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Metabolic and physiological adaptations to renal failure - Research Paper Example

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INTRODUCTION Cells need to be at certain specific conditions before they can function normally. Unlike plants or bacteria, animals cell do not have cell walls covering their plasma membranes. Thus, they are more prone to changes in the ionic concentrations of the interstitial fluid bathing them…
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Metabolic and physiological adaptations to renal failure
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Metabolic and physiological adaptations to renal failure

Download file to see previous pages... Thus, humans employ organs that protect the cells by maintaining the ion concentrations within normal levels and removing toxins from the extracellular environment. Both of these functions are done by kidneys. As organisms evolve, the kidneys become more complex, making them more capable of adapting to changes in the body. Although this is beneficial in terms of mitigating the potential of developing CKD, this prevents the early detection of disease since the kidney is still capable of adapting to its condition during the early stages of CKD. This paper summarizes the pathophysiology and symptomatology of chronic kidney disease, as well as the biochemical and physiological adaptations that the body enforce to cope with a dysfunctional kidney. CHRONIC KIDNEY DISEASE (CKD) Pathophysiology Chronic Kidney Disease, according to chronic hypoxia hypothesis, starts with a postglomerular flow obstruction, affecting the associated glomerulus and injuring the peritubular capillary network (Fine and Norman, 2008). Thus, the defective arterial-venous oxygen shunting reduces parenchymal oxygen, facilitating the progress to chronic renal disease (Masaomi, 2006). The resulting hypoxic environment causes the fibrotic response characterizing CKD. In this disease, the extracellular matrix (ECM) accumulates enough to disrupt the normal architecture of renal tissue. Renal fibrosis, specifically glomerulosclerosis and tubulointerstitial fibrosis, is the hallmark of the disease. The latter is characterized by an abundance of inflammatory cell infiltrates, increase in interstitial fibroblasts, and presence of myofibroblasts. The increase in number of fibroblasts is critical in the development of the disease as these cells are the major ECM-producing cells in tubulointerstitium. Specifically, ECM accumulation is caused by increased production and decreased turnover of matrix proteins by fibroblasts and proximal tubular epithelial cells. On the other hand, tubular atrophy is caused by apoptosis and epithelial-mesenchymal transdifferentiation. In summary, the development of fibrosis is associated with increased levels of proinflammatory, vasoconstrictive and profibrotic factors (Fine and Norman, 2008; Deng et al., 2010). Symptomatology CKD clinically manifests as a progressive decrease in glomerular filtration rate (GFR) for at least 3 months duration, usually with albuminuria. As a result, there is a decreased renal phosphate excretion, subsequently increasing serum phosphate levels. In effect, the conversion of vitamin D to active 1, 25-dihydroxyvitamin D is also decreased, depleting intestinal calcium absorption and serum calcium levels. This will then signal the release of parathyroid hormone (Abboud and Henrich, 2010). The loss of calcium levels, in turn, may cause the weight loss and loss of muscle mass seen among uremic patients (Rajan and Mitch, 2008). ADAPTATIONS TO CKD Protein catabolism Protein catabolism is usually seen with among individuals afflicted with CKD, this is because it is induced by inflammation, together with other conditions such as metabolic acidosis, insulin resistance, increased glucocorticoid production, and high serum concentrations of angiotensinogen II. The rapid degradation of proteins allows adaptation to rapid changes in physiological conditions. Such changes can happen in renal ...Download file to see next pagesRead More
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