The Bloody Mystery of Glomerular Tuft Development

2021 ◽  
Vol 32 (9) ◽  
pp. 2104-2106
Author(s):  
Denise K. Marciano
Keyword(s):  
Glomerular Tuft

Histological Comparative of Kidney of Neonatal Mice Exposed to Silver Nanoparticles During Fetal Development

2019 ◽  
Vol 10 (01) ◽  
Author(s):  
Najat F. Mohammed Salih ◽  
Gazwa D. Al-Nakeeb
Keyword(s):  
Silver Nanoparticles ◽  
Fetal Development ◽  
High Dose ◽  
Histopathological Analysis ◽  
Histological Changes ◽  
Newborn Mice ◽  
The Third ◽  
Tubular Necrosis ◽  
Neonatal Kidney ◽  
Glomerular Tuft

This study aimed to compare the histological changes in the neonatal kidney after their mothers exposed to different doses of silver nanoparticles colloidal solution (AgNPs) during the three stages of pregnancy. Pregnant Swiss albino mice (n=60) were randomly divided into three treated groups. They were intraperitoneally injected with AgNPs for 7 days during each stage of the gestational period. The newborn mice were sacrificed immediately after the birth, and the kidneys were being collected for histopathological analysis. The results showed that the AgNPs caused histological changes in the neonatal kidneys; vacuolation of some renal vesicles and cortical tubules, cystic tubular dilation, glomerular tuft shrinkage, and focal tubular necrosis in the first week-dose exposed pregnant. Disintegrating of immature glomeruli, distention of Bowman’s space of mature glomeruli, tubular necrosis, loss of renal parenchyma, medullar tubules containing hyaline casts, and subcapsular haemorrhage in the second week-dose exposed pregnant. Massive hypercellularity in the deeper part of the renal cortex, cortical and medullary tubules dilation, atrophy of subcapsular immature tubules, cortical cyst formation, glomerular tuft necrosis, dilation of Bowman’s space with evidence of crescent formation, and medullar portion replaced by scant loose connective tissue containing few numbers of tubules the third week-dose exposed pregnant. The results showed that the AgNPs has more negative effects on the kidney development at the third week-high dose and comparing the histological changes in the neonatal kidney were appeared in a time-depended manner and in a dosedepended manner. More researches must be carried out to obtain better understanding of AgNPs toxicity on fetal development and its ability as a teratogenic agent to induce external and internal abnormalities in the fetus.

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.

Abstract 256: Rbp-j Controls the Fate of the Kidney Vasculature

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Eugene Lin ◽  
Maria Luisa S Sequeira Lopez ◽  
Roberto A Gomez
Keyword(s):  
Stromal Cells ◽  
Mesangial Cells ◽  
Notch Signaling Pathway ◽  
Renal Vasculature ◽  
Arterial Tree ◽  
Mural Cells ◽  
Vascular Markers ◽  
Renal Abnormalities ◽  
Glomerular Tuft

Proper assembly of the renal vasculature is essential for post-natal life, and alterations to the renal vasculature are at the root of many types of cardiovascular disease. However, the mechanisms underlying the establishment, assembly and maintenance of the renal blood vessels are poorly understood. We have identified a population of renal stromal cells (marked by their expression of the transcription factor Foxd1) that differentiate to form the mural cells of the kidney arterial tree (excluding endothelial cells) and the glomerular mesangium. We previously demonstrated that RBP-J, the final transcriptional effector of the Notch signaling pathway, controls the phenotype of renin cells which are also derived from the Foxd1 lineage. We therefore hypothesized that RBP-J regulates the differentiation of stromal cells into the mural cells of the kidney arterioles. To answer this question, we deleted RBP-J in the metanephric stromal precursor cells, and found that mutant mice displayed striking kidney abnormalities in early life. Staining for vascular markers showed a significant decrease in the number of arteries and arterioles. Vessel walls were thinner due to a decrease in both the size and number of smooth muscle cells. We also noted a near absence of renin cells, supporting our earlier findings regarding the key role of RBP-J in establishing the differentiated renin cell endowment. These findings were accompanied by delayed nephrogenesis and other renal abnormalities including tubular dilation. In addition, mutant kidneys lacked Foxd1-lineage cells within the glomeruli, resulting in a depletion of mesangial cells and glomerular aneurysms. Thus, we conclude that RBP-J in Foxd1+ stromal cells plays a key role in the development of the kidney vasculature, and regulates the fate of cells that compose the arterial tree and the glomerular tuft.

Crescentic glomerulonephritis

2009 ◽  
pp. 399-434
Author(s):  
Patrick Nachman ◽  
Richard J. Glassock
Keyword(s):  
Renal Function ◽  
End Stage Renal Disease ◽  
Crescentic Glomerulonephritis ◽  
Rapidly Progressive Glomerulonephritis ◽  
Clinical Syndrome ◽  
Aggressive Treatment ◽  
Stage Renal Disease ◽  
End Stage ◽  
Glomerular Tuft

The term crescentic glomerulonephritis (CrGN) refers to a diverse collection of disorders of widely different etiology and pathogenesis having in common the development of extensive proliferation of cells within Bowman's space (Couser, 1988; Glassock et al., 1995; Nachman et al., 1998; Pusey and Rees, 1998; Morgan et al., 2006; Lionaki, et al., 2007). The resulting accumulation of cells gives rise to a ‘crescent’ enveloping the glomerular tuft itself. Polymerization of fibrinogen in Bowman's space due to passage of fibrinogen through gaps in the capillary wall, the elaboration of procoagulant factors by infiltrating monocytes and impaired fibrinolysis all contribute to the pathogenesis of the crescent (Couser, 1988, Glassock et al., 1995). Usually 〉50% of glomeruli are involved with crescentic lesions. Such patients also frequently manifest rapid and progressive deterioration of renal function leading to the clinical syndrome of rapidly progressive glomerulonephritis. Early and aggressive treatment can often delay or prevent the development of end-stage renal disease (ESRD). See Table 10.1 for an etiologic and pathogenetic classification of CrGN.

scholarly journals Spontaneous Mesangioproliferative Glomerulonephritis in Pigtailed Macaques (Macaca nemestrina)

1981 ◽  
Vol 18 (6_suppl) ◽  
pp. 82-88 ◽  
Author(s):  
J. T. Boyce ◽  
W. E. Giddens ◽  
R. Seifert
Keyword(s):  
Renal Dysfunction ◽  
Cause Of Death ◽  
Immune Complexes ◽  
Mesangial Cells ◽  
Macaca Nemestrina ◽  
Mesangial Matrix ◽  
Ultrastructural Studies ◽  
Mesangioproliferative Glomerulonephritis ◽  
Glomerular Tuft

Mesangioproliferative glomerulonephritis was found in 28 of 113 pigtailed macaques (Macaca nemestrina) that died in 1977. In five it was considered severe enough to cause significant renal dysfunction; in two of these it was the cause of death. The basic lesion was a proliferation of mesangial cells and deposition of mesangial matrix in the mesangial stalk, resulting in various degrees of stalk expansion and increased lobulation of the glomerular tuft. Preliminary immunofluorescence and ultrastructural studies suggest the pathogenesis of the lesion may involve deposition of antigen-IgM immune complexes in the mesangial region.

scholarly journals II. RENAL THRESHOLD FOR HEMOGLOBIN IN DOGS UNINFLUENCED BY MERCURY POISONING

1932 ◽  
Vol 55 (4) ◽  
pp. 617-625 ◽  
Author(s):  
William H. Havill ◽  
John A. Lichty ◽  
Gordon B. Taylor ◽  
George H. Whipple
Keyword(s):  
Blood Plasma ◽  
Mercuric Chloride ◽  
Renal Injury ◽  
Active Part ◽  
Tubular Epithelium ◽  
Mercury Poisoning ◽  
Renal Threshold ◽  
Convoluted Tubules ◽  
Hemoglobin Threshold ◽  
Glomerular Tuft

The minimal or depression renal threshold for dog hemoglobin is not modified by moderate doses of mercuric chloride. This type of renal injury involves the epithelium of the convoluted tubules but the glomeruli escape. We are unable to explain our findings if we assume that the tubular epithelium takes an active part in the passage of dog hemoglobin from the blood into the urine. The evidence points toward the glomerular tuft as responsible for the passage of the hemoglobin from the blood plasma into the tubules. The glomerular tuft establishes the true hemoglobin threshold under these conditions. If the convoluted tubules are normal, we note that hemoglobin is taken into the epithelium and this explains the high initial renal threshold. With repeated hemoglobin injections this tubular epithelium becomes stuffed with hemoglobin pigment fractions and can absorb no more, which explains the minimal or depression threshold. Further injury of this tubular epithelium with mercury causes no change in this minimal renal threshold, unless we produce actual tubular obstruction.

scholarly journals Urinary excretion of viable podocytes in health and renal disease

2003 ◽  
Vol 285 (1) ◽  
pp. F40-F48 ◽  
Author(s):  
Stefanie U. Vogelmann ◽  
W. James Nelson ◽  
Bryan D. Myers ◽  
Kevin V. Lemley
Keyword(s):  
Cultured Cells ◽  
Growth Behavior ◽  
Glomerular Disease ◽  
Glomerular Sclerosis ◽  
Tunel Staining ◽  
Healthy Controls ◽  
Podocyte Loss ◽  
The Difference ◽  
Glomerular Tuft ◽  
Quiescent Disease

The loss of glomerular visceral epithelial cells (podocytes) has been associated with the development of glomerular sclerosis and loss of renal function. Viability of podocytes recovered from urine of subjects with glomerular disease and of healthy controls was investigated by propidium iodide exclusion and TUNEL staining. Podocyte loss was quantified by cytospin. The growth behavior in culture of urinary cells and their expression of specific markers were examined. The majority of urinary podocytes are viable, although apoptosis occurs in about one-half of the cells. Patients with active glomerular disease excreted up to 388 podocytes/mg creatinine, whereas healthy controls and patients with quiescent disease generally excreted <0.5 podocytes/mg creatinine. The identity of cultured cells was confirmed by their morphology, growth behavior, and expression of podocyte-specific markers. The difference in growth behavior between healthy controls and subjects with active glomerular disease suggests that in active disease viable podocytes detach from the glomerular tuft due to local environmental factors rather than defects in the podocytes per se, whereas in healthy individuals mostly senescent podocytes are shed.

Glomerular tuft ballooning in mitomycin-C-induced renal impairment

1992 ◽  
Vol 420 (6) ◽  
pp. 545-551 ◽  
Author(s):  
Hideo Shiiki ◽  
Kazuhiro Dohi ◽  
Hisayuki Nishioka ◽  
Takashi Matsuda ◽  
Masao Kanauchi ◽  
...  
Keyword(s):  
Renal Impairment ◽  
Mitomycin C ◽  
Glomerular Tuft

scholarly journals How Do Mesangial and Endothelial Cells Form the Glomerular Tuft?

2008 ◽  
Vol 19 (1) ◽  
pp. 24-33 ◽  
Author(s):  
Michael R. Vaughan ◽  
Susan E. Quaggin
Keyword(s):  
Endothelial Cells ◽  
Glomerular Tuft

Mammalian target of rapamycin complex 1 activation in podocytes promotes cellular crescent formation

2014 ◽  
Vol 307 (9) ◽  
pp. F1023-F1032 ◽  
Author(s):  
Junhua Mao ◽  
Zhifeng Zeng ◽  
Zhuo Xu ◽  
Jiangzhong Li ◽  
Lei Jiang ◽  
...  
Keyword(s):  
Mammalian Target Of Rapamycin ◽  
Hypoxia Inducible Factor ◽  
Target Of Rapamycin ◽  
Crescent Formation ◽  
Glomerular Diseases ◽  
Mtorc1 Signaling ◽  
Cellular Crescent ◽  
Underlying Mechanisms ◽  
Mtorc1 Activation ◽  
Glomerular Tuft

Podocytes play a key role in the formation of cellular crescents in experimental and human diseases. However, the underlying mechanisms for podocytes in promoting crescent formation need further investigation. Here, we demonstrated that mammalian target of rapamycin complex 1 (mTORC1) signaling was remarkably activated and hypoxia-inducible factor (HIF) 1α expression was largely induced in cellular crescents from patients with crescentic glomerular diseases. Specific deletion of Tsc1 in podocytes led to mTORC1 activation in podocytes and kidney dysfunction in mice. Interestingly, 33 of 36 knockouts developed cellular or mixed cellular and fibrous crescents at 7 wk of age (14.19 ± 3.86% of total glomeruli in knockouts vs. 0% in control littermates, n = 12–36, P = 0.04). All of the seven knockouts developed crescents at 12 wk of age (30.92 ± 11.961% of total glomeruli in knockouts vs. 0% in control littermates, n = 4–7, P = 0.002). Most notably, bridging cells between the glomerular tuft and the parietal basement membrane as well as the cellular crescents were immunostaining positive for WT1, p-S6, HIF1α, and Cxcr4. Furthermore, continuously administrating rapamycin starting at 7 wk of age for 5 wk abolished crescents as well as the induction of p-S6, HIF1α, and Cxcr4 in the glomeruli from the knockouts. Together, it is concluded that mTORC1 activation in podocytes promotes cellular crescent formation, and targeting this signaling may shed new light on the treatment of patients with crescentic glomerular diseases.

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