Renal Function and the Number of Glomeruli in the Human Kidney

Hayman, J. M.; Martin, J. W.; Miller, Max

doi:10.1001/archinte.1939.00190010079007

Cited by 44 publications

(29 citation statements)

References 23 publications

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“…Denic et al (23) recently reported that aging (>70 years) US transplant donors have nearly 50% fewer nonsclerosed glomeruli than 18-to 40-year-old donors, and this nephron loss is the result of nephrosclerosis with global glomerulosclerosis. Old, obsolescent glomeruli are thought to be absorbed without trace from the kidney, such that the extent of glomerular loss is unaccounted for by the amount of glomerulosclerosis (23,34). Given that 2 of the 9 normotensive subjects were older than 70 years, it is possible that our low nephron counts in normotensive Japanese may also be explained by age-related nephron loss.…”

Section: Discussionmentioning

confidence: 99%

New insights on glomerular hyperfiltration: a Japanese autopsy study

Kanzaki¹,

Puelles²,

Cullen‐McEwen³

et al. 2017

JCI Insight

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Section: Discussionmentioning

confidence: 99%

New insights on glomerular hyperfiltration: a Japanese autopsy study

Kanzaki¹,

Puelles²,

Cullen‐McEwen³

et al. 2017

JCI Insight

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“…The nephron number is inversely related to glomerular volume [63] , and glomerular enlargement is found in these ethnic groups with a high incidence of hypertension and progressive renal disease [91,92] , both associated with IUGR [5, 6] . Hayman et al [93] described in 1939 an association between nephron number and hypertension. An autopsy study in humans from Keller et al [94] confirms the link between hypertension and fewer, but larger glomeruli, providing evidence for a low number of glomeruli as an explanation for primary hypertension.…”

Section: Intrauterine Growth Restrictionmentioning

confidence: 99%

Consequences of Intrauterine Growth Restriction for the Kidney

Schreuder

Waal

Wijk

2006

Kidney Blood Press Res

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Low birth weight due to intrauterine growth restriction is associated with various diseases in adulthood, such as hypertension, cardiovascular disease, insulin resistance and end-stage renal disease. The purpose of this review is to describe the effects of intrauterine growth restriction on the kidney. Nephrogenesis requires a fine balance of many factors that can be disturbed by intrauterine growth restriction, leading to a low nephron endowment. The compensatory hyperfiltration in the remaining nephrons results in glomerular and systemic hypertension. Hyperfiltration is attributed to several factors, including the renin-angiotensin system (RAS), insulin-like growth factor (IGF-I) and nitric oxide. Data from human and animal studies are presented, and suggest a faltering IGF-I and an inhibited RAS in intrauterine growth restriction. Hyperfiltration makes the kidney more vulnerable during additional kidney disease, and is associated with glomerular damage and kidney failure in the long run. Animal studies have provided a possible therapy with blockage of the RAS at an early stage in order to prevent the compensatory glomerular hyperfiltration, but this is far from being applicable to humans. Research is needed to further unravel the effect of intrauterine growth restriction on the kidney.

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“…The "nephron endowment" is determined by 36 weeks of gestation (1), although new nephron formation after birth in humans has been suggested (2). Low birth weight (from any cause, including preterm birth) is strongly correlated with reduced nephron endowment (3,4) and results in hyperfiltration from birth (5), leading to an increase risk of essential hypertension (6)(7)(8)(9) and chronic kidney disease later in life (10,11); these infants are thus placed at long-term risk for disease. Currently, there is no known method to increase nephron number in newborn or adult humans.…”

Section: Introductionmentioning

confidence: 99%