Health and Medicine

Health and Medicine
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 Health and Medicine
Introduction
Chronic kidney disease has become a health concern in the world today. The disease has been majorly linked to increase risk of developing cardiovascular related symptoms. Further, chronic kidney disease is also associated with chronic renal dysfunction. According to an American journal, it is approximated that 1 out of 9 individuals in USA have shown signs of chronic kidney disease. According to Reynolds et al (2004), these symptoms range from proteinuria with renal clearance to advanced renal failure that requires replacing the renal organ either by transplant or dialysis, which is, referred to as end-stage renal disease (ESRD), Gross J, Azevedo M, Silveiro S, et al (2005). It has been noted that, the disease has prevalence has increased, with poor medication response by the patients and increased cost of management and treatment of the disease. Mortality due to related conditions such as cardiovascular diseases have been in the rise, Culleton and Hemmelgarn (2003)
Discuss the pathophysiology of chronic kidney disease and how it interrelates pathophysiologically with diabetes and obesity
Chronic kidney disease may be caused by successive renal dysfunction, farmilalial disease or may result due to hereditary condition affecting glomerulo tubular functions that develops over a long period. In cats, the most common histopathology linked to chronic kidney disease is tubule interstitial nephritis, Gross J, Azevedo M, Silveiro S, et al (2005). The main cause of chronic kidney disease has not been identified. However, the associated lesions to chronic kidney disease are permanent and usually progressive.
Though the kidney nephrons remain intact, they undergo hypertrophy to compensate for the lost neprones so as to maintain their functionality. Though neprones undergo this adaptive mechanism to maintain their functionality, this result to increase neprone damage and hence resulting increased kidney dysfunction. This results to homeostatic regulation failure thus, leading to increased mineral imbalance in the blood. This is due to retention of mineral due to failure of the kidney neprones to function normally, Retnakaran et al. (2006), Schiffrin et al (2007). Although there is no known treatment which can restore the permanent renal lesions, resultant clinical symptoms to the patients resulting from renal dysfunction may be minimized by subjecting the patients to the right disease management practices.
Among children, chronic kidney disease results to retarded growth, thus children do not attain the hereditary height even after medication. The growth failure is correlated to the degree of renal dysfunction. Patients suffering from chronic kidney disease have high chances of being victims of cardiovascular disease, Gross et al (2005). Further, uremia metabolism, linked to chronic kidney disease is partially explainable by use of one factor like dyslipidemia or another factors linked to disease. However, the conditions that develop to patients with CKD like hypertension worsen the health of chronic kidney disease victims. Researchers associate both the diminishing glomerular filtration rate and hypertension conditions of individual to development of cardiovascular problems among such individuals.
In patients with CKD, increased glucose concentrations in the kidney unusually stimulate renal cells that produce more TGF-β1, a growth factor that increases the work of glucose transporter GLUT-1, thus stimulating high glucose uptake, and further accelerates mesangial cell production. TGF-β1 thickens the basement membrane of glomerular by promoting extracellular matrix protein accumulation in the basement membranes of the mesangial regions of glomerulus, resulting in fibrosis, hence glomerulo sclerosis condition. Reduction in the blood flow in glomerulo sclerosis decreases the density of the glomeruli and the glomerular filtration area, Culleton and Hemmelgarn (2003). This also causes deposition of extracellular matrix proteins at the tubular basal membrane and the interstitial space, thus promoting tubule interstitial fibrosis.
According to Nephrol (2005), Diabetes and hypertension, are two common co-morbidities associated with obesity. This is primarily linked with the onset and increase in the rate of progression of chronic kidney disease. Further, Hypertension causes CKD as well as complicates its condition, Reynolds et al (2004). Other risk factors like Smoking leads to the development of micro albuminuria. Further, smoking lead to progression of renal disease especially to diabetic individuals. In addition, smoking individuals who are non-diabetic have high risk of CKD progression than their counterparts who do not smoke. Renal injuries caused by smoking increases glomerular hyper-filtration. Further, the injury is linked to increase in intra-glomerular capillary pressure and production of angiotensin II amoung other clinical conditions, as stated by Retnakaran et al. (2006) and Schiffrin, Lipman and Mann J (2007). However, stopping smoking has been associated with decreased kidney neprone in T2DM. These calls for promotion of behavior and lifestyle change in affected victims and also prevention of new cases of smoking among the diabetic patients.
Obesity leads to proteinuria development and chronic kidney disease. However, obesity also accelerates the development of CKD individuals suffering from it. Morbid obesity for instance, may cause glomerular sclerosis, even when the individual is not suffering from renal dysfunction. Further, in obese individual weight losses is linked to decreased proteinuria. In addition, obesity has been thought to have beneficial survival attributes to stage five patients. And thus, use of such strategies in management of CKD should be applied with great precaution. Reynolds et al (2004)
High dietary salt intake in the body is linked to hypertension among other cardiovascular diseases. Further, high dietary salt for CKD patients worsen the condition, Schiffrin, Lipman and Mann (2007). Further, salt intake may lead to more damage of neprones due to the increase production of TGF-β
Nutritional deficit & fluid & electrolyte imbalance related to lack of knowledge of disease processes and how to self manage limitations; & how to maintain daily limitations
Subjective data of Mrs. Douglas’s remark that she takes little amounts of fluid and low food intake, unbalanced diet intake , high intake of sweets may confirm that she may have gout and azotemia among other symptoms such as Proteinuria and hematuria, (Cannon and Kumar, 2009). This denotes lack of knowledge or adequate information about good eating habits to manage her condition. Excessive weight and lack of exercise of Mrs. Douglas may be the cause of fatigue and her inability to walk. Adhering to the recommended diet for patients with CKD and taking the right amounts of fluid may prolong her life and also aid her coup with to side effects resulting from medication. Psychiatric disorders are common to patients and may interfere with treatment for Mrs. Douglas, Reynolds et al (2004).
With the patient’s history we may con...