High salt intake in pregnancy alters maturation of glomeruli in the rat offspring

• Main Authors: Nadezda Koleganova, Grzegorz Piecha, Eberhard Ritz
• Format: Article
• Language: English
• Published: The Korean Society of Nephrology 2012-06-01
• Series: Kidney Research and Clinical Practice
• Online Access: http://www.sciencedirect.com/science/article/pii/S2211913212005657

There is currently discussion on the optimal salt intake and uncertainty whether both high and low salt intake is associated with adverse effects. One aspect has so far not be considered, i.e. the potential impact of salt intake during pregnancy on kidney function and blood pressure in the offspring. Faulty fetal programming, amongst others by high or low salt intake, leads to alterations in kidney morphology and albuminuria in the offspring. A low number of glomeruli is known to cause high blood pressure later in life. It was the purpose of the present study to clarify whether very high (or low) salt intakes in pregnancy affect kidney development in the offspring. Sprague-Dawley rats were fed normal (0.15%), medium (1.3%), or high (8.0%) salt diet during pregnancy and weaning. The number of glomeruli (mature, immature, and S-shape bodies) was assessed at 1 week postnatally. The expression of proteins of interest was assessed (by western blotting) at 1 week postnatally and at term. There was no difference between the groups with respect to litter size, birth weight, and placenta size. At age 1 week the number of S-shaped bodies was significantly lower (405±308) and the number of mature glomeruli (818±405) and layers of developing glomeruli (7.1±0.6) was significantly higher in the offspring of mothers on high-salt compared to the medium or low salt groups (1044±490, 460±304, and 5.9±0.9 respectively). As a net result the total number of glomeruli was significantly lower in the offspring of mothers on high-salt (9476±1264) compared to the medium or low salt groups (11175±1920). At 1 week of age in the offspring of mothers on high salt the glomeruli were bigger compared to lower salt intake. The expression of Pax-2 (54±23% vs. 100±28%) and FGF-2 (72±33% vs. 100±30%) was significantly lower in the offspring of mothers on high-salt consistent with their causative role. We conclude that high maternal salt intake during pregnancy accelerates maturation of glomeruli in the offspring, but reduces the final number of glomeruli.