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      Age Trends of Renal Arteriolar Hyalinization Explored with the Aid of Serial Sections

      Nephron Clinical Practice

      S. Karger AG

      Human aging, Arteriolosclerosis, Hypertension, Nephrosclerosis

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          Abstract

          Background: Hyalinized renal arterioles (Hy) can be counted per unit area of PAS-stained paraffin sections. The percentages of nephrons having hyalinized afferent and efferent arterioles can be assessed in serial sections. Methods: Slides of renal tissue were assessed for Hy in 559 basal forensic autopsies, i.e. those with no condition known to correlate with hypertension. Serial sections in a series of 20 cases were used to measure afferent and efferent arterioles and determine formulas to relate afferent and efferent arterioles to Hy. The formulas were used in the 559 cases to assess the trends on age of Hy in terms of percentage of affected nephrons. Results: Hy increased rapidly from ages 15 to 34 years, but stabilized from ages 35 to 102 years at levels implying afferent arterioles of about 2/5 of nephrons and efferent arterioles of about 1/5. Most of the nephrons in the kidney were deduced to be supplied by hyalinized afferent arterioles in nearly half of all subjects from ages 35 to 102 years, and the rates were the same at all ages. Conclusion: These data provide for the first time provisional estimates for the prevalence of Hy to be used as baselines for biopsy comparisons. Failure of numerous kidneys to enter end-stage nephrosclerosis in spite of several decades of involvement by hyalinization in half or more of their arterioles does not support the view that hyalinization induces ischemic nephron atrophy.

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          Most cited references 4

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          Insudative lesions--their pathogenesis and association with glomerular obsolescence in diabetes: a dynamic hypothesis based on single views of advancing human diabetic nephropathy.

          Kidneys from 74 consecutive, primarily non-insulin-dependent diabetics at autopsy and 59 age-, sex, and ethnic group-matched controls were examined qualitatively and semiquantitatively to determine the prevalence and severity of insudative lesions (ILs) and obsolescent glomeruli with (OGcFC) and without (OGsFC) insudative (fibrin cap) lesions. A subset of 25 cases with advanced diabetic changes was examined using serial sections, immunohistochemical stains, and electron microscopy to determine the pathogenesis of ILs and OGcFCs. Insudative lesions consisted of intramural accumulations (hereafter called deposits) of presumably imbibed plasma proteins and lipids within renal arterioles, glomerular capillaries, Bowman's capsule, and proximal convoluted tubules. Insudative lesions in Bowman's capsule are called capsular drop lesions (CDs), in glomerular capillaries they are called fibrin cap lesions (FC), and in afferent and efferent arterioles they are called hyalinized afferent (HA) and hyalinized efferent (HE) arterioles, respectively. All ILs were much more numerous and/or larger in diabetics than in controls. Contrary to previous opinion, CDs and HE arterioles were not specific for diabetes, being present in small numbers in nine (15%) controls. Controls with CD/HE arterioles had far more HA arterioles and focal mesangiolyses (FMs) than those without. Insudative lesions consisted of the well known homogenous eosinophilic deposits (homogenous eosinophilic ILs) and the less familiar foamy, reticulated, and vacuolar deposits (heterogenous lucent ILs). Homogenous eosinophilic ILs were predominant in afferent arterioles and more so in efferent arterioles, and were segregated into globules of varying density with the denser deposits located peripherally. Two types of CDs, which differed sharply in location and composition, were found. The first was mostly homogenous eosinophilic, usually without capsular adhesions and located near the vascular pole close to preglomerular arterioles. The second was mostly heterogenous lucent, located away from the vascular pole, and consistently connected by adhesions to the capillary tuft usually near FMs and/or Kimmelstiel-Wilson (KW) nodules. The latter ILs sometimes extended in continuity along the internal surface of the basement membrane from Bowman's capsule into the proximal convoluted tubule. It was hypothesized that ILs traveled centrifugally through the walls of preglomerular arterioles to form the first type of CD and longitudinally within the walls of afferent arterioles and glomerular capillaries and through adhesions to form the second. Contrary to previous opinion, FCs were consistently intramural. When numerous, FCs were associated with a form of glomerular obsolescence called OGcFC.(ABSTRACT TRUNCATED AT 400 WORDS)
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            What is 'nephrosclerosis'? lessons from the US, Japan, and Mexico.

            Selected features of 'nephrosclerosis' can be quantitated morphometrically in renal histology at autopsy. Specimens are available from Japan, Mexico, and the US (blacks and whites). Autopsies of men and women aged 15-79 years provided renal samples for paraffin sectioning. These were assembled in New Orleans for objective evaluation after standardized staining with PAS-Alcian blue and interspersion with each other. Obsolescence of glomeruli, interstitial fibrosis, fibroplastic intimal thickenings of arteries, and arteriolar hyalinization, as operationally defined, were measured by objective morphometry. Obsolescence of glomeruli and interstitial fibrosis displayed the expected correlation with arterial intimal fibroplasia, but failed to confirm any direct association with arteriolar hyalinization. Some of the variation of 'nephrosclerosis', within and between populations, cannot be fully explained by microvascular defects. Arterial intimal fibroplasia appeared to promote 'nephrosclerosis', in the sense of fibrous replacement of atrophied nephrons, but arteriolar hyalinization did not. Hyaline deposits in arterioles may offer little or no threat to the integrity of the affected nephrons. 'Nephrosclerosis' appears to be multifactorial; it may be, in part, a consequence of fibroplasia in microscopic arteries causing ischaemic injury to scattered nephrons, but may also be a confluence of basically separate conditions, only some of which are known.
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              The epidemiologic necropsy for abdominal aortic aneurysm.

              The epidemiologic necropsy measures the occurrence of unsuspected disease through the examination of necropsy records. The estimates of unsuspected disease should approximate what occurs in the living population. The necropsy records of the University of Kansas Medical Center (Kansas City) from 1950 to 1984 were examined for the occurrence rate of abdominal aortic aneurysms. Each adult patient was categorized as (1) without abdominal aortic aneurysm, (2) abdominal aortic aneurysm discovered as a necropsy surprise, or (3) abdominal aortic aneurysm diagnosed or suspected during life. Necropsy detection rates of unsuspected abdominal aortic aneurysms were compared with those found in five published screening surveys. The necropsy detection rate in men was 81 (0.019) of 4155 and was 28 (0.009) of 3142 in women, a difference that was statistically significant. When the necropsy series was adjusted to reflect the same demographic composition as the screening surveys, the results from necropsy and screening were statistically similar. In particular, two surveys from the United Kingdom showed screening detection rates among white men of 0.072 compared with a necropsy detection rate of 0.058. These results further support the use of the epidemiologic necropsy as a research tool for estimating the reservoir of disease in the population.
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                Author and article information

                Journal
                NEC
                Nephron Clin Pract
                10.1159/issn.1660-2110
                Nephron Clinical Practice
                S. Karger AG
                1660-2110
                2007
                March 2007
                29 January 2007
                : 105
                : 4
                : c171-c177
                Affiliations
                Department of Pathology, Louisiana State University Health Sciences Center, New Orleans, La., USA
                Article
                99036 Nephron Clin Pract 2007;105:c171–c177
                10.1159/000099036
                17264518
                © 2007 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 4, Tables: 2, References: 15, Pages: 1
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/99036
                Categories
                Original Paper

                Cardiovascular Medicine, Nephrology

                Nephrosclerosis, Hypertension, Arteriolosclerosis, Human aging

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