Chronic and Complex Health

Diabetes is the main cause of chronic renal failure and the frequency of both conditions is increasing worldwide. Chronic renal disease affected more than 50 million people globally (Dirks, 2005). In the same token, diabetes affects over 171 million people globally (Wild, 2004).  Diabetes is implicated in renal diseases and it is the primary cause for over 45 percent of individuals undergoing dialysis. Renal failure is the most significant long term complications in relation to mortality and morbidity for diabetic individual patients. However, not all people with type 2 diabetes develop renal disease during their lifespan.
Diabetes Mellitus Pathophysiology
Diabetes mellitus (type 2 diabetes) is a group of metabolic diseases characterized by abnormalities in fat and carbohydrate metabolism. This progressive condition makes the body to become resistant to normal impacts of insulin or to gradually lose its capability to generate insulin. The precise cause of type 2 diabetes is unknown, albeit modifiable risk factors have been implicated. Risk factors associated with diabetes mellitus include family history with type 2 diabetes, advanced age, ethnicity, hypertension, sedentary lifestyle, unhealthy diet, overweight and impaired blood glucose tolerance (Batuman, 2016). In the case of Luigi, the underlying risk factors include sedentary lifestyle, ageing, overweight, ethnicity, stress and smoking.
Beta-cells are sensitive to high levels of free fatty acids and glucose. Defects in beta-cell function and mass result in the pathophysiology of diabetes. Dysfunction of islet cell results in to a relative diabetes of insulin activity. Progress decrease in number and weight of beta-cells takes place in T2D (Huether & McCance, 2012). Dysfunctional beta-cell predicts the onset and progression of T2D and beta-cell failure has been confirmed in obese individuals.
Diabetes mellitus develops gradually over a protracted duration of time. During this duration insulin resistance begins and the pancreas reacts by secreting greater quantities of insulin. This overproduction of insulin wears out the pancreas. By the time an individual is diagnosed with type 2 diabetes, the body has lost 50{b347ee882963fc078925bef44838eb079b614d3dde11dc0714b595823c2ade58} of the insulin producing cells (Batuman, 2016). Clinical manifestations such as high blood glucose become apparent.
Another clinical manifestation of diabetes is blurred vision (Braun, & Anderson, 2007). Type 2 diabetes increases the levels of blood glucose in the bloodstream, causing damage to the blood vessels located in the eyes, feet and kidney (Poretsky, 2010). The swelling of retinal blood vessels due to retina damage cuts off the supply of oxygen and cause the blood vessels to swell and bleed, a condition called retinopathy, as evidenced in Luigi’s case (Van Buren, & Toto, 2012). Other clinical manifestations of individual with T2D include hypertension, dyslipid and overweight. Polydipsia and polyuria may also be present.
Diabetes also affects the kidneys through causing harm to the glomerular and kidney tubules. This damage eventually reaches the glomerular base membrane causing the development of proteinuria, hemoptysis, and progressive hematuria (Coca, Ismail-Beigi, Haq, et al (2012). Hyperglycemia produces strong resistance and its prevalence continues to cause harm to internal lining of endothelial cell (Braun, & Anderson, 2007). This causes changes to the characteristics of the basement membrane, and glomerular capillaries.
Chronic Renal Failure Pathophysiology
Chronic renal failure is the progressive loss of kidney function due to the decrease in the glomerular filtration rate. There are several causes of chronic renal failure and each cause has its pathophysiology. These causes include metabolic injuries, systemic hypertension, fibrosis, proteinuria, loss of renal cells, extensive production of angiotensin II, and ischemia (Cavanaugh, 2007).  Proteinuria is caused by elevated capillary pressure and elevated glomerular permeability (Braun, & Anderson, 2007). The predisposing risk factors of renal failure include type 2 diabetes, old age, family history of renal failure, and ethnicity, while precipitating factors are sedentary lifestyle, diet and uncontrolled diabetes. Luigi’s age (77 years), hypertension, presence of diabetes mellitus, sedentary lifestyle, and overweight makes him the right candidate for chronic renal failure.
Early abnormalities in renal function include rising transglomerular resulting in hyperfiltration, appearing at first with small amounts of albumin and increased glomerular filtration rate (Braun, & Anderson, 2007). Renal structural abnormalities seen in diabetic patients with renal failure such as thickening of basement membrane, mesangial expansion, arteriosclerosis, podocyte abnormalities, and changes in tubular and endothelial cells, fibrosis, and interstitial inflammation occur in renal compartments (Lewis et al., 2007). Mesangial expansion, which is caused by mesangial cell hyperthrophy, is the leading cause of reduced glomerular filtration.
Glomerular hemodynamic changes, such as hyperfiltration and hyperoerfusion, lead to the development of leakage of albumin from the glomerular capillary (Lewis et al., 2007). A reduction both efferent and afferent resistance leads to an increase in glomerular capillary pressures and increased flow of glomerular plasma (Lewis et al., 2007). Increase in pressure causes hypertension within the kidney and chronic renal hypertension leads to hypoxia, glomerular sclerosis and ultimately chronicle renal failure. The thickened capillaries become leaky. These changes in microvascular result in diabetic nephropathy and eventually chronic renal failure. The liver begins to elevate protein synthesis to offset the loss in vain proximal convoluted tubular cells start to metabolize the filtered proteins as other molecules are allowed passage in urine (Wolf, 2012). Because the level of protein synthesis cannot keep pace with hypoalbuminemia, the compensatory mechanism is thrown off balance (Lerma, & Batuman, 2014). This results in osmotic pressures of hypoproteinemia and circulatory system, manifested as generalized edema (Inzucchi, Bergenstal, Buse, et al.  2012). Edema is characterized by the swellings of the legs and hands, initially clinically manifested as edema of the eyes.
Decreases in renal perfusion and blood flow lead to the activation of rennin-angiotensin axis. Angiotensin II causes the blood vessels to become narrow causing increased edema (Lewis, et al., 2007). Aldosterone activates the re-absorption of water and salt by nephron cells causing the blood volume to increase and hence edema (Lewis, et al., 2007).  Through cross-talking, podocytes, endothelial cells, and mesangial cells are involved in mesangial expansion and thickening of the glomerular basement membrane (Lewis et al., 2007).
Microvascular Complications that Lead To Renal Failure
Diabetes increases the risk of developing permanent complications due to degenerative alterations in the body. Furthermore, chromic complications occur in organs and tissues that experience high echelons of glucose circulating in the blood. Diabetes complications fall into two categories-microvascular and macrovascular. Microvascular complications concern the damage to small blood vessels causing damage to the nerves, kidney and eyes. The damage to the kidney is called nephropathy and the condition can lead to renal failure (Cade, 2008). If left for a long period without treated, microalbuminuria progresses to proteinuria and consequently diabetic rephropathy.

 

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