Mesangial Cells Initiate Compensatory Tubular Cell Hypertrophy

Sinuani, Inna; Beberashvili, Ilia; Averbukh, Zhan; Cohn, M.; Gitelman, Inna; Weissgarten, Joshua

doi:10.1159/000287229

Cited by 20 publications

(21 citation statements)

References 105 publications

(80 reference statements)

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“…22 Such changes stimulate the mesangial cells in nephrons, and the induction of chemokines including transforming growth factor-ß elevates SNGFR and eventually causes compensatory tubular hypertrophy. 16,23 This series of events is believed to encompass the "signal" proposed by Takagi et al 24 However, in their study the signal was defined only as a factor inducing structural hypertrophy. Nevertheless, as demonstrated in this study, this signal simultaneously induces structural hypertrophy and functional hyperfiltration.…”

Section: Discussionmentioning

confidence: 99%

Compensatory Structural and Functional Adaptation after Radical Nephrectomy for Renal Cell Carcinoma According to Preoperative Stage of Chronic Kidney Disease

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Compensatory Structural and Functional Adaptation after Radical Nephrectomy for Renal Cell Carcinoma According to Preoperative Stage of Chronic Kidney Disease

et al. 2015

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“…In addition, the mesangium serves as a source and target of vasoactive hormones, growth factors, cytokines and ECM proteins and thus contributes to the pathophysiology of a variety of glomerular diseases (Sinuani et al 2010;Schlöndorff and Banas 2009). These factors activate mesangial cells in an autocrine manner and mediate interactions with glomerular endothelial and epithelial cells and with blood-borne inflammatory cells.…”

Section: Effect Of Tgf-β On Mesangial Cellsmentioning

confidence: 99%

Role of TGF-β in chronic kidney disease: an integration of tubular, glomerular and vascular effects

2011

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Transforming growth factor beta (TGF-β) has been recognized as an important mediator in the genesis of chronic kidney diseases (CKD), which are characterized by the accumulation of extracellular matrix (ECM) components in the glomeruli (glomerular fibrosis, glomerulosclerosis) and the tubular interstitium (tubulointerstitial fibrosis). Glomerulosclerosis is a major cause of glomerular filtration rate reduction in CKD and all three major glomerular cell types (podocytes or visceral epithelial cells, mesangial cells and endothelial cells) participate in the fibrotic process. TGF-β induces (1) podocytopenia caused by podocyte apoptosis and detachment from the glomerular basement membrane; (2) mesangial expansion caused by mesangial cell hypertrophy, proliferation (and eventually apoptosis) and ECM synthesis; (3) endothelial to mesenchymal transition giving rise to glomerular myofibroblasts, a major source of ECM. TGF-β has been shown to mediate several key tubular pathological events during CKD progression, namely fibroblast proliferation, epithelial to mesenchymal transition, tubular and fibroblast ECM production and epithelial cell death leading to tubular cell deletion and interstitial fibrosis. In this review, we re-examine the mechanisms involved in glomerulosclerosis and tubulointerstitial fibrosis and the way that TGF-β participates in renal fibrosis, renal parenchyma degeneration and loss of function associated with CKD.

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“…Karşı böbrekte kompansatris hipertrofi intrauterin dönemde başlar ve çocukluk çağı boyunca devam eder (14)(15)(16) . Yapılan çalışmalarda, tek böbrekli insan fetüslerinde yaklaşık olarak %11'lik bir volüm artışı olduğu gösterilmiştir.…”

Section: Discussionunclassified

Clinical characteristics and follow-up results of unilateral renal agenesis and hypoplasia of children

Evrengül¹,

Ertan²,

Serdaroğlu³

et al. 2016

BUCH

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ÖZAmaç: Az nefron sayısına sahip çocuklarda, yaşamlarının ilerleyen dönemlerinde hipertansiyon, proteinüri ve kronik böbrek yetmezliği gelişme riski yüksektir. Bu renal hasar, glomerüler hiperfiltrasyondam kaynaklanmaktadır. Bu çalışmanın amacı, tek taraflı agenezik ve hipoplazik böbreği olan çocukların klinik özelliklerinin ve izlem sonuçlarının değerlendirilmesidir. Yöntem: Celal Bayar Üniversitesi Tıp Fakültesi ve Dr. Behçet Uz Çocuk Hastanesinde takip edilen, tek taraflı renal agenezisi ve hipoplazisi olan hastaların klinik, radyolojik ve nükleer tıp inceleme bulguları değerlendirildi. Bulgular: Bu çalışma ortalama yaşı 8,9±4 yıl olan 30 (%60) erkek ve 20 (%40) kız hastadan oluşmaktaydı. Yirmi beş hasta renal agenezi, 25 hasta renal hipoplazi tanısı aldı. Laboratuvar incelemesinde ortalama serum kreatinin düzeyi 0,45±0,22 mg/dl ve tahmin edilen glomerüler filtrasyon hızı (eGFR) 144±30,3 ml/dk. idi. Yirmi dokuz (%58) hastada hiperfiltrasyon saptandı. Proteinüri ve hipertansiyonu olan 1 (%4) hasta vardı. On beş (%30) hastada ürolojik anamoli mevcuttu. Sonuç: Bu çalışmada, tek taraflı renal agenezisi ve hipoplazisi olan hastaların serum kreatinin düzeyi normal bulundu. Ancak bu hastaların 29 (%58) hiperfiltrasyon vardı. Hiperfiltasyonu olan çocukların çoğunda yaşamlarının ilerleyen döneminde renal hasar geliştiği için bu çocuk-ların doğumdan itibararen klinik takiplerinin yapılması gerekmektedir.Anahtar kelimeler: Konjenital böbrek hastalıkları, renal agenezi, renal hipoplazi ABSTRACT Objective: Children with an inadequate number of nephrons have an increased risk of developing hypertension, proteinuria and chronic kidney disease in later life. This renal injury is caused by glomerular hyperfiltration. The aim of this study is to evaluate clinical characteristics and follow-up results of the children with unilateral renal agenesis and hypoplasia. Methods: We evaluated the clinical, radiological, and nuclear medicine findings of the children with unilateral agenetic or hypoplastic kidneys who were followed at Celal Bayar University School of Medicine and Dr. Behcet Uz Children's Hospital between 2005 and 2012. Results: The study consisted of 30 (60%) males and 20 (40%) females with a mean age of 8.9±4 years. A total of 25 patients were with renal agenesis and 25 with renal hypoplasia were diagnosed. On laboratory evaluation, mean serum creatinine level was 0.45±0.22 mg/ dl and the mean estimated glomerular filtration rate (eGFR) was 144±30.3 ml/min. 29 patient (58%) had hyperfiltration according to an eGFR. Proteinuria and hypertension were noted in 1 (4%) patient. Urological anomalies were found in 15 patients (30%). Conclusion: Our study has determined that children with unilateral renal agenesis and hypoplasia had normal serum creatinine values. Howewer 29 patients (58%) had hyperfiltration according to eGFR. Because many children with hiperfiltration develop renal injury in later life, we emphasize the need for clinical follow-up in these patients starting at birth.

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Mesangial Cells Initiate Compensatory Tubular Cell Hypertrophy

Cited by 20 publications

References 105 publications

Compensatory Structural and Functional Adaptation after Radical Nephrectomy for Renal Cell Carcinoma According to Preoperative Stage of Chronic Kidney Disease

Compensatory Structural and Functional Adaptation after Radical Nephrectomy for Renal Cell Carcinoma According to Preoperative Stage of Chronic Kidney Disease

Role of TGF-β in chronic kidney disease: an integration of tubular, glomerular and vascular effects

Clinical characteristics and follow-up results of unilateral renal agenesis and hypoplasia of children

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