Matches in SemOpenAlex for { <https://semopenalex.org/work/W2029182408> ?p ?o ?g. }
- W2029182408 endingPage "1036" @default.
- W2029182408 startingPage "1027" @default.
- W2029182408 abstract "Morphometric study of arterioles and glomeruli in the aging kidney suggests focal loss of autoregulation.BackgroundIn the past it was widely assumed that hyaline afferent arteriolosclerosis was responsible for ischemic glomerulosclerosis in the aging and hypertensive kidney. However, glomerular lesions of focal segmental glomerulosclerosis are now recognized in essential hypertension. Experimentally, such lesions are associated with loss of autoregulation of blood flow and glomerular hyperperfusion, as well as initial glomerular hypertrophy. These observations challenge the notion of ischemia as a unitary explanation for glomerulosclerosis.MethodsA morphometric study was performed on normal portions of eight kidneys removed for tumors in aging, normotensive patients. Measurements were made of 126 pairs of afferent arterioles and their associated glomeruli. In addition, the amount of extracellular matrix (ECM) in the immediate periglomerular region was quantitated.ResultsAfferent arterioles were divided into three types according to the presence or absence of hyaline deposits and whether these did or did not obstruct the lumen. Arterioles with nonobstructive hyaline deposits had lumens over twice as large as those without deposits (482 ± 240 μ2 vs. 204 ± 160 μ2, P = 0.0000). Their associated glomeruli had significantly greater total capillary area, particularly the hilar capillaries (1276 ± 797 μ2 vs. 667 ± 492 μ2, P = 0.002), but with larger individual capillaries elsewhere as well (P = 0.03). Arterioles with obstructive deposits differed from those with nonobstructive deposits by their smaller lumens (P = 0.001) and walls (P = 0.004), with a higher proportion of ECM in the periglomerular region (P = 0.001), all consistent with a later stage of lesion. Glomeruli were divided into four basic types: normal, hypertrophic, glomeruli with features of focal segmental glomerulosclerosis (FSGS-type), and ischemic. Compared to normal glomeruli, hypertrophic glomeruli were larger, with greater total capillary area (P = 0.0005), particularly the hilar capillaries (P = 0.0000), and larger capillaries in the remainder of the tuft (P = 0.003), but showed no evident lesions. FSGS-type glomeruli were also larger, with larger hilar capillaries (P = 0.0005), but showed an increase in ECM due to sclerotic lesions (P = 0.004). The remaining capillaries showed an inverse relation with the amount of mesangial matrix, showing a spectrum of sizes from enlarged to shrunken. As anticipated, ischemic glomeruli were significantly smaller than normal ones in every parameter measured. There was a strong association between hypertrophic/FSGS-type glomeruli and hyaline arteriolosclerosis, found in 90.3% of such glomeruli, versus 29.1% for the remaining glomeruli (P = 0.0001). The great majority of hyaline deposits were of the nonobstructive variety (86.2%), but some were obstructive (13.8%), particularly in FSGS-type glomeruli, consistent with a more advanced lesion.ConclusionsWe believe we have demonstrated in the aging kidney of humans the morphologic correlates of loss of autoregulation, occurring on a focal basis, with afferent arteriolar dilatation and increase in glomerular capillary size and subsequent focal segmental glomerulosclerosis. Hyaline arteriolosclerosis of the nonobstructive sort is strongly associated with these changes and may play a role in their pathogenesis. Morphometric study of arterioles and glomeruli in the aging kidney suggests focal loss of autoregulation. In the past it was widely assumed that hyaline afferent arteriolosclerosis was responsible for ischemic glomerulosclerosis in the aging and hypertensive kidney. However, glomerular lesions of focal segmental glomerulosclerosis are now recognized in essential hypertension. Experimentally, such lesions are associated with loss of autoregulation of blood flow and glomerular hyperperfusion, as well as initial glomerular hypertrophy. These observations challenge the notion of ischemia as a unitary explanation for glomerulosclerosis. A morphometric study was performed on normal portions of eight kidneys removed for tumors in aging, normotensive patients. Measurements were made of 126 pairs of afferent arterioles and their associated glomeruli. In addition, the amount of extracellular matrix (ECM) in the immediate periglomerular region was quantitated. Afferent arterioles were divided into three types according to the presence or absence of hyaline deposits and whether these did or did not obstruct the lumen. Arterioles with nonobstructive hyaline deposits had lumens over twice as large as those without deposits (482 ± 240 μ2 vs. 204 ± 160 μ2, P = 0.0000). Their associated glomeruli had significantly greater total capillary area, particularly the hilar capillaries (1276 ± 797 μ2 vs. 667 ± 492 μ2, P = 0.002), but with larger individual capillaries elsewhere as well (P = 0.03). Arterioles with obstructive deposits differed from those with nonobstructive deposits by their smaller lumens (P = 0.001) and walls (P = 0.004), with a higher proportion of ECM in the periglomerular region (P = 0.001), all consistent with a later stage of lesion. Glomeruli were divided into four basic types: normal, hypertrophic, glomeruli with features of focal segmental glomerulosclerosis (FSGS-type), and ischemic. Compared to normal glomeruli, hypertrophic glomeruli were larger, with greater total capillary area (P = 0.0005), particularly the hilar capillaries (P = 0.0000), and larger capillaries in the remainder of the tuft (P = 0.003), but showed no evident lesions. FSGS-type glomeruli were also larger, with larger hilar capillaries (P = 0.0005), but showed an increase in ECM due to sclerotic lesions (P = 0.004). The remaining capillaries showed an inverse relation with the amount of mesangial matrix, showing a spectrum of sizes from enlarged to shrunken. As anticipated, ischemic glomeruli were significantly smaller than normal ones in every parameter measured. There was a strong association between hypertrophic/FSGS-type glomeruli and hyaline arteriolosclerosis, found in 90.3% of such glomeruli, versus 29.1% for the remaining glomeruli (P = 0.0001). The great majority of hyaline deposits were of the nonobstructive variety (86.2%), but some were obstructive (13.8%), particularly in FSGS-type glomeruli, consistent with a more advanced lesion. We believe we have demonstrated in the aging kidney of humans the morphologic correlates of loss of autoregulation, occurring on a focal basis, with afferent arteriolar dilatation and increase in glomerular capillary size and subsequent focal segmental glomerulosclerosis. Hyaline arteriolosclerosis of the nonobstructive sort is strongly associated with these changes and may play a role in their pathogenesis." @default.
- W2029182408 created "2016-06-24" @default.
- W2029182408 creator A5059751677 @default.
- W2029182408 creator A5074883217 @default.
- W2029182408 creator A5089507696 @default.
- W2029182408 date "2003-03-01" @default.
- W2029182408 modified "2023-10-16" @default.
- W2029182408 title "Morphometric study of arterioles and glomeruli in the aging kidney suggests focal loss of autoregulation11See Editorial by Olson, p. 1162." @default.
- W2029182408 cites W1972957271 @default.
- W2029182408 cites W1981643883 @default.
- W2029182408 cites W1985133368 @default.
- W2029182408 cites W1993196935 @default.
- W2029182408 cites W1995976380 @default.
- W2029182408 cites W1996170341 @default.
- W2029182408 cites W2010451625 @default.
- W2029182408 cites W2011497717 @default.
- W2029182408 cites W2020397175 @default.
- W2029182408 cites W2027957168 @default.
- W2029182408 cites W2034961623 @default.
- W2029182408 cites W2060140375 @default.
- W2029182408 cites W2081864124 @default.
- W2029182408 cites W2087167475 @default.
- W2029182408 cites W2089707588 @default.
- W2029182408 cites W2096816041 @default.
- W2029182408 cites W2144403565 @default.
- W2029182408 cites W2144823962 @default.
- W2029182408 cites W2319716687 @default.
- W2029182408 cites W2325113966 @default.
- W2029182408 doi "https://doi.org/10.1046/j.1523-1755.2003.00831.x" @default.
- W2029182408 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12631084" @default.
- W2029182408 hasPublicationYear "2003" @default.
- W2029182408 type Work @default.
- W2029182408 sameAs 2029182408 @default.
- W2029182408 citedByCount "102" @default.
- W2029182408 countsByYear W20291824082012 @default.
- W2029182408 countsByYear W20291824082013 @default.
- W2029182408 countsByYear W20291824082014 @default.
- W2029182408 countsByYear W20291824082015 @default.
- W2029182408 countsByYear W20291824082016 @default.
- W2029182408 countsByYear W20291824082017 @default.
- W2029182408 countsByYear W20291824082018 @default.
- W2029182408 countsByYear W20291824082019 @default.
- W2029182408 countsByYear W20291824082020 @default.
- W2029182408 countsByYear W20291824082021 @default.
- W2029182408 countsByYear W20291824082022 @default.
- W2029182408 countsByYear W20291824082023 @default.
- W2029182408 crossrefType "journal-article" @default.
- W2029182408 hasAuthorship W2029182408A5059751677 @default.
- W2029182408 hasAuthorship W2029182408A5074883217 @default.
- W2029182408 hasAuthorship W2029182408A5089507696 @default.
- W2029182408 hasBestOaLocation W20291824081 @default.
- W2029182408 hasConcept C105702510 @default.
- W2029182408 hasConcept C118494813 @default.
- W2029182408 hasConcept C126322002 @default.
- W2029182408 hasConcept C12722491 @default.
- W2029182408 hasConcept C131631996 @default.
- W2029182408 hasConcept C142724271 @default.
- W2029182408 hasConcept C2777390665 @default.
- W2029182408 hasConcept C2778305430 @default.
- W2029182408 hasConcept C2779134260 @default.
- W2029182408 hasConcept C2779561371 @default.
- W2029182408 hasConcept C2780091579 @default.
- W2029182408 hasConcept C2780636983 @default.
- W2029182408 hasConcept C2780793064 @default.
- W2029182408 hasConcept C2908929049 @default.
- W2029182408 hasConcept C71924100 @default.
- W2029182408 hasConcept C84393581 @default.
- W2029182408 hasConceptScore W2029182408C105702510 @default.
- W2029182408 hasConceptScore W2029182408C118494813 @default.
- W2029182408 hasConceptScore W2029182408C126322002 @default.
- W2029182408 hasConceptScore W2029182408C12722491 @default.
- W2029182408 hasConceptScore W2029182408C131631996 @default.
- W2029182408 hasConceptScore W2029182408C142724271 @default.
- W2029182408 hasConceptScore W2029182408C2777390665 @default.
- W2029182408 hasConceptScore W2029182408C2778305430 @default.
- W2029182408 hasConceptScore W2029182408C2779134260 @default.
- W2029182408 hasConceptScore W2029182408C2779561371 @default.
- W2029182408 hasConceptScore W2029182408C2780091579 @default.
- W2029182408 hasConceptScore W2029182408C2780636983 @default.
- W2029182408 hasConceptScore W2029182408C2780793064 @default.
- W2029182408 hasConceptScore W2029182408C2908929049 @default.
- W2029182408 hasConceptScore W2029182408C71924100 @default.
- W2029182408 hasConceptScore W2029182408C84393581 @default.
- W2029182408 hasIssue "3" @default.
- W2029182408 hasLocation W20291824081 @default.
- W2029182408 hasLocation W20291824082 @default.
- W2029182408 hasOpenAccess W2029182408 @default.
- W2029182408 hasPrimaryLocation W20291824081 @default.
- W2029182408 hasRelatedWork W1852486766 @default.
- W2029182408 hasRelatedWork W1996120316 @default.
- W2029182408 hasRelatedWork W2009420095 @default.
- W2029182408 hasRelatedWork W2029182408 @default.
- W2029182408 hasRelatedWork W2075327813 @default.
- W2029182408 hasRelatedWork W2325113966 @default.
- W2029182408 hasRelatedWork W2413901792 @default.
- W2029182408 hasRelatedWork W2417603516 @default.
- W2029182408 hasRelatedWork W2419468104 @default.
- W2029182408 hasRelatedWork W255922607 @default.