Barker, DJ, Osmond, C, Golding, J, Kuh, D, Wadsworth, ME. Growth in utero, blood pressure in childhood and adult life, and mortality from cardiovascular disease. Br Med J. 1989; 298, 564–567.
Barker, DJ, Eriksson, JG, Forsén, T, Osmond, C. Fetal origins of adult disease: strength of effects and biological basis. Int J Epidemiol. 2002; 31, 1235–1239.
Langley-Evans, SC, McMullen, S. Developmental origins of adult disease. Med Princip Pract. 2010; 19, 87–98.
Nuñez, P, Arguelles, J, Perillan, C. Offspring’s hydromineral adaptive responses to maternal undernutrition during lactation. J Dev Orig Health Dis. 2015; 6, 520–529.
You, L, Zhu, X, Shrubsole, MJ, et al. Renal function, bisphenol A, and alkylphenols: results from the National Health and Nutrition Examination Survey (NHANES 2003–2006). Environ Health Perspect. 2011; 119, 527–533.
Gowder, SJ. Nephrotoxicity of bisphenol A (BPA) – an updated review. Curr Mol Pharmacol. 2013; 6, 163–172.
Li, M, Bi, Y, Qi, L, et al. Exposure to bisphenol A is associated with low-grade albuminuria in Chinese adults. Kidney Int. 2012; 81, 1131–1139.
Trasande, L, Attina, TM, Trachtman, H. Bisphenol A exposure is associated with low-grade urinary albumin excretion in children of the United States. Kidney Int. 2013; 83, 741–748.
Nyengaard, JR, Bendtsen, TF. Glomerular number and size in relation to age, kidney weight, and body surface in normal man. Anat Rec. 1992; 232, 194–201.
Beeman, SC, Zhang, M, Gubhaju, L, et al. Measuring glomerular number and size in perfused kidneys using MRI. Am J Physiol Renal Physiol. 2011; 300, 1454–1457.
Bertram, JF. Analyzing renal glomeruli with the new stereology. Int Rev Cytol. 1995; 161, 111–172.
Hard, GC, Khan, KN. A contemporary overview of chronic progressive nephropathy in the laboratory rat, and its significance for human risk assessment. Toxicol Pathol. 2004; 32, 171–180.
Bonventre, JV, Vaidya, VS, Schmouder, R, Feig, P, Dieterle, F. Next-generation biomarkers for detecting kidney toxicity. Nat Biotechnol. 2010; 28, 436–440.
Hughson, MD, Douglas-Denton, R, Bertram, JF, et al. Hypertension, glomerular number, and birth weight in African Americans and white subjects in the southeastern United States. Kidney Int. 2006; 69, 671–678.
Kataria, A, Trasande, L, Trachtman, H. The effects of environmental chemicals on renal function. Nat Rev Nephrol. 2015; 11, 610–625.
vom Saal, FS, Welshons, WV. Evidence that bisphenol A (BPA) can be accurately measured without contamination in human serum and urine, and that BPA causes numerous hazards from multiple routes of exposure. Mol Cell Endocrinol. 2014; 398, 101–113.
Schecter, A, Malik, N, Haffner, D, et al. Bisphenol A (BPA) in U.S. food. Environ Sci Technol. 2010; 44, 9425–9430.
Martínez-Castelao, A, Navarro-González, JF, Górriz, JL, de Alvaro, F. The concept and the epidemiology of diabetic nephropathy have changed in recent years. J Clin Med. 2015; 4, 1207–1216.
Alonso-Magdalena, P, Quesada, I, Nadal, A. Endocrine disruptors in the etiology of T2DM mellitus. Nat Rev Endocrinol. 2011; 7, 346–353.
Heindel, JJ, Skalla, LA, Joubert, BR, Dilworth, CH, Gray, KA. Review of developmental origins of health and disease publications in environmental epidemiology. Reprod Toxicol. 2016; 68, 34–48.
Gore, AC, Chappell, VA, Fenton, SE, et al. EDC-2: the Endocrine Society’s second scientific statement on endocrine-disrupting chemicals. Endocr Rev. 2015; 36, 1–150.
Firmin, S, Bahi-Jaber, N, Abdennebi-Najar, L. Food contaminants and programming of T2DM: recent findings from animal studies. J Dev Orig Health Dis. 2016; 7, 505–512.
Hu, J, Yang, S, Wang, Y, et al. Serum bisphenol A and progression of type 2 diabetic nephropathy: a 6-year prospective study. Acta Diabetol. 2015; 52, 1135–1141.
Hu, J, Wang, Y, Xiang, X, et al. Serum bisphenol A as a predictor of chronic kidney disease progression in primary hypertension: a 6-year prospective study. J Hypertens. 2016; 34, 332–337.
Alonso-Magdalena, P, Vieira, E, Soriano, S, et al. Bisphenol A exposure during pregnancy disrupts glucose homeostasis in mothers and adult male offspring. Environ Health Perspect. 2010; 118, 1243–1250.
García-Arevalo, M, Alonso-Magdalena, P, Rebelo Dos Santos, J, et al. Exposure to bisphenol-A during pregnancy partially mimics the effects of a high-fat diet altering glucose homeostasis and gene expression in adult male mice. PLoS One. 2014; 9, e100214.
Liu, XL, Chen, XY, Wang, ZC, Shen, T, Zhao, H. Effects of exposure to bisphenol A during pregnancy and lactation on the testicular morphology and caspase-3 protein expression of ICR pups. Biomed Rep. 2013; 1, 420–424.
Tran, S, Chen, Y-W, Chenier, I, Chan, JSD, Quaggin, S. Maternal diabetes modulates renal morphogenesis in offspring. J Am Soc Nephrol. 2008; 19, 943–952.
Chen, YW, Chenier, I, Chang, SY, Tran, S, Ingelfinger, JR. High glucose promotes nascent nephron apoptosis via NF-κB and p53 pathways. Am J Physiol Renal Physiol. 2011; 300, 147–156.
Kanwar, YS, Nayak, B, Lin, S, Akagi, S, Xie, P. Hyperglycemia: its imminent effects on mammalian nephrogenesis. Pediatr Nephrol. 2005; 20, 858–866.
Amri, K, Freund, N, Vilar, J, Merlet-Benichou, C, Lelievre-Pegorier, M. (1999) Adverse effects of hyperglycemia on kidney development in rats. Diabetes. 1999; 48, 2240–2245.
Hokke, SN, Armitage, JA, Puelles, VG, et al. Altered ureteric branching morphogenesis and nephron endowment in offspring of diabetic and insulin-treated pregnancy. PLoS One. 2013; 8, e58243.
Hokke, S, Arias, N, Armitage, JA, et al. Maternal glucose intolerance reduces offspring nephron endowment and increases glomerular volume in adult offspring. Diabetes Metab Res Rev. 2016; 32, 816–826.
García-Arévalo, M, Alonso-Magdalena, P, Servitja, JM, et al. Maternal exposure to bisphenol-A during pregnancy increases pancreatic β-cell growth during early life in male mice offspring. Endocrinology. 2016; 157, 4158–4171.
Fernández García, MT, Núñez Martínez, P, García de la Fuente, V, et al. Practical application of stereological methods in experimental kidney animal models. Nefrologia. 2017; 37, 29–33.
Sugimoto, H, Shikata, K, Matsuda, M, et al. Increased expression of endothelial cell nitric oxide synthase (ecNOS) in afferent and glomerular endothelial cells is involved in glomerular hyperfiltration of diabetic nephropathy. Diabetologia. 1998; 41, 1426–1434.
Yamashita, T, Kawashima, S, Miwa, Y, et al. A 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitor reduces hypertensive nephrosclerosis in stroke-prone spontaneously hypertensive rats. J Hypertens. 2002; 20, 2465–2473.
Hard, GC, Alden, CL, Bruner, RHG, et al. Non-proliferative lesion of the kidney and lower urinary tract in the rat. Guides for Toxicologic Pathology. 1999. STP/ARP/AFIP: Washington, DC.
Frazier, KS, Seely, JC, Hard, GC, et al. Proliferative and non-prolferative lesions of the rat and mouse urinary system. Toxicologic Pathol. 2012; 40, 14–86.
Thornburg, KL. The programming of cardiovascular disease. J Dev Orig Health Dis. 2015; 6, 366–376.
Kanzaki, G, Tsuboi, N, Haruhara, K, et al. Factors associated with a vicious cycle involving a low nephron number, hypertension and chronic kidney disease. Hypertens Res. 2015; 38, 633–641.
Moritz, KM, Dodic, M, Wintour, EM. Kidney development and the fetal programming of adult disease. Bioessays. 2003; 25, 212–220.
Chen, YW, Chenier, I, Tran, S, et al. Maternal diabetes programs hypertension and kidney injury in offspring. Pediatr Nephrol. 2010; 25, 1319–1329.
Hoy, WE, Ingelfinger, JR, Hallan, S. The early development of the kidney and implications for future health. J Dev Orig Health Dis. 2010; 1, 216–233.
Zandi-Nejad, K, Luyckx, VA, Brenner, BM. Adult hypertension and kidney disease: the role of fetal programming. Hypertension. 2006; 47, 502–508.
Fong, D, Denton, KM, Moritz, KM, Evans, R, Singh, RR. Compensatory responses to nephron deficiency: adaptive or maladaptive?
Nephrology (Carlton). 2014; 19, 119–128.
McMullen, S, Langley-Evans, SC. Essential hypertension: defending the contribution of a congenital nephron deficit. Hypertension. 2005; 46, e4.
Cagampang, FR, Torrens, C, Anthony, FW, Hanson, MA. Developmental exposure to bisphenol A leads to cardiometabolic dysfunction in adult mouse offspring. J Dev Orig Health Dis. 2012; 3, 287–292.
Johnson, SA, Painter, MS, Javurek, AB, et al. Sex-dependent effects of developmental exposure to bisphenol A and ethinyl estradiol on metabolic parameters and voluntary physical activity. J Dev Orig Health Dis. 2015; 6, 539–552.
Lemley, KV. A basis for accelerated progression of diabetic nephropathy in Pima Indians. Kidney Int Suppl. 2003; 83, S38–S42.
Chen, HM, Li, SJ, Chen, HP, et al. Obesity-related glomerulopathy in China: a case series of 90 patients. Am J Kidney Dis. 2008; 52, 58–65.
Schmitz, A, Nyengaard, JR, Bendtsen, TF. Glomerular volume in type 2 (noninsulin-dependent) diabetes estimated by a direct and unbiased stereologic method. Lab Invest.. 1990; 62, 108–113.
Keller, G, Zimmer, G, Mall, G, et al. Nephron number in patients with primary hypertension. N Engl J Med. 2003; 348, 101–108.
Rochester, JR, Bisphenol, A. and human health: a review of the literature. J Steroid Biochem Mol Biol. 2011; 127, 204–215.
Frazier, KS, Seely, JC. Urinary system. In Monographs on Pathology of Laboratory Animals, 2nd edn, (eds. Jones TC, Hard GC, Mohr U), 1998; pp. 37–57. Springer: Berlin, Germany.
Hard, GC, Alden, CL, Stula, EF, Trump, BF. Proliferative lesions of the kidney in rats. In Guides for Toxicologic Pathology, 1995; pp. 1–19.
Sahota, PS, Popp, JA, Hardisty, JF, Gopinath, C, (eds.). Toxicologic Pathology: Nonclinical Safety Assessment. 2013. CRC Press: Boca Raton, USA.
Kilkenny, C, Browne, WJ, Cuthill, IC, et al. Improving biscience research reporting: the ARRIVE guidelines for reporting animal research. PLoS Biol. 2002; 8, e1000412.