Atubular glomeruli in a rat model of polycystic kidney disease

Atubular glomeruli in a rat model of polycystic kidney disease.BackgroundAutosomal-dominant polycystic kidney disease (ADPKD) is associated with a progressive decline in glomerular filtration rate (GFR) that often leads to end-stage renal disease. The basis for this decline in GFR is poorly understood.MethodsGlomeruli in heterozygous Han:SPRD rats with ADPKD and their normal litter mates were studied by light microscopy, using serial sectioning techniques. The connections of the renal corpuscles to proximal tubules were classified as normal, atrophied, or absent (atubular glomerulus). Renal corpuscles also were examined by scanning electron microscopy. Single nephron glomerular blood flows were determined using microspheres.ResultsIn the kidneys of six-month-old rats with ADPKD, 50% of the glomeruli were atubular and another 26% were associated with atrophied neck segments; these glomeruli were most often smaller in size than normal. About 16% of the glomeruli were hypertrophied and had normal connections to proximal tubules. Sclerotic changes in cystic kidney glomeruli were usually mild or moderate, and belied the failure of glomerular function. Glomerular blood flow in the cystic kidneys averaged half of normal and was markedly heterogeneous; the majority of small glomeruli displayed very low blood flows and a few showed relatively high blood flows. Fewer glomerular abnormalities were found in rats treated for five months with potassium citrate in their drinking water.ConclusionsThe diminished GFR in the rat with ADPKD can be accounted for largely by the formation of atubular glomeruli. Compensatory glomerular hypertrophy also is present and may contribute to the progression of the renal disease

Study of Bacterial Adhesion on Different Glycopolymer Surfaces by Quartz Crystal Microbalance with Dissipation

Protein-carbohydrate interactions are involved in a wide variety of cellular recognition processes including cell growth regulation, differentiation and adhesion, the immune response, and viral or bacterial infections. A common way for bacteria to achieve adhesion is through their fimbriae which possess cellular lectins that can bind to complementary carbohydrates on the surface of the host tissues. In this work, we synthesized glycopolymers using reversible addition-fragmentation chain transfer (RAFT) polymerization which were subsequently immobilized on a sensor surface for studies of bacterial adhesion by quartz crystal microbalance with dissipation (QCM-D). Ricinus communis Agglutinin (RCA120), a galactose specific lectin, was first studied by QCM-D to determine the specific lectin interactions to the different glycopolymers-treated surfaces. Subsequently, Pseudomonas aeruginosa PAO1 (a Gram-negative bacterium with galactose-specific binding C-type lectin (PA-IL)) and Escherichia coli K-12 (a Gram-negative bacterium with mannose-specific binding lectin) were then used as model bacteria to study bacterial adhesion mechanisms on different polymer-treated sensor surfaces by the coupled resonance theory. Our results showed that lectin-carbohydrate interactions play significant roles in comparison to the nonspecific interactions, such as electrostatic interactions. A significantly higher amount of P. aeruginosa PAO1 could adhere on the glycopolymer surface with strong contact point stiffness as compared to E. coli K-12 on the same surface. Furthermore, in comparison to E. coli K-12, the adhesion of P. aeruginosa PAO1 to the glycopolymers was found to be highly dependent on the presence of calcium ions due to the specific C-type lectin interactions of PA-IL, and also the enhanced bacterial adhesion is attributed to the stiffer glycopolymer surface in higher ionic strength condition.</p