Glomerular pathology: recent advances

Gibson, Ian W.; More, I. A. R.

doi:10.1002/(sici)1096-9896(199802)184:2<123::aid-path16>3.0.co;2-x

Cited by 22 publications

(12 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The origin of primary FSGS has not yet been elucidated. Glomerulosclerosis is characterized by an accumulation of extracellular matrix proteins plus a paucity of glomerular mesangial cells and can be seen as an end-result of glomerular injury and of aging (Gibson and More 1998). Oxidative stress and alterations in membrane lipid homeostasis are thought to be important events in aging process and aging related degenerative disease as FSGS or a diabetic nephropathy (Rohrmoser and Mayer 1996;Ha and Lee 2001;Mason and Wahab 2003).…”

Section: Discussionmentioning

confidence: 99%

Abnormal basement membrane in the inner ear and the kidney of the Mpv17-/- mouse strain: ultrastructural and immunohistochemical investigations

Gottesberge

Felix

2005

Histochem Cell Biol

View full text Add to dashboard Cite

The loss of the function of the peroxisomal Mpv17-protein and associated imbalanced radical oxygen species (ROS) homeostasis leads to an early onset of focal segmental glomerulosclerosis and sensorineural deafness associated with severe degeneration of cochlear structures. An excessive enlargement of basal laminae of the stria vascularis capillaries and glomeruli indicates numerous changes in their molecular composition. The basement membrane (BM) of the glomeruli and the stria vascularis are simultaneously affected in early stages of the disease and the lamination, splitting of the membrane and formation of the "basket weaving" seen at the onset of the disease in the kidney are similar to the ultrastructural alterations characteristic for Alporta9s syndrome. The progressive alteration of the BMs is accompanied by irregularity in the distribution of the collagen IV subunits and by an accumulation of the laminin B2(gamma1) in the inner ear and B(beta1) in the kidney. Since Mpv17 protein contributes to ROS homeostasis, further studies are necessary to elucidate downstream signaling molecules activated by ROS. These studies explain the cellular responses to missing Mpv17-protein, such as accumulation of the extracellular matrix, degeneration, and apoptosis in the inner ear.

show abstract

Section: Discussionmentioning

confidence: 99%

Abnormal basement membrane in the inner ear and the kidney of the Mpv17-/- mouse strain: ultrastructural and immunohistochemical investigations

Gottesberge

Felix

2005

Histochem Cell Biol

View full text Add to dashboard Cite

show abstract

“…Although these pathologic changes are present in several renal disorders (43), tubular dilation and glomerulosclerosis also develop in response to renal ischemia (44). The vascular defects in VEGF 120/120 mice likely impaired kidney oxygenation, and ultrastructural signs of ischemia in mutant mice were indeed observed in the proximal tubules and loops of Henleknown to be most susceptible to ischemic stress (44).…”

Section: Discussionmentioning

confidence: 99%

Loss of the VEGF164 and VEGF188 Isoforms Impairs Postnatal Glomerular Angiogenesis and Renal Arteriogenesis in Mice

Mattot¹,

Moons²,

Lupu

et al. 2002

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

ABSTRACT. Vascular endothelial growth factor (VEGF) is transcribed in the VEGF120, VEGF164, or VEGF188 isoforms, which differ in receptor binding, matrix association, and angiogenic activity. This vascular growth factor has been implicated in the development of the renal vasculature, but the role of the distinct VEGF isoforms remains unknown. In the present report, renal angiogenesis and arteriogenesis were studied in VEGF120/120 mice, expressing only the short VEGF120 isoform. In VEGF120/120 mice, ingrowth and survival of capillaries in glomeruli, remodeling of peritubular capillaries, vascular coverage by pericytes, and branching of renal arteries were all severely impaired, causing abnormal glomerular filtration and impairing renal function. The arterial branching defect might be related to a reduced expression of renin, a presumed renal arterial branching factor. Glomerulosclerosis and tubular dilation possibly resulted from renal ischemia caused by vascular defects. Thus, VEGF164 and VEGF188 not only mediate angiogenesis, but they also play an essential role in renal branching arteriogenesis.

show abstract

“…12 The presence of tubulo-interstitial injury and fibrosis has prognostic significance in CG. 13 Among the previously reported cases of CG in SLE, two achieved clinical remission with Collapsing glomerulopathy occurring in HIV-negative patients R Gupta et al…”

Section: Discussionmentioning

confidence: 99%

Collapsing glomerulopathy occurring in HIV-negative patients with systemic lupus erythematosus: report of three cases and brief review of the literature

Gupta

Sharma

Bhowmik

et al. 2011

Lupus

View full text Add to dashboard Cite

Collapsing glomerulopathy (CG), once recognized as a distinct renal disease in HIV-positive patients, has since been described in association with a number of other conditions, including autoimmune diseases. Among the latter, CG has been reported in Still's disease. Extensive search of the literature revealed only three patients with renal biopsy diagnosis of CG in the presence of clinical and serological evidence of SLE (HIV-negative). This case report presents three adult female HIV-negative patients with SLE who were detected as having significant proteinuria and underwent renal biopsy. In all three cases, renal biopsy showed features of diffuse lupus nephritis. In addition, variable numbers of glomeruli showed segmental collapse of glomerular tuft with hyperplasia of overlying visceral epithelial cells and were diagnosed as CG. The patients were managed with aggressive immunosuppressive therapy, including intravenous steroids in two patients and tacrolimus and cyclophosphamide in one patient. All three patients achieved partial remission of proteinuria with maintained renal function at the last follow-up. Collapsing glomerulopathy is a rare occurrence in patients with SLE, which should be considered in patients with lupus nephritis and significant proteinuria. A timely performed renal biopsy allows accurate diagnosis and appropriate therapeutic modifications.

show abstract

Glomerular pathology: recent advances

Cited by 22 publications

References 74 publications

Abnormal basement membrane in the inner ear and the kidney of the Mpv17-/- mouse strain: ultrastructural and immunohistochemical investigations

Abnormal basement membrane in the inner ear and the kidney of the Mpv17-/- mouse strain: ultrastructural and immunohistochemical investigations

Loss of the VEGF164 and VEGF188 Isoforms Impairs Postnatal Glomerular Angiogenesis and Renal Arteriogenesis in Mice

Collapsing glomerulopathy occurring in HIV-negative patients with systemic lupus erythematosus: report of three cases and brief review of the literature

Contact Info

Product

Resources

About