical marker levels. Digoxin treatment significantly reduced the liver enzyme ALT, plasma TNF-α, TGF-β, PTX3, and MDA levels and decreased histological changes in the liver tissue with MTX-induced hepatotoxicity in the rat model. Conclusion. We suggest that digoxin has an anti-inflammatory and antihepatotoxic effect on the MTX-induced liver injury model.

Kidney Outcome in Primary Focal Segmental Glomerulosclerosis (FSGS) by Using a Predictive Model

2020 ◽  
Author(s):  
Shahrzad Ossareh ◽  
Mansoureh Yahyaei ◽  
Mojgan Asgari ◽  
Hanri Afghahi
Keyword(s):  
Kidney Disease ◽  
Predictive Model ◽  
Focal Segmental Glomerulosclerosis ◽  
Interstitial Fibrosis ◽  
Cox Model ◽  
Tubular Atrophy ◽  
Model Interaction ◽  
Segmental Glomerulosclerosis ◽  
End Stage ◽  
Adjusted Model

Abstract Background: Focal segmental glomerulosclerosis (FSGS) is one of the important causes of end stage kidney disease (ESKD). We evaluated the risk factors of progression of primary FSGS to chronic kidney disease (CKD) or ESKD with a predictive model including clinical and histological predictors.Methods: 201 patients with primary FSGS (59% male, mean age: 38±15 years), were studied. Time-dependent Cox model and C statistics were used for the predictive model. Interaction and correlation between independent variables were estimated.Results: During 55±27 months of follow-up, 82 patients (41%) developed CKD (46) or ESKD (36) patients. In adjusted model, 1 unit of higher serum creatinine (SCr) at baseline (HR:1.39, 95%CI: 1.15-1.70) and 1% increase in glomeruli with segmental glomerulosclerosis (SGS) (HR: 1.03, 95% CI: 1.02-1.04) or interstitial fibrosis/tubular atrophy (IF/TA) (HR: 1.03, 95% CI: 1.01-1.05) increased the risk of CKD/ESKD. In adjusted model, higher baseline proteinuria and collapsing variant were not associated with risk of CKD/ESKD. By adding SGS and IF/TA scores to baseline SCr in the model, discrimination by C statistics was 0.83 (95%CI: 0.77-0.90). Median renal survival was 3.1 years (95% CI: 2.2-4.1 years) in patients with highest risks score (baseline eGFR<25 ml/min/1.73 m2+ IF/TA/SGS> 50%), and 8.1 years (95% CI: 7.7-8.6 years).in those with lowest score (baseline eGFR>75 ml/min/1.73 m2+ IF/TA/SGS <5%).Conclusion: In primary FSGS, higher baseline SCr, increased SGS and IF/TA, but not baseline proteinuria and collapsing pathology, were the predictors for CKD/ESKD. These findings indicated the importance of timely detection and referral in prognosis of primary FSGS.

Abstract 514: Jak2 Tyrosine Kinase Mediates Angiotensin II Renal Pathogenesis via its Pressor Dependent Actions

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Peter P Sayeski ◽  
Sung O Park ◽  
Annet Kirabo ◽  
Rebekah Baskin ◽  
Dale M Seth ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renal Injury ◽  
Interstitial Fibrosis ◽  
Critical Role ◽  
Glomerular Sclerosis ◽  
Control Group ◽  
Mrna Levels ◽  
Ang Ii ◽  
Urine Albumin ◽  
Independent Events

We previously found that Jak2 kinase, expressed within vascular smooth muscle cells (VSMC), plays a critical role in angiotensin II (Ang II)-mediated hypertension. Given that Jak2 mediates both pressor-dependent and pressor-independent events, we sought to determine the role of blood pressure (BP), per se, on the deleterious effects of Jak2 within the kidney. To investigate this, three groups of mice were examined; i) wild type mice (Controls) that received Ang II infusion, ii) mice lacking Jak2 expression within the VSMC (VSMC Jak2 Null) that also received Ang II, and iii) Control mice that received Ang II plus an anti-hypertensive triple therapy (3Rx). After baseline BP recordings, Ang II was infused (1000 ng/kg/min, SC) to all groups and the 3Rx regimen (80 mg/L hydralazine, 5 mg/L reserpine, 30 mg/L hydrochlorothiazide in the drinking water) was initiated two days later to the 3Rx group, in order to maintain BP at similar levels to the VSMC Jak2 Null group. After 28 days of Ang II, mice were euthanized and the kidneys were assessed via histological, molecular, and functional approaches. Chronic Ang II infusion significantly increased the levels of intrarenal Ang II in all three groups; Control = 1,262±283 fmol/g, VSMC Jak2 Null = 1,655±666 fmol/g, and 3Rx = 2,174±588. While Ang II infusion significantly increased the mean BP in the Control group (152 ± 2 mm Hg), it was significantly, and similarly, lower in both the VSMC Jak2 Null and 3Rx groups (125 ± 5 mm Hg and 131 ± 5 mm Hg, respectively). Glomerular sclerosis was absent and interstitial fibrosis ranged from absent- mild- moderate, and was similar in all groups. The increases in i) perivascular infiltration of CD3+ lymphocytes, ii) CTGF gene expression, iii) tubule casts and iv) albuminuria that were observed in the Control mice, were significantly reduced in both the VSMC Jak2 Null and 3Rx groups. [CTGF mRNA Levels: Control = 100%±17, VSMC Jak2 Null = 70%±12*, 3Rx= 56%±17*. Urine Albumin (ng/day): Control = 414 ± 262, VSMC Jak2 Null = 138 ± 172*, 3Rx= 101 ± 89* (*, p<0.05 vs. Control)]. Thus, the early renal injury due to chronic Ang II infusion correlates with increased BP and not with the expression of VSMC-derived Jak2, suggesting that Jak2 contributes to early Ang II-mediated renal injury via its pressor-dependent actions.

Minimal-change nephropathy and focal segmental glomerulosclerosis

2020 ◽  
pp. 4919-4928
Author(s):  
Moin Saleem ◽  
Lisa Willcocks
Keyword(s):  
Nephrotic Syndrome ◽  
Focal Segmental Glomerulosclerosis ◽  
Parasitic Infection ◽  
Genetic Mutation ◽  
Minimal Change ◽  
Response To Treatment ◽  
Glomerular Sclerosis ◽  
Protein Factor ◽  
Segmental Glomerulosclerosis ◽  
Published Evidence

Minimal-change nephrotic syndrome (MCNS) is an immune-mediated condition, usually of unknown cause. On light microscopy the glomeruli appear normal, and on electron microscopy there is effacement of epithelial cell foot processes over the outer surface of the glomerular basement membrane. MCNS is the cause of about 75% of cases of nephrotic syndrome in children and 17% in adults. Management and prognosis—treatment in adults is with prednisolone at an initial dose of 80 mg/day, then tapering. This leads to complete remission in 90 to 95% of patients, but 50 to 75% of glucocorticoid-responsive adults will have a relapse. Progression to renal failure is not expected and would call the diagnosis of MCNS into question. Focal segmental glomerulosclerosis (FSGS) is not a specific disease entity but a histological lesion, often of unknown aetiology, which is characterized by segmental areas of glomerular sclerosis. It may be (1) primary—either due to genetic mutation, or associated with an unknown circulating protein factor that causes an increase in glomerular permeability; or (2) secondary—the end product of a variety of pathological processes including glomerular hyperfiltration, healed glomerulonephritis, viral (including HIV) infection, or parasitic infection. Management and prognosis—corticosteroid and immunosuppressive therapy should be considered only in patients with primary FSGS and nephrotic syndrome. The steroid regimen is as used for MCNS, but with lesser success. Steroid-resistant cases are treated with ciclosporin (for which there is most published evidence), mycophenolate mofetil, or cyclophosphamide. Prognosis depends on histology and response to treatment.

Role of autophagy and evaluation the effects of microRNAs 214, 312, 34c and prorenin receptor in a rat model of focal segmental glomerulosclerosis

Life Sciences ◽  
2021 ◽  
pp. 119671
Author(s):  
Derya Yildirim ◽  
Onur Bender ◽  
Zehra Firat Karagoz ◽  
Fatma Helvacioglu ◽  
Mukadder Ayse Bilgic ◽  
...  
Keyword(s):  
Focal Segmental Glomerulosclerosis ◽  
Rat Model ◽  
Segmental Glomerulosclerosis ◽  
Prorenin Receptor

scholarly journals Regulation of Mild Moxibustion on Uterine Vascular and Prostaglandin Contents in Primary Dysmenorrhea Rat Model

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Xuemei Li ◽  
Sha Guo ◽  
Zhaoheng Chen ◽  
Kuiyu Ren ◽  
Hong Zhang ◽  
...  
Keyword(s):  
Rat Model ◽  
Prostaglandin F2α ◽  
Female Rats ◽  
Saline Control ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Primary Dysmenorrhea ◽  
Uterine Tissue ◽  
Moxibustion Group ◽  
Mild Moxibustion

Objective. Primary dysmenorrhea (PD) is a common and high incidence disease in gynecology, which seriously affects the quality of life in young women. Our previous study found that mild moxibustion could treat abdominal pain of PD patients, but the mechanism is still unclear. Therefore, this study aims to partly investigate the treatment mechanism of moxibustion for PD, especially on uterine microcirculation. Methods. Forty 3-month-old Sprague Dawley female rats were randomly divided into four groups, including group A (saline control group, n = 10), group B (control plus moxibustion group, n = 10), group C (PD model group, n = 10), group D (PD. model plus moxibustion group, n = 10). The PD rat model was established by injecting estradiol benzoate and oxytocin. Mild moxibustion on Sanyinjiao (SP6) and Guanyuan (CV4) acupoints was once a day, 20 minutes per time, for 10 consecutive days. A vaginal smear was used to test the estrous cycle of rats. Uterine microvascular thickness was observed by stereomicroscope. And we detected the content of prostaglandin F2α (PGF2α) and prostaglandin E2 (PGE2) in uterine tissue by enzyme-linked immunosorbent assay. Results. Mild moxibustion can enlarge the microvessels, improve the microcirculation disturbance, and relieve the swelling of the uterus in PD rats. During the mild moxibustion intervention, the contents of PGF2α and PGE2 in uterus issues were synchronous increases or decreases and the changes of PGE2 were more obvious, but the changes of uterine microvasculature and morphology caused by the decrease of PGF2α were greater than PGE2. Conclusion. Mild moxibustion at SP6 and CV4 acupoints may relax uterine microvascular obstacle by reducing the content of PGF2α in uterine tissue, improve the microcirculation disorder, and then alleviate the PD rat’s uterine swelling.

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