The epidemiology of chronic kidney disease

The epidemiology of chronic kidney disease. The world's disease profile is changing, and chronic diseases now account for the majority of global morbidity and mortality, rather than infectious diseases. The causes of chronic kidney diseases reflect this change and diabetes, together with hypertension, is now the major cause of end-stage renal failure worldwide, not only within the developed world, but also increasingly within the emerging world.Diabetes is of epidemic proportions, and its prevalence will double in the next 25 years, particularly in the developing countries. This will place an enormous financial burden on countries, including the cost of the management of end-stage renal failure. Thus, it is medically and economically imperative for awareness, detection, and prevention programs to be introduced across the world, particularly in the developing countries. This will require concerted action from global institutions, governments, health service providers, and medical practitioners

Initiation and evolution of interstitial leukocytic infiltration in experimental glomerulonephritis

Initiation and evolution of interstitial leukocytic infiltration in experimental glomerulonephritis. Most forms of glomerulonephritis have a significant interstitial leukocytic infiltrate which is associated with disease progression. However, there is little data concerning the timing, initial location, and development of this interstitial component. Therefore, we have addressed these issues in a study of passive accelerated anti-GBM glomerulonephritis in the rat. In this model, interstitial leukocytic infiltration was an early event in the disease process with a significant infiltrate apparent at 12 hours after administration of nephrotoxic serum (NTS). This initial infiltrate was restricted to a perivascular sheath surrounding the hilar arterioles. The sheath infiltrate then spread to include the whole hilar area by day 1, the entire periglomerular area by day 3, and became widespread throughout the cortical tubulointerstitium by day 7. The early sheath infiltrate was composed of macrophages and T cells. Both cell types continued to increase as the infiltrate expanded, and a significant accumulation of activated cells (IL-2R+) was evident from day 7 onwards. There was a highly significant correlation between interstitial macrophage infiltration and renal function impairment, proteinuria, and histologic damage. Interstitial T cell infiltration correlated with proteinuria and histologic damage, while the appearance of immune-activated mononuclear cells (IL-2R+) exhibited a highly significant correlation with all disease parameters. This study demonstrates the importance of the glomerular hilar arteriolar region as a focus for mononuclear leucocytic migration and accumulation which not only affects the structure and function of the glomerulus but subsequently the entire tubulointerstitium

Regulation of human renal adenocarcinoma cell growth by retinoic acid and its interactions with epidermal growth factor

Regulation of human renal adenocarcinoma cell growth by retinoic acid and its interactions with epidermal growth factor. Retinoic acid (RA) is a natural derivative of vitamin A which regulates the growth and differentiation of epithelia. We have previously proposed that RA participates in compensatory kidney growth and reported that RA inhibits rat mesangial cell growth. This paper describes the effects of RA on a human renal adenocarcinoma cell line (PAD) under different growth conditions, and its interactions with epidermal growth factor (EGF). PAD cells were shown to express RA receptors α and β by Northern blot analysis. In serum free cultures, addition of RA (10-7 M) markedly increased thymidine incorporation by PAD cells (155 ± 7% mean ± se vs. control in 6 separate experiments; P < 0.0001). RA also caused a significant increase in thymidine incorporation by PAD cells under conditions of rapid growth in serum supplemented medium (115 ± 2% vs. control; P < 0.001). RA by itself was unable to reverse contact inhibition of PAD cell growth (NS vs. control), but it synergistically enhanced the mitogenic effect of EGF on confluent monolayers (110 ± 0.6% vs. EGF alone; P < 0.05). Northern blot analysis demonstrated that PAD cells express EGF receptor mRNA, and this was not significantly modified by the addition of RA. Growth arrested (serum starved) PAD cells expressed RAR-α mRNA which was up-regulated eightfold at three hours following the addition of 10% FCS. Thus, our data show that RA is directly mitogenic for serum starved human renal adenocarcinoma cells and that it exerts complex modulation of cell growth in the presence of EGF and serum components

Nutritional Therapies for Ulcerative Colitis: Literature Review, Chart Review Study, and Future Research

Few clinical studies suggest a significant influence of diet or nutritional supplementation on ulcerative colitis. One reason is that ulcerative colitis, like many chronic diseases, is multifactorial. This article reviews the relevant literature and presents the results of a retrospective chart review study that was done at a complimentary medicine office

Effects of a Sugar-Free Hypoallerdenic Diet and Nutrtional Supplementation on Ulcerative Colitis

Few clinical studies have found that dietary or nutritional factors significantly influence ulcerative colitis (UC}(l,2}. It is noteworthy, however, that a range of factors have been researched including dietary components such as refined sugars (3,4}, allergenic foods (1,5,6} and fast foods (7), as well as nutritional supplement effects from fish oil (2), zinc (8), glutamine (9), folate (10, 11} and alpha-tocopherolquinone (12}. More recently investigators have also examined the interelationships between bowel flora and UC, including factors such as flora changes (13,14), endotoxemia (15} and supplementation effects with Lactobacillous species (16,17). These studies taken together and a recent review of UC (18) suggest that nutritional influences on UC may likely be multifactorial. We therefore report the findings of a retrospective chart review study of 24 consecutive UC patients who presented to an outpatient medical office in which treatment emphasized a comprehensive nutritional regimen, including a sugar-free hypoallergenic diet and nutritional supplementatio

Crack tip effective strain rates in rate sensitive materials

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42755/1/10704_2004_Article_BF00033853.pd

De novo glomerular osteopontin expression in rat crescentic glomerulonephritis

De novo glomerular osteopontin expression in rat crescentic glomerulonephritis. Osteopontin (OPN) is a secreted acidic glycoprotein that has potent monocyte chemoattractant and adhesive properties. Up-regulation of tubular OPN expression is thought to promote interstitial macrophage infiltration in experimental nephritis; however, the role of OPN in glomerular lesions, particularly crescent formation, is unknown. The present study used Northern blotting, in situ hybridization and immunohistochemistry to examine OPN expression in a rat model of accelerated anti-GBM glomerulonephritis. Osteopontin mRNA and protein is expressed by some parietal epithelial cells, thick ascending limbs of Henle and medullary tubules and collecting ducts in normal rat kidney. De novo OPN mRNA and protein expression was evident in glomerular visceral and parietal epithelial cells in anti-GBM glomerulonephritis. Glomerular OPN expression preceded and correlated with macrophage infiltration in the development of hypercellularity, focal and segmental lesions and, notably, crescent formation. There was marked up-regulation of OPN expression by tubular epithelial cells that also preceded and correlated with interstitial macrophage (r = 0.93, P < 0.001) and T-cell infiltration (r = 0.85, P < 0.001). Both glomerular and tubular OPN expression correlated significantly with proteinuria (P < 0.001) and a reduction in creatinine clearance (P < 0.01). In addition, double immunohistochemistry showed co-expression of osteopontin and one of its ligands, CD44, in intrinsic renal cells. CD44 and OPN expression by parietal epithelial cells was evident in crescent formation, while virtually all OPN-positive tubules expressed CD44. Infiltrating macrophages and T-cells were CD44-positive, but only a small proportion of T-cells and few macrophages showed OPN expression. Interestingly, strong OPN mRNA and protein expression was seen in macrophage multinucleated giant cells. In summary, this study suggests that OPN promotes macrophage and T-cell infiltration in the development of renal lesions in rat anti-GBM glomerulonephritis, including glomerular crescent and multinucleated giant cell formation