Background: Developmental programming shows that influences during critical periods of development confer susceptibility to disease in adulthood. Maternal cigarette smoking has deleterious effects on fetal growth and development. However, its impact on renal development and function in adulthood is unknown.

Aim: To study the effect of maternal cigarette smoke exposure (SE) on renal development in early postnatal life and determine if this, in turn, can lead to renal dysfunction in adulthood in female and male offspring.

Method: Female Balb/c mice (6 weeks) were exposed to either smoke or sham 6 weeks prior to mating and during gestation and lactation. Offspring were sacrificed at three different time points, at postnatal day 1 (P1), weaning age (P20), and 13 weeks (W13, mature age). Blood and urine samples were collected to assess renal function. Kidneys were harvested to determine structural change and the expression of mRNA related to renal development and disorders.

Results: kidney/body weight ratio was significantly reduced in male offspring exposed to smoke. Both male and female offspring’s kidneys from SE dams had fewer vascularised and mature glomeruli compared to control at P1 and P20. At w13, males exposed to smoke had subtle tubulointertitial fibrosis. mRNA expression of the development markers bone morphogenetic protein 4, fibroblast growth factor 10, Wingles type protein 4, and Wilm’s tumour inhibitory protein 1 were significantly increased in the SE offspring compared to control at P20 and P1 in both genders. There was no difference in serum creatinine levels, however, urine albumin/creatinine ratio was significantly increased in offspring of SE dams in both genders. This correlated with increased mRNA expression of  the pro-inflammatory marker (MCP-1).

Conclusion: Maternal SE leads to kidney underdevelopment in female and male offspring at least until weaning and induces renal dysfunction at adulthood. This was more significant in male offspring.