Age Changes in the Human Kidney of the Different Races

Tauchi, Hisashi; Tsuboi, Kazuhito; Okutomi, J.

doi:10.1159/000211811

Cited by 154 publications

(61 citation statements)

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“…However, because there were only a few subjects over age 60 and none over age 65, we cannot exclude a decline after age 60. The effect of age on renal parenchymal volume has not been determined in normal individuals, and the results of sonographic or autopsy studies of total renal mass are variable, ranging from a linear decline after age 40 (30) to no decline (20). Measurements of total volume or weight can be misleading in this regard, because sinus fat increases with age (28) and, as shown in this study, varies inversely with parenchymal volume.…”

Section: Discussionmentioning

confidence: 66%

Determinants and Functional Significance of Renal Parenchymal Volume in Adults

Johnson

Rishi

Andone

et al. 2011

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives The significance of renal parenchymal volume and the factors that influence it are poorly understood.Design, setting, participants, & measurements Renal parenchymal volume (RPV) was measured on contrastenhanced CT scans after exclusion of sinus fat and vessels in 224 healthy subjects evaluated as kidney donors and in a separate cohort of 22 severely obese individuals before and after 6 months of weight loss. GFR was measured by iohexol clearance in 76 of the transplant donors. RPV was correlated with age, GFR, and various anthropometric parameters. ResultsIn potential transplant donors, RPV correlated with body surface area (BSA; r ϭ 0.68) and was 7% larger in men but did not vary with age or race. Gender and body size were independent determinants of RPV. RPV correlated well with GFR (r ϭ 0.62) and accounted for almost all of the variability in a model of GFR that included age, race, gender, and body surface area. GFR correlated more strongly with RPV than with creatinine-based equations. The same relationship between RPV and BSA was observed in obesity, and RPV decreased with weight loss. ConclusionsIn healthy adults younger than 65 years, renal parenchymal volume is governed by body size and gender but not age or race and is strongly correlated with GFR. This indicates that renal parenchymal volume varies to meet metabolic demand and is closely linked to renal function.

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Section: Discussionmentioning

confidence: 66%

Determinants and Functional Significance of Renal Parenchymal Volume in Adults

Johnson

Rishi

Andone

et al. 2011

Clinical Journal of the American Society of Nephrology

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“…Evidence from autopsy studies suggests a wide range in the number of nephrons in the 'normal' kidney Nyengaard & Bendtsen, 1992). Nephrons are lost both with ageing (Moore, 1931;Nyengaard & Bendtsen, 1992;Tauchi, Tsuboi, & Okutomi, 1971) and due to a variety of nephropathic insults. Damage to the glomerulus, the filtration segment of the nephron, is marked by protein leakage into the urine, making the appearance of urinary protein or albumin a marker of early renal disease.…”

Section: Early Development Explanationsmentioning

confidence: 99%

Exploring the pathways leading from disadvantage to end-stage renal disease for Indigenous Australians

Cass

Cunningham

Snelling³

et al. 2004

Social Science & Medicine

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Indigenous Australians are disadvantaged, relative to other Australians, over a range of socio-economic and health measures. The age-and sex-adjusted incidence of end-stage renal disease (ESRD) -the irreversible preterminal phase of chronic renal failure -is almost nine times higher amongst Indigenous than it is amongst non-indigenous Australians. A striking gradient exists from urban to remote regions, where the standardised ESRD incidence is from 20 to more than 30 times the national incidence. We discuss the profound impact of renal disease on Indigenous Australians and their communities. We explore the linkages between disadvantage, often accompanied by geographic isolation, and both the initiation of renal disease, and its progression to ESRD. Purported explanations for the excess burden of renal disease in indigenous populations can be categorised as:(1) primary renal disease explanations; (2) genetic explanations; (3) early development explanations; and (4) socio-economic explanations.We discuss the strengths and weaknesses of these explanations and suggest a new hypothesis which integrates the existing evidence. We use this hypothesis to illuminate the pathways between disadvantage and the human biological processes which culminate in ESRD, and to propose prevention strategies across the life-course of Indigenous Australians to reduce their ESRD risk.Our hypothesis is likely to be relevant to an understanding of patterns of renal disease in other high-risk populations, particularly indigenous people in the developed world and people in developing countries. Furthermore, analogous pathways might be relevant to other chronic diseases, such as diabetes and cardiovascular disease. If we are able to confirm the various pathways from disadvantage to human biology, we will be better placed to advocate evidence-based interventions, both within and beyond the scope of the health-care system, to address the excess burden of renal and other chronic diseases among affected populations.

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“…After 40, there was a steady loss of nephrons. Tauchi et al 20 examined the kidneys of Japanese and Caucasians and reported a decrease in the number of parenchymal cells and tendency to increase in the size of cells as the main characteristics of senile changes. The size of glomeruli did not show any marked change with age in Caucasians, whereas in Japanese, there a significant decrease was evident in their size.…”

Section: Discussionmentioning

confidence: 99%