Glomerular basement membrane thickness in children: A stereologic assessment

Ramage, Ian; Howatson, Allan G.; McColl, John H.; Maxwell, Heather; Murphy, Anna V.; Beattie, Tom F.

doi:10.1046/j.1523-1755.2002.00527.x

Cited by 42 publications

(42 citation statements)

References 22 publications

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“…Although TBMN is considered to have a good prognosis owing to a nonprogressive nephropathy, numerous hints in the literature suggest a reduced lifespan in affected individuals. First, the possibility that TBMN may not be benign in terms of ultimate prognosis has been considered before (13,14,18,30,25), and ESRD similar to that seen in AS was reported in adults with heterozygote COL4A3/A4 mutations (occasionally also referred to as "autosomal dominant Alport syndrome") (15,34 -37). It should be noted that it was suggested that the molecular type of COL4A3/A4 mutations and additional modifier genes are likely to influence the severity of the renal phenotype eventually (35,36,37).…”

Section: Discussionmentioning

confidence: 99%

Chronic Renal Failure and Shortened Lifespan in COL4A3+/− Mice

Beirowski¹,

Weber²,

Groß³

2006

Journal of the American Society of Nephrology

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Section: Discussionmentioning

confidence: 99%

Chronic Renal Failure and Shortened Lifespan in COL4A3+/− Mice

Beirowski¹,

Weber²,

Groß³

2006

Journal of the American Society of Nephrology

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“…Type 2 diabetic patients in both the early and the late stages of disease, although the mechanisms leading to increase in glomerular size may differ (Moriya et al 2000; Ramage et al 2002). Previous studies (Osterby & Gunderson, 1980;Hirose et al 1982;Nyengaard & Rasch, 1993) provide convincing evidence of glomerular capillary growth and glomerular hypertrophy as an earliest response to hyperglycaemia in diabetic nephropathy.…”

Section: Glomerular Hypertrophy Occurs In Both Type 1 Andmentioning

confidence: 97%

A stereological study of the renal glomerular vasculature in the db/db mouse model of diabetic nephropathy

et al. 2005

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In diabetic nephropathy, glomerular hypertrophy is evident early in response to hyperglycaemia. Alterations of capillary length and vascular remodelling that may contribute to glomerular hypertrophy and the subsequent development of glomerulosclerosis remain unclear. The present study used the db/db mouse model of Type 2 diabetes to examine the glomerular microvascular changes apparent with long-term diabetic complications. Unbiased stereological methods and high-resolution light microscopy were used to estimate glomerular volume, and glomerular capillary dimensions including length and surface area in 7-month-old db/db diabetic mice and age-matched db/m control mice. The db/db diabetic mice showed significant glomerular hypertrophy, corresponding with elevated blood glucose levels, and increased body weight and kidney weight, compared with db/m control mice.

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“…The thickness of glomerular basement membrane (GBM) was determined by the orthogonal intercept method as described previously. 26,27 In brief, the shortest distance between endothelial cytoplasmic membrane and the outer lining of the lamina rara externa underneath the cytoplasmic membrane of the epithelial foot processes was measured with a logarithmic ruler where gridlines transected the GBM. The true harmonic mean thickness (Th) was estimated from the apparent harmonic mean thickness (lh) using the following equation: Th ϭ 8/3 ϫ 10mesangiolysis were excluded from the measurements.…”

Section: Evaluation Of Morphological Changesmentioning

confidence: 99%

Deficiency of Endothelial Nitric-Oxide Synthase Confers Susceptibility to Diabetic Nephropathy in Nephropathy-Resistant Inbred Mice

Kanetsuna

Takahashi

Nagata

et al. 2007

The American Journal of Pathology

166

150

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Recent studies have implicated dysfunctional endothelial nitric-oxide synthase (eNOS) as a common pathogenic pathway in diabetic vascular complications. However, functional consequences are still incompletely understood. To determine the role of eNOS-derived nitric oxide (NO) in diabetic nephropathy, we induced diabetes in eNOS knockout (KO) and wild-type (WT) mice on the C57BL6 background, using low-dose streptozotocin injection, and we investigated their glomerular phenotype at up to 20 weeks of diabetes. Although the severity of hyperglycemia in diabetic eNOS KO mice was similar to diabetic WT mice, diabetic eNOS KO mice developed overt albuminuria, hypertension, and glomerular mesangiolysis, whereas diabetic WT and nondiabetic control mice did not. Glomerular hyperfiltration was also significantly reduced in diabetic eNOS KO mice. Electron micrographs from diabetic eNOS KO mice revealed an injured endothelial morphology, thickened glomerular basement membrane, and focal foot process effacement. Furthermore, the anionic sites at glomeru- Nitric oxide (NO) is a free radical that mediates diverse functions in a range of biological systems.1 NO is produced by a family of nitric-oxide synthase (NOS) enzymes to catalyze the stoichiometric five-electron oxidation of the terminal quanidino group of L-arginine to produce NO and L-citrulline. Three NOS isoforms have been distinguished in mammalian species: neuronal NOS, inducible NOS, which is expressed in a variety of activated tissues, and endothelial NOS (eNOS).1 In the vasculature, NO is mostly generated by eNOS, and the generated NO plays a crucial role in maintaining vascular homeostasis, including vascular tone, leukocyte adhesion to endothelium, proliferation of vascular smooth muscle cells, and platelet aggregation and adhesion to the vessel wall.

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Glomerular basement membrane thickness in children: A stereologic assessment

Abstract: Stereologic methods are superior to model based techniques in estimating GBM thickness and should be regarded as the technique of choice in this area. GBM thickness was observed to increase during childhood with no gender effect demonstrable as a main effect or interaction.

Cited by 42 publications

References 22 publications

Chronic Renal Failure and Shortened Lifespan in COL4A3+/− Mice

Chronic Renal Failure and Shortened Lifespan in COL4A3+/− Mice

A stereological study of the renal glomerular vasculature in the db/db mouse model of diabetic nephropathy

Deficiency of Endothelial Nitric-Oxide Synthase Confers Susceptibility to Diabetic Nephropathy in Nephropathy-Resistant Inbred Mice

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