See the published version of this preprint at Nutrition Journal.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research
Kalkidan Hassen Abate
Jimma University College of Public Health and Medical Sciences
Corresponding Author
ORCiD: https://orcid.org/0000-0001-9752-5417
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: 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.
Methods: 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/1.73m2 on at least in two occasions of ninety 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.
Results: 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).
Conclusion: 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.
Keywords
prenatal famine, eGFR: Chronic kidney disease
Figure 1
This is a list of supplementary files associated with this preprint. Click to download.
Loading...
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Nutrition Journal.
Version 2
Posted 12 Feb, 2021
No community comments so far
Editor assigned
On 06 Feb, 2021
Reviewers invited
Invitations sent on 06 Feb, 2021
Submission checks complete
On 06 Feb, 2021
Editor invited
On 06 Feb, 2021
First submitted
On 28 Oct, 2020
Version (no preprint)
Posted 03 Feb, 2021
Review #2 received
Received 03 Feb, 2021
Editorial decision: Minor revision
On 03 Feb, 2021
Reviewer #4 agreed
On 28 Jan, 2021
Reviewer #3 agreed
On 23 Dec, 2020
Reviewer #2 agreed
On 02 Nov, 2020
Review #1 received
Received 01 Nov, 2020
Editor assigned
On 29 Oct, 2020
Reviewers invited
Invitations sent on 29 Oct, 2020
Reviewer #1 agreed
On 29 Oct, 2020
Submission checks complete
On 28 Oct, 2020
Editor invited
On 28 Oct, 2020
This version was not preprinted
No comments provided
Review #2 received
Received 19 Oct, 2020
Reviewer #2 agreed
On 01 Oct, 2020
Reviewer #3 agreed
On 01 Oct, 2020
Review #1 received
Received 01 Oct, 2020
Reviewer #1 agreed
On 29 Sep, 2020
Reviewers invited
Invitations sent on 23 Sep, 2020
Editor assigned
On 15 Sep, 2020
Submission checks complete
On 14 Sep, 2020
Editor invited
On 14 Sep, 2020
First submitted
On 11 Sep, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Nutrition & Dietetics
Learn more about our company.
See the published version of this preprint at Nutrition Journal.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research
Kalkidan Hassen Abate
Jimma University College of Public Health and Medical Sciences
Corresponding Author
ORCiD: https://orcid.org/0000-0001-9752-5417
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Nutrition Journal.
Version 2
Posted 12 Feb, 2021
No community comments so far
Editor assigned
On 06 Feb, 2021
Reviewers invited
Invitations sent on 06 Feb, 2021
Submission checks complete
On 06 Feb, 2021
Editor invited
On 06 Feb, 2021
First submitted
On 28 Oct, 2020
Version (no preprint)
Posted 03 Feb, 2021
Review #2 received
Received 03 Feb, 2021
Editorial decision: Minor revision
On 03 Feb, 2021
Reviewer #4 agreed
On 28 Jan, 2021
Reviewer #3 agreed
On 23 Dec, 2020
Reviewer #2 agreed
On 02 Nov, 2020
Review #1 received
Received 01 Nov, 2020
Editor assigned
On 29 Oct, 2020
Reviewers invited
Invitations sent on 29 Oct, 2020
Reviewer #1 agreed
On 29 Oct, 2020
Submission checks complete
On 28 Oct, 2020
Editor invited
On 28 Oct, 2020
This version was not preprinted
No comments provided
Review #2 received
Received 19 Oct, 2020
Reviewer #2 agreed
On 01 Oct, 2020
Reviewer #3 agreed
On 01 Oct, 2020
Review #1 received
Received 01 Oct, 2020
Reviewer #1 agreed
On 29 Sep, 2020
Reviewers invited
Invitations sent on 23 Sep, 2020
Editor assigned
On 15 Sep, 2020
Submission checks complete
On 14 Sep, 2020
Editor invited
On 14 Sep, 2020
First submitted
On 11 Sep, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Nutrition & Dietetics
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Nutrition Journal.
Background: 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.
Methods: 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/1.73m2 on at least in two occasions of ninety 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.
Results: 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).
Conclusion: 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.
Figure 1
This is a list of supplementary files associated with this preprint. Click to download.
Loading...