Maternal protein restriction is often associated with structural and functional sequelae in offspring, particularly affecting growth and renal-cardiovascular function. However, there is little understanding as to whether hypertension and kidney disease occur because of a primary nephron deficit or whether controlling postnatal growth can result in normal renal-cardiovascular phenotypes. To investigate this, female Sprague-Dawley rats were fed either a low-protein (LP, 8.4% protein) or normal-protein (NP, 19.4% protein) diet prior to mating and until offspring were weaned at postnatal day (PN) 21. Offspring were then fed a non ‘growth’ (4.6% fat) which ensured that catch-up growth did not occur. Offspring growth was determined by weight and dual energy X-ray absorptiometry. Nephron number was determined at PN21 using the disector-fractionator method. Kidney function was measured at PN180 and PN360 using clearance methods. Blood pressure was measured at PN360 using radio-telemetry. Body weight was similar at PN1, but by PN21 LP offspring were 39% smaller than controls (Pdiet < 0.001). This difference was due to proportional changes in lean muscle, fat, and bone content. LP offspring remained smaller than NP offspring until PN360. In LP offspring, nephron number was 26% less in males and 17% less in females, than NP controls (Pdiet < 0.0004). Kidney function was similar across dietary groups and sexes at PN180 and PN360. Blood pressure was similar in LP and NP offspring at PN360. These findings suggest that remaining on a slow growth trajectory after exposure to a suboptimal intrauterine environment does not lead to the development of kidney dysfunction and hypertension.

Stroke is one of the leading causes of death worldwide. Currently more than two thirds of the burden of stroke occurs in developing countries. Development of strategies for prevention and management of stroke in these countries requires data on incidence, risk factors and management practices that are relevant to the specific socioeconomic and cultural factors present in these populations. Yet currently available data come almost exclusively from developed countries. Herein, we aim to discuss some of the issues, impediments and opportunities faced by researchers undertaking population-based studies on the burden of stroke in developing countries. Important criteria to be addressed include the establishment of productive working relationships with both local collaborators and the community; the identification of an appropriate population group; and development of a working protocol which takes into account potential language barriers and the need for cultural sensitivity. When possible the protocol should include similar methods to studies conducted elsewhere so that comparisons can be made between regions. Furthermore, the results of such studies should be disseminated in an appropriate and timely manner to the local community and appropriate government and nongovernment organisations. This will enable the development and implementation of prevention and intervention programs to reduce the impact of stroke in these nations.