scholarly journals Glomerular Hypertrophy

2020 ◽  
Author(s):  
Keyword(s):  
Glomerular Hypertrophy

Histomorphometry of Feline Chronic Kidney Disease and Correlation With Markers of Renal Dysfunction

2012 ◽  
Vol 50 (1) ◽  
pp. 147-155 ◽  
Author(s):  
S. Chakrabarti ◽  
H. M. Syme ◽  
C. A. Brown ◽  
J. Elliott
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Image Analysis ◽  
Renal Function ◽  
Kidney Disease ◽  
Renal Dysfunction ◽  
Interstitial Fibrosis ◽  
Glomerular Hypertrophy ◽  
Renal Lesions ◽  
Postmortem Examinations

Chronic kidney disease is common in geriatric cats, but most cases have nonspecific renal lesions, and few studies have correlated these lesions with clinicopathological markers of renal dysfunction. The aim of this study was to identify the lesions best correlated with renal function and likely mediators of disease progression in cats with chronic kidney disease. Cats were recruited through 2 first-opinion practices between 1992 and 2010. When postmortem examinations were authorized, renal tissues were preserved in formalin. Sections were evaluated by a pathologist masked to all clinicopathological data. They were scored semiquantitatively for the severity of glomerulosclerosis, interstitial inflammation, and fibrosis. Glomerular volume was measured using image analysis; the percentage of glomeruli that were obsolescent was recorded. Sections were assessed for hyperplastic arteriolosclerosis and tubular mineralization. Kidneys from 80 cats with plasma biochemical data from the last 2 months of life were included in the study. Multivariable linear regression ( P < .05) was used to assess the association of lesions with clinicopathological data obtained close to death. Interstitial fibrosis was the lesion best correlated with the severity of azotemia, hyperphosphatemia, and anemia. Proteinuria was associated with interstitial fibrosis and glomerular hypertrophy, whereas higher time-averaged systolic blood pressure was associated with glomerulosclerosis and hyperplastic arteriolosclerosis.

Prevention of Glomerular Hypertrophy and Glomerulosclerosis in Milan Normotensive Rats by Low-Protein Diet, but Not by Low-Dose Captopril Treatment

Nephron ◽  
1995 ◽  
Vol 71 (2) ◽  
pp. 208-212 ◽  
Author(s):  
V. Kliem ◽  
R. Brunkhorst ◽  
G. Ehlerding ◽  
K. Kühn ◽  
K.H. Neumann ◽  
...  
Keyword(s):  
Low Dose ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Glomerular Hypertrophy ◽  
Low Protein ◽  
Captopril Treatment

scholarly journals UJI EFEKTIVITAS EKSTRAK BIJI KETUMBAR (CORIANDRUM SATIVUM L.) TERHADAP GAMBARAN HISTOPATOLOGI GINJAL TIKUS HIPERKOLESTEROLEMIA DIABETES

2020 ◽  
Vol 4 (2) ◽  
pp. 357
Author(s):  
Syarifah Nazira ◽  
Maria Selvester Thadeus ◽  
Niniek Hardini
Keyword(s):  
Oxidative Stress ◽  
Blood Sugar ◽  
Blood Sugar Level ◽  
Seed Extract ◽  
Coriandrum Sativum ◽  
Blood Cholesterol ◽  
Glomerular Hypertrophy ◽  
Blood Cholesterol Level ◽  
High Fat ◽  
Coriander Seed

Diabetes Mellitus (DM) is metabolic disease characterized hyperglicemia caused by abnormalities of insulin secretion, insulin sensitivity, or both of them.  Persistent hyperglicemia can trigger the production of oxidative stress. Oxidative stress can cause  glomerular hypertrophy. Coriander seed extract has the potential to overcome oxidative stress. This study aims to determine the effect of coriander seed extract to kidney histopathological examination, blood cholesterol, and blood sugar level in hypercholestrolemia diabetic rats. Samples consist of 30 males wistar rats were divided into five treatments i.e: (K1) standard feed and aquades, (K2) high-fat feed, alloxan, and  glibenclamid 0,045 mg/day, (K3) high-fat feed, alloxan, and coriander seed extract 300 mg/kgBW/day, (K4) high-fat feed, alloxan, and coriander seed extract 500mg/kgBW/day, (K5) high-fat feed, alloxan, and  coriander seed extract 700mg/kgBW/day. Coriander seed extract was given for 28 days. The result of Wilcoxon test showed that coriander seed extract can reduce blood cholesterol level in diabetic hypercholesterolemia, meanwhile the result of paired T-test showed that it can reduce blood sugar level. Measurement of kidney’s histopathological structure as glomerular area was analyzed by Kruskal Wallis test (p=0,001) and continued with Mann-Whitney test. Group K4 can reduce glomerular area significantly compared with group K3 and K5. In conclussion, coriander seed extract can reduce blood cholesterol, blood sugar level and effectively reduce glomerular hypertrophy at dose of 500mg/kgBW/day. Keyword : Coriandrum sativum L.; coriander seed extract; glomerular hypertrophy; blood cholesterol level; blood  glucose level ABSTRAK Diabetes Melitus (DM) merupakan suatu penyakit metabolik dengan karakteristik  hiperglikemi yang terjadi karena kelainan sekresi insulin, kerja insulin atau kedua-duanya. Hiperglikemi persisten dapat memicu produksi stres oksidatif. Stres oksidatif dapat menyebabkan terjadinya hipertrofi glomerulus. Ekstrak biji ketumbar (Coriandrum sativum L.) berpotensi mengatasi stres oksidatif. Penelitian ini bertujuan untuk mengetahui efek pemberian esktrak biji ketumbar (Coriandrum sativum L.) terhadap gambaran histopatologi ginjal, kadar kolesterol darah, dan kadar gula darah tikus model hiperkolesterolemia diabetes. Sebanyak 30 ekor tikus putih jantan galur wistar, dikelompokkan menjadi lima kelompok dengan perlakuan berbeda yaitu: (K1) pakan standar dan aquades, (K2) pakan tinggi lemak, aloksan, dan glibenklamid 0,045mg/hari, (K3) pakan tinggi lemak, aloksan dan ekstrak biji ketumbar 300mg/kgBB/hari, K4) pakan tinggi lemak, aloksan dan ekstrak biji ketumbar 500mg/kgBB/hari, (K5) pakan tinggi lemak, aloksan, dan ekstrak biji ketumbar 700mg/kgBB/hari. Ekstrak biji ketumbar diberikan selama 28 hari. Hasil uji Wilcoxon menunjukkan ekstrak biji ketumbar dapat menurunkan kadar kolesterol darah, sedangkan hasil uji T berpasangan menunjukkan ekstrak biji ketumbar dapat menurunkan kadar guka darah sewaktu pada tikus model hiperkolesterolemia diabetes. Histopatologi ginjal dianalisis menggunakan uji Kruskal Wallis didapatkan (p=0,001) dan dilanjutkan dengan uji Mann-Whitney. Pada kelompok K4 terdapat penurunan luas glomerulus yang signifikan dibanding kelompok K3 dan K5. Kesimpulannya, esktrak biji ketumbar dapat menurunkan kadar kolesterol darah, kadar gula darah, dan pada dosis 500mg/kgBB/hari paling efektif untuk menurunkan hipertrofi gomerulus. 

scholarly journals LncRNA NEAT1 Promotes High Glucose-Induced Mesangial Cell Hypertrophy by Targeting miR-222-3p/CDKN1B Axis

2021 ◽  
Vol 7 ◽  
Author(s):  
Lin Liao ◽  
Jie Chen ◽  
Chuanfu Zhang ◽  
Yue Guo ◽  
Weiwei Liu ◽  
...  
Keyword(s):  
High Glucose ◽  
Noncoding Rna ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Morphological Alteration ◽  
Glomerular Hypertrophy ◽  
Cell Hypertrophy ◽  
Rna Immunoprecipitation ◽  
Lncrna Neat1

Glomerular hypertrophy is an early morphological alteration in diabetic nephropathy. Cyclin-Dependent Kinases have been shown to be required for high glucose (HG)-induced hypertrophy; however, the upstream regulators of CDKN1B in glomerular hypertrophy remain unclear. Herein we describe a novel pathway in which Long noncoding RNA (lncRNA) NEAT1 regulates the progression of mesangial cell hypertrophy via a competing endogenous RNA (ceRNA) mechanism. Real-time PCR was performed to detect the relative NEAT1 and miR-222-3p expressions and further confirmed the relationship between NEAT1 and miR-222-3p. Cell cycle was evaluated by flow cytometry. The related mechanisms were explored by Western blot, RNA immunoprecipitation and chromatin immunoprecipitation assay. We show that NEAT1 forms double stranded RNA (dsRNA) with miR-222-3p, thus limiting miR-222-3p’s binding with CDKN1B. This release of CDKN1B mRNA leads to elevated CDKN1B protein expression, resulting in hypertrophy. In addition, we demonstrated that STAT3 which is activated by HG induces the transcription of NEAT1 by binding to its promoter. Our findings underscore an unexpected role of lncRNAs on gene regulation and introduce a new mode of proliferation regulation in mesangial cells.

scholarly journals Reversible glomerular hypertrophy in adult patients with primary focal segmental glomerulosclerosis.

1997 ◽  
Vol 8 (11) ◽  
pp. 1668-1678
Author(s):  
K Nishimoto ◽  
H Shiiki ◽  
T Nishino ◽  
H Uyama ◽  
M Iwano ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Focal Segmental Glomerulosclerosis ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Cell Number ◽  
Glomerular Hypertrophy ◽  
Control Subjects ◽  
Segmental Glomerulosclerosis ◽  
The Mean ◽  
Glomerular Tuft

The present study was performed to assess the pathogenetic role of glomerular hypertrophy in patients with primary focal segmental glomerulosclerosis (FSGS). We studied 14 patients with FSGS by morphometry. In seven patients, minimal change nephrotic syndrome (MCNS) was diagnosed on the first renal biopsy, but FSGS was diagnosed on the second biopsy (MCNS-FSGS group). Seven other patients with FSGS on the first biopsy underwent second biopsies while in remission (FSGS-R group). Biopsy results were compared with biopsies from 10 patients with MCNS and seven control subjects. Nonsclerotic glomeruli were examined. The mean glomerular tuft area, whole glomerular area, and number of mesangial cells were significantly increased in both biopsies from the MCNS-FSGS group and in the first biopsies obtained during the nephrotic stage of the FSGS-R group, compared with control subjects and patients with MCNS. Biopsies from FSGS patients in remission showed that the mean glomerular tuft area and number of mesangial cells were significantly decreased. The fractional extracellular matrix area (extracellular matrix area/glomerular tuft area) and mesangial cell density (mesangial cell number/glomerular tuft area) in FSGS during both nephrotic and remission stages were the same as those in control subjects and patients with MCNS. The present study suggests that glomerular hypertrophy precedes the development of glomerulosclerosis in FSGS and is reversible when patients are in remission. These features support the pathogenetic importance of glomerular hypertrophy in patients with primary FSGS.

Reversal of Renal Fibrosis, Inflammation, and Glomerular Hypertrophy by Kallikrein Gene Delivery

2006 ◽  
Vol 17 (5) ◽  
pp. 545-555 ◽  
Author(s):  
Grant Bledsoe ◽  
Bo Shen ◽  
Yuyu Yao ◽  
Jenny J. Zhang ◽  
Lee Chao ◽  
...  
Keyword(s):  
Gene Delivery ◽  
Renal Fibrosis ◽  
Glomerular Hypertrophy

scholarly journals Reduced Autophagy by a microRNA-mediated Signaling Cascade in Diabetes-induced Renal Glomerular Hypertrophy

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Supriya Deshpande ◽  
Maryam Abdollahi ◽  
Mei Wang ◽  
Linda Lanting ◽  
Mitsuo Kato ◽  
...  
Keyword(s):  
Signaling Cascade ◽  
Glomerular Hypertrophy

scholarly journals Early Enhanced Leucine-Rich α-2-Glycoprotein-1 Expression in Glomerular Endothelial Cells of Type 2 Diabetic Nephropathy Model Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Sona haku ◽  
Hiromichi Wakui ◽  
Kengo Azushima ◽  
Kotaro Haruhara ◽  
Sho Kinguchi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Diabetic Nephropathy ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Early Stage ◽  
Endothelial Cell Proliferation ◽  
Glomerular Hypertrophy ◽  
Vegf Expression ◽  
Initial Development ◽  
Glomerular Endothelial Cells

Abnormal angiogenesis plays a major role in the development of early stage diabetic nephropathy. Vascular endothelial growth factor (VEGF) is a classical proangiogenic factor that regulates abnormal glomerular angiogenesis linked to glomerular hypertrophy in the early stage of diabetic nephropathy. Leucine-rich α-2-glycoprotein-1 (LRG1) was recently reported as a novel proangiogenic factor that is expressed in endothelial cells and promotes angiogenesis by modulating the transforming growth factor-β signaling pathway. However, the pathophysiology of LRG1 in diabetic nephropathy remains largely unknown. In the present study, we investigated intrarenal expression of the novel proangiogenic factor LRG1 in diabetic db/db mice by immunohistochemistry and a laser capture microdissection method during the development of diabetic nephropathy. We hypothesized that glomerular LRG1 expression is increased earlier than VEGF expression under conditions of pathological angiogenesis in the early stage of diabetic nephropathy. Thus, we compared glomerular expression of VEGF and LRG1 in diabetic db/db mice at 16 and 24 weeks of age. At 16 weeks, diabetic db/db mice exhibited glomerular hypertrophy with abnormal angiogenesis characterized by endothelial cell proliferation, which was concomitant with an increase in LRG1 expression of glomerular endothelial cells. However, glomerular VEGF expression was not increased at this early stage. At 24 weeks, the features of early diabetic nephropathy in db/db mice had developed further, along with further enhanced glomerular LRG1 expression. At this late stage, glomerular VEGF and fibrosis-related-gene expression was also significantly increased compared with nondiabetic db/m mice. These results suggest that LRG1 plays a pivotal role in the initial development of diabetic nephropathy by promoting abnormal angiogenesis, thereby suggesting that LRG1 is a potential preemptive therapeutic target of diabetic nephropathy.

Glomerular surface area is normalized in mice born with a nephron deficit: no role for AT1 receptors

2009 ◽  
Vol 296 (3) ◽  
pp. F583-F589 ◽  
Author(s):  
Amany Shweta ◽  
Luise A. Cullen-McEwen ◽  
Michelle M. Kett ◽  
Roger G. Evans ◽  
Kate M. Denton ◽  
...  
Keyword(s):  
Surface Area ◽  
Time Course ◽  
Receptor Activation ◽  
Compensatory Hypertrophy ◽  
Glomerular Hypertrophy ◽  
Capillary Surface ◽  
Glomerular Capillary ◽  
Additional Group ◽  
Nephron Deficit ◽  
Glomerular Capillaries

We examined whether deficits in glomerular capillary surface area associated with a congenital nephron deficit could be corrected by glomerular hypertrophy. Using unbiased stereological techniques, we examined the time course and mode of glomerular hypertrophy in mice lacking one allele for glial cell line-derived neurotrophic factor (GDNF). These GDNF heterozygous (Het) mice are born with ∼30% less nephrons than wild-type (WT) littermates. An additional group of GDNF Het mice received the angiotensin type 1 (AT1)-receptor antagonist candesartan (Cand; 10 mg·kg−1·day−1) from 5 wk of age to determine the role of AT1 receptors in the compensatory hypertrophy. At 10 wk of age, the total volume of renal corpuscles, glomerular capillary surface area, and length of glomerular capillaries in the kidneys of GDNF Het mice were all markedly (∼45%) less than that of WT mice ( P < 0.001). However, by 30 wk, and persisting at 60 wk of age, GDNF Het and WT mice did not significantly differ in any of these parameters. Furthermore, conscious 24-h mean arterial pressure (MAP) did not differ between GDNF Het and WT mice at any time point. MAP of GDNF Het-Cand mice was 20–30 mmHg less than that of GDNF Het-vehicle mice at all three ages, but Cand treatment did not significantly alter glomerular capillary dimensions. In conclusion, we have demonstrated that the deficit in glomerular capillary surface area associated with a congenital nephron deficit can be corrected for in adulthood by an increase in the total length of glomerular capillaries. This process does not require AT1 receptor activation.

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