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, ). 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, ). Studies have shown that the angiotensin II of the renin-angiotensin system shows increased activities during diabetes (Carey & Siragy, ). 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, ). These events lead to the destruction of the renal tissues, leading to chronic kidney disease.