Various studies have suggested a strong link between diabetes and kidney diseases. As described above, more than 44% of the incidences of kidney disease are associated with diabetes (Centers for Disease Control and Prevention, 2010). Diabetes is known to cause chronic diabetic nephropathy due to the damages caused on the nephrons by the rise in sugar levels, causing microalbuminuria and proteinuria (Ziyadeh, 2003).
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While the relationship between chronic kidney disease/kidney failure and diabetes is known, the actual pathophysiological mechanism involved is not clear. Nevertheless, a number of theories have attempted to explain the relationship between the two conditions. First, it is suggested that high glucose levels in circulation forces superfiltration of excessive blood in the nephrons, causing excessive pressure on the microfilters.
The excessive pressure causes the nephrons to leak, releasing quantifiable amounts of electrolytes and proteins from the blood to the urine (Ziyadeh, 2003). The damage caused by the excessive pressure on the glomeruli of the nephrons increases with time, leading to kidney failure.
A second theoretical explanation of the relationship between chronic kidney failure/disease and diabetes involves the renin-angiotensin system, a hormonal system involved in the regulation of blood pressure and fluid substance in circulation (Luño, 2004). Studies have shown that the angiotensin II of the renin-angiotensin system shows increased activities during diabetes (Carey & Siragy, 2013). The increased activity causes hypertrophy of a number of renal cells.
It also increases the pressure on the arteriolar smooth muscles of the kidney, which increases the vascular pressure. Angiotensin II also induces excessive cell growth, inflammation, apoptosis, migration and differentiation (Carey & Siragy, 2013). These events lead to the destruction of the renal tissues, leading to chronic kidney disease.
Review of literature
Although managing diabetes does not mean that kidney failure will be treated, a growing volume of research provides an indication of the possibility of controlling the condition from a number of perspectives.
One of the major areas of study that has shown promise in controlling the condition is the realization that a number of pathophysiological growth factors are involved in the development and progress of diabetic kidney disease. Flyvberg (2010) found that some cytokines and putative growth factors play a significant role in the development of kidney diseases in diabetic people.
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For instance, growth hormone, insulin-like growth factors and transformational growth factors have significant effects on the development of kidney failure in diabetic humans. The study suggests that the control and management of the condition could be achieved using antagonist protein agents that target and inhibit the action of these growth factors and cytokines.
Studies have found that blocking the rampamycin pathway can slow down the profession of diabetic kidney disease in rats, which gives some promise for the treatment of the problem in humans (National Institute of Diabetes and Digestive and Kidney Diseases, 2010).
A major alternative method of controlling the condition is the focus on moderate diets. It has been shown that people with diabetes should avoid consumption of excessive proteins. Studies have shown that high-protein diets are harmful to the nephrons, which means that dietary allowance should be considered in managing the condition. In addition, studies have shown that intensive management of blood glucose is an important intervention with significant impact on the control of diabetic kidney disease.
A major method of avoiding the condition involves the identification and mitigation of the risks of developing kidney disease in diabetic individuals. Studies have shown that some human genes predispose individuals to diabetic kidney diseases. According to Seaquist, Goetz, Rich and Barbosa (2009), a study of familial clustering of kidney failure provides evidence of genetic susceptibility to diabetic nephropathy.
Potential intervention method
Since the relationship between diabetes and chronic kidney disease/failure is caused by more than one factor, it is important to involve multiple intervention methods to reduce the number of diabetic people with kidney diseases. As such, it is suggested that dietary interventions be combined with genetic testing (to identify genetic risks) and drug therapy to mitigate the health risk of developing kidney disease in diabetic people.
Carey, R. M., & Siragy, H. M. (2013). The intrarenal renin–angiotensin system and diabetic nephropathy. Trends in Endocrinology & Metabolism, 14(6), 274-281.
Centers for Disease Control and Prevention. (2010). National diabetes fact sheet: general information and national estimates on diabetes in the United States, 2005. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention.
Flyvberg, A. (2010). Putative pathophysiological role of growth factors and cytokines in experimental diabetic kidney disease. Diabetologia, 43(10), 1205-1223.
Luño, J. (2004). Renin-angiotensin system in diabetic nephropathy. Nefrologia: publicacion oficial de la Sociedad Espanola Nefrologia, 25(2), 73-81.
National Institute of Diabetes and Digestive and Kidney Diseases (2010). National Diabetes Statistics, 2007. Bethesda, MD: National Institutes of Health, U.S. Department of Health and Human Services.
Seaquist, E. R., Goetz, F. C., Rich, S., & Barbosa, J. (2009). Familial clustering of diabetic kidney disease. New England Journal of Medicine, 320(18), 1161-1165.
Ziyadeh, F. N. (2003). The extracellular matrix in diabetic nephropathy. American journal of kidney diseases, 22(5), 736-744.