Department of Nutrition and Dietetics, Institute of Health, Jimma University, Jimma, Ethiopia.
Department of Population and Family Heath, Institute of Health, Jimma University, Jimma, Ethiopia.
Nutr J. 2021 Mar 2;20(1):19. doi: 10.1186/s12937-021-00675-8.
The impact of an adverse prenatal environment such as famine exposure on the development of adulthood non-communicable chronic illnesses, including diabetes and hypertension has been well articulated in the recent past and supported by evidence. However, there exist few longitudinal studies conducted on the long term consequences of prenatal famine exposure on adulthood kidney function. Hence, we set out to examine whether prenatal exposure to the Ethiopian Great Famine (1983-1985) was associated with changes in estimated glomerular filtration rate (eGFR) and the risk of developing chronic kidney disease (CKD) later in adult life.
The study was conducted in 219 famine exposed and 222 non exposed cohorts in Raya Kobo district, North Wollo Zone, Northern Ethiopia. Estimated GFR was computed from standardized serum creatinine using the CKD Epidemiology Collaboration (CKD-EPI) equation. The definition of CKD includes those with an eGFR of less than 60 ml/min/1.73 m2 on at least in two occasions of 90 days apart (with or without markers of kidney damage). Linear and logistic regression analyses were employed to examine the independent effect of prenatal famine exposure on eGFR and CKD respectively.
The mean (SD) serum creatinine of exposed and non-exposed groups were 0.78 (0.2) and 0.75 (0.2) respectively. The mean (SD) eGFR of exposed groups was 107.95 (27.49) while the non-exposed 114.48 (24.81) ml/min. In linear regression, the unadjusted model to examine the association between famine exposure and eGFR resulted in a significant negative beta coefficient (β = - 0.124: 95% CI: - 11.43, - 1.64). Adjusting the exposure for outstanding covariates of kidney health, including systolic blood pressure, fasting blood sugar and blood glucose did not alter the inverse relationship (β = -.114 95% CI: - 10.84, - 1.17). In the unadjusted bivariate logistic regression model, famine exposure resulted in nearly 2.7 times higher odds of developing CKD (OR: 2.68, 95% CI: 1.16, 6.2). The odds remained equivalent after adjusting for systolic blood pressure, fasting blood glucose and body mass index (OR = 2.61: 95% CI: 1.120, 6.09).
In the study setting, prenatal exposure to the Great Ethiopian Famine was associated with decreased eGFR and higher risk of developing CKD among survivors. These findings may imply that famine in early life may play a significant role in the development of kidney dysfunction in adulthood.
最近的研究表明,产前环境(如饥荒暴露)对成年期非传染性慢性疾病(包括糖尿病和高血压)的发展有重大影响,这一观点已得到充分论证,并得到了证据的支持。然而,关于产前饥荒暴露对成年期肾功能的长期影响,目前仅有少数纵向研究。因此,我们着手研究 1983-1985 年埃塞俄比亚大饥荒是否与成年后肾小球滤过率(eGFR)的变化以及慢性肾脏病(CKD)的发生风险有关。
在北沃洛州拉亚科博地区的 219 名暴露于饥荒的队列和 222 名未暴露于饥荒的队列中进行了这项研究。使用 CKD 协作流行病学(CKD-EPI)方程,根据标准化血清肌酐计算估计的肾小球滤过率(eGFR)。CKD 的定义包括至少两次相隔 90 天的 eGFR 低于 60ml/min/1.73m2(有或没有肾脏损伤标志物)的人群。采用线性和逻辑回归分析分别检验产前饥荒暴露对 eGFR 和 CKD 的独立影响。
暴露组和未暴露组的平均(标准差)血清肌酐分别为 0.78(0.2)和 0.75(0.2)。暴露组的平均(标准差)eGFR 为 107.95(27.49),未暴露组为 114.48(24.81)。在未调整模型中,线性回归分析显示,饥荒暴露与 eGFR 之间存在显著的负相关关系(β= -0.124:95%置信区间:-11.43,-1.64)。在调整了包括收缩压、空腹血糖和血糖在内的肾脏健康的显著混杂因素后,暴露对 eGFR 的影响并没有改变(β= -0.114,95%置信区间:-10.84,-1.17)。在未调整的二元逻辑回归模型中,饥荒暴露使 CKD 的发病风险增加了近 2.7 倍(OR:2.68,95%置信区间:1.16,6.2)。调整收缩压、空腹血糖和体重指数后,这一比值仍然相当(OR=2.61:95%置信区间:1.120,6.09)。
在研究环境中,产前暴露于埃塞俄比亚大饥荒与幸存者的 eGFR 下降和 CKD 发病风险增加有关。这些发现可能意味着生命早期的饥荒可能在成年期肾功能障碍的发展中起重要作用。