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…
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 ...
Cite this document
(“Metabolic and physiological adaptations to renal failure Research Paper”, n.d.)
Retrieved from https://studentshare.net/health-sciences-medicine/47740-metabolic-and-physiological-adaptations-to-renal
(Metabolic and Physiological Adaptations to Renal Failure Research Paper)
“Metabolic and Physiological Adaptations to Renal Failure Research Paper”, n.d. https://studentshare.net/health-sciences-medicine/47740-metabolic-and-physiological-adaptations-to-renal.
GOUT Word Count 2766 INTRODUCTION Gout is a metabolic disorder classically represented as acute inflammatory monarthritis (Rott & Agudelo, 2003); that is known to be initiated by the crystallization of uric acid (UA) within the joints. Uric acid is the end product of metabolism of purine.
880). Once kidney function has declined for a long period of time, the entire body is affected, resulting to systemic manifestations of CRF. Among several systemic manifestations is anemia, which could complicate the status of a client with renal disease.
Renal Transplants Transplants Worldwide Renal transplantation started in 1954 when Ronald Herrick donated a kidney to his identical brother, Richard. Joseph Murray was their surgeon was the first to perform successful living kidney transplantation Peter Bent Brigham Hospital in Boston, Massachusetts.
The author states that metabolic syndrome refers to a group of risk factors that increases an individual’s risk for coronary heart disease, stroke, diabetes and other health perils that temper with a person’s normal life. Age and genetic factors are some of the uncontrollable causes of metabolic syndrome.
Nephrotic syndromes comprise two words, which have different meanings. Nephros is a Greek word meaning kidney while syndrome is a word meaning a collection of symptoms. Causes of nephrotic syndrome Nephrotic syndrome cannot itself be termed as a disease but a set of symptoms which reflect or indicate a failure in the kidneys.
Kidneys form urine through the absorption of water and waste from blood. Adolf, Schunke and Schunke (2004) outline other functions of the kidney as regulation of body blood pressure and acid base balance, and stimulating the formation of red blood cells. The normal breakdown of body tissues and food are responsible for formation of waste in the blood.
These experiences are often noted observed by people who suffered from some chronic illnesses such as diabetes, various type of cancer, arthritis and renal failure.
An individual's diet, lifestyle and habits may contribute to acquiring various diseases.
ey function, progress in several years and usually asymptomatic and is detected only in the later course of the disease (Rolfes, Pinna, & Whitney, 2009, p. 880). Once kidney function has declined for a long period of time, the entire body is affected, resulting to systemic