Animal Models Of Renal Disease Research Articles

Interaction of antibodies with renal cell surface antigens

Over the past ten years it has been increasingly recognized that immune complex nephritides, characterized by the accumulation of granular immune deposits in renal structures, may not only be the consequence of deposition of circulating immune complexes but also of antigen-antibody complexes aggregated locally or formed in situ [1]. One of the sites at which antibodies may interact locally with antigens in the kidney is at the surface of renal cells [1, 2]. There is an abundance of antigens on cells: part of them are intrinsic plasma membrane proteins, while others may be present because they are secretion products or they have been ‘planted on the cell surface for immunological or physico-chemical reasons. In this article renal lesions that may arise from the binding of antibodies with these various kinds of cell surface antigens will be reviewed. Most of our insights come from animal models of renal disease. In the closing section the potential impact of data derived from experimental pathology on our concepts of human nephropathies will be evaluated.

Metabolic adaptations of the nephron in renal disease

Morphological and physiological studies have shown that various nephron segments are different functionally and metabolically. Major advances to understand renal metabolism have required improved techniques to study the problem of tissue heterogeneity in the kidney. The degree of heterogeneity within the kidney in renal disease may increase because pathological processes are many times focal or they produce histological changes in certain areas and adaptive changes in other zones of the kidney. Hence, methodological problems have hampered the studies of renal metabolism, particularly at the nephron level, in kidney diseases. Most metabolic studies have been done in experimental animal models of renal disease. This article provides an overview of changes in renal metabolism that occur in urinary tract obstruction, nephrotoxic or ischemic-induced acute renal failure, and in chronic models of reduced renal mass. The information available is limited and the existence of major gaps in our understanding of renal metabolism in diseases of the kidney is evident.

Role of dietary factors in the progression of chronic renal disease

AbstractIn diseases of the kidney characterized by irreversible injury, it appears that once a critical level of renal functional deterioration is reached, progression to endstage disease invariably occurs even if the initiating event or condition is resolved or eradicated. Immunopathogenetic mechanisms probably account for most forms of primary glomerular disease in humans. Although immunologic events and the mediators of glomerular damage that they induce might be responsible for initiating most glomerular diseases, certain clinical and experimental observations suggest that the rate of progression of these diseases is influenced by several nonimmunologic factors. In certain diseases, such as proliferative glomerulonephritis, the relentless decrease in renal function is due very likely to the initial underlying process; in other entities characterized mainly by interstitial scarring and glomerular sclerosis, the cause of progressive loss of renal function is less apparent. Recent experimental evidence suggests that dietary manipulations, such as reductions in protein and/or phosphate intake, can halt or attenuate the progression of chronic renal insufficiency in experimental animal models. Therefore, the exciting possibility exists that the natural history of some renal diseases may be altered by changes in the diet. We review current information regarding the role of manipulations of dietary protein, phosphorus, or lipid content on the progression of chronic renal disease. Most of the experimental observations to be reviewed have been made in animal models of renal disease. The literature on the role of dietary manipulations on the progression of renal disease in patients is somewhat limited and will not be emphasized here.