In our unpublished meta-analysis, we searched PubMed using the key words ‘birthweight’, ‘intrauterine growth retardation’, ‘intrauterine growth restriction’, ‘creatinine clearance’, ‘glomerular filtration rate’ and ‘renal function’; five studies which observed 2733 subjects aged 18 years or older were included, and we found that

GFR of LBW people was approximately 3 mL/min per 1.73 m2 lower than that of normal counterparts (Fig. 1). One study compared the birthweight between 1230 end-stage renal disease (ESRD) patients and 2460 healthy controls and revealed that birthweight less than 2.5 kg or higher than 4.0 kg was associated with the highest ESRD risk selleck chemical and birthweight between 3.5–4.0 kg was associated with the lowest ESRD risk.34

Whereas another matched case–control study did not reveal the association between birthweight and ESRD in a population of 1162 subjects.35 A longitudinal study with a duration of 38 years observed over 2 million people, and results showed that Protein Tyrosine Kinase inhibitor LBW people had 1.5 times higher risk of ESRD. However, in this study, ESRD mainly occurred before the age of 14 years old, which was possibly due to the higher incidence of congenital or inherited renal disease in the LBW population.36 In a study on the familial aggregation of ESRD, LBW was not an influence factor but high birthweight was considered as a protective factor.37 Three meta-analyses showed that birthweight was negatively associated with blood pressure in different age stages, with every 1 kg increase of birthweight resulting in a 1.2–2 mmHg decrease of blood pressure,38–40 possibly old resulting from kidney hyperfiltration caused by glomerulosclerosis and damage of renal sodium excretion capacity. The risk of diabetes and dyslipidaemia was also higher in LBW people.41,42 This could be explained by their susceptibility to obesity and insulin resistance and their special growth process, namely,

malnutrition in uterine, relative over-nutrition after birth and excessive fast growth in the early stage of life.43 LBW also influenced the structure and function of the cardiovascular system,44 such as the damage of vessel dilation function and the turbulence of endo-epithelial function. It is a reasonable speculation that this kind of abnormality could also exist in the capillary of nephrons and the function of glomerular endothelium. LBW also influences sympathetic nerve45 and renin–angiotensin system activity.46 Some researchers owed the higher risk of CKD in certain races such as black people47 and goajiro Indians48 to their higher LBW mortality. However, one study revealed that low nephron number and LBW may play a role in the development of hypertension in white subjects but not in black.49 Another study showed that the more severe hypertension found in black subjects could not be attributed to racial differences in number of glomeruli or birthweight.