Schreuder Michiel, Delemarre-van de Waal Henriette, van Wijk Ans
Department of Pediatric Nephrology, VU University Medical Center, Amsterdam, The Netherlands.
Kidney Blood Press Res. 2006;29(2):108-25. doi: 10.1159/000094538. Epub 2006 Jul 12.
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.
因子宫内生长受限导致的低出生体重与成年期的多种疾病相关，如高血压、心血管疾病、胰岛素抵抗和终末期肾病。本综述的目的是描述子宫内生长受限对肾脏的影响。肾发生需要多种因素的精细平衡，而这些因素可能会因子宫内生长受限而受到干扰，导致肾单位数量减少。剩余肾单位的代偿性高滤过会导致肾小球和全身性高血压。高滤过归因于多种因素，包括肾素 - 血管紧张素系统（RAS）、胰岛素样生长因子（IGF - I）和一氧化氮。本文呈现了来自人类和动物研究的数据，提示在子宫内生长受限中IGF - I功能失常以及RAS受到抑制。高滤过使肾脏在额外发生肾脏疾病时更易受损，从长远来看还与肾小球损伤和肾衰竭相关。动物研究提供了一种在早期阶段阻断RAS以预防代偿性肾小球高滤过的可能疗法，但这远不能应用于人类。需要开展研究以进一步阐明子宫内生长受限对肾脏的影响。
