Response to Birth Weight and Renal Functional Reserve in Adults

In this issue Tsuboi and Bertram have commented on our paper “Renal functional response – association with birth weight and kidney volume”. We would like to thank the authors for the appreciation of our research and for questioning the level of prematurity of our low birth weight (LBW) cohort. It is argued that being born close to term, yet premature; the kidneys of the LBW group may have been too well developed to allow for a reduced renal functional response (RFR). This is a valid argument that unfortunately was not discussed in our paper.Sup.ref1Terstappen F, Lely AT. Long-term renal disease after prematurity or fetal growth restriction: who is at risk? Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2020; 35: 1087-1090.Google Scholar However, we did not find any association between gestational age and RFR, and with a range of gestational age in the LBW group from 27 to 43 weeks, with a median of 34 weeks, this should have been picked up. Using the same cohort, we have previously shown that women born LBW had lower measured GFR and lower kidney volume than their normal birth weight counterparts.Sup.ref2Ryan D. Sutherland M.R. Flores T.J. et al.Development of the Human Fetal Kidney from Mid to Late Gestation in Male and Female Infants.EBioMedicine. 2018; 27: 275-283Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar, 3Manalich R. Reyes L. Herrera M. et al.Relationship between weight at birth and the number and size of renal glomeruli in humans: a histomorphometric study.Kidney international. 2000; 58: 770-773Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar In these papers both LBW and small for gestational age (SGA) were important variables, while gestational age was not. This suggests an important contribution of the birth weight alone, regardless of the gestational age. LBW is commonly used as an umbrella including both fetal growth restriction, prematurity and small for gestational age.1Terstappen F, Lely AT. Long-term renal disease after prematurity or fetal growth restriction: who is at risk? Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2020; 35: 1087-1090.Google Scholar Premature birth – and especially very premature birth – disrupts the natural nephrogenesis.2Ryan D. Sutherland M.R. Flores T.J. et al.Development of the Human Fetal Kidney from Mid to Late Gestation in Male and Female Infants.EBioMedicine. 2018; 27: 275-283Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar Although, there are evidence of postnatal nephrogenesis in premature children, this is both qualitatively and quantitatively insufficient to merit a normal nephron endowment.Sup.ref4 Therefore, prematurity is an important determinant of nephron number. Other studies have shown reduced nephron number and impaired kidney health later in life associated with LBW and SGA both with and without prematurity.3Manalich R. Reyes L. Herrera M. et al.Relationship between weight at birth and the number and size of renal glomeruli in humans: a histomorphometric study.Kidney international. 2000; 58: 770-773Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar,4Hughson M. Farris 3rd, A.B. Douglas-Denton R. et al.Glomerular number and size in autopsy kidneys: the relationship to birth weight.Kidney international. 2003; 63: 2113-2122Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar,Sup.ref5Crump C. Sundquist J. Winkleby M.A. et al.Preterm birth and risk of chronic kidney disease from childhood into mid-adulthood: national cohort study.Bmj. 2019; 365: l1346Crossref PubMed Scopus (120) Google Scholar A Swedish registry study showed not only an increased risk of chronic kidney disease of both extremely early and late preterm, but also for those born early term compared to full term.5Crump C. Sundquist J. Winkleby M.A. et al.Preterm birth and risk of chronic kidney disease from childhood into mid-adulthood: national cohort study.Bmj. 2019; 365: l1346Crossref PubMed Scopus (120) Google Scholar Therefore, intrauterine growth restriction as evidenced by either LBW or SGA may be as important determinants of nephron endowment as prematurity. Download .pdf (.15 MB) Help with pdf files Birth Weight and Renal Functional Reserve in AdultsKidney International ReportsPreviewWe read with great interest the paper “ Renal Functional Response-Association With Birth Weight and Kidney Volume ” by Lillås et al. Low birth weight (LBW) is a well-known surrogate marker for nephron endowment and is associated with impaired salt handling and glomerular hyperfiltration, leading to the development of hypertension and progression to end-stage kidney disease in later life (1, 2). Because the number of nephrons in humans does not increase after term birth, individuals with a low nephron number are thought to have limited adaptive capacity to maintain normal renal function under various stress conditions. Full-Text PDF Open Access