Diabetes Mellitus and Chronic Kidney Disease: A Case Study

RUNNING HEAD: A CASE STUDY
A CASE STUDY
Name of Student
Name of University
Author note

A CASE STUDY1
CASE STUDY A
Response to Question 1:
Diabetes mellitus is a metabolic disease that occurs due to insulin insufficiency or
deficiency in the body. Diabetes is insidiously related to the development of chronic renal
disease (Thomas, Cooper and Zimmet 2016) and the two pathologies are very much
interrelated to each other. Accumulation elevated Parathyroid hormone levels has been seen
to develop insulin resistance in the body tissues, especially in skeletal muscle. Insulin
resistance causes damage to the insulin binding process (De Meyts 2015), disrupting glucose
metabolism in the body. Anemic state impacted by chronic renal failure hinders the insulin
resistance even more (Yaffe et al. 2016) Correcting the anemia with medication has shown to
better insulin sensitivity in the body. Insulin secretion has been reported to have diminished
in patients suffering with chronic renal disease. The pathophysiological factors interlacing
both the pathologies together are – high parathyroid hormone levels (Campbell et al. 2016),
metabolic acidosis and diminished Vitamin D levels. There is an increased oxidative stress in
the tissues leading to a causation of diabetic - kidney disease. Diabetic nephropathy (Feldman
et al.2017) has been shown to be associated with a bodily state of oxidative stress fuelled by a
hyperglycemic persistence in the body. Hyperglycemia has been reported to shift the state of
redox equilibrium that is the crucial inductor of a severe oxidative stress that over a
prolonged period of persistence, lead to nephropathy and chronic kidney damage. Increase in
Reactive Oxygen Species (ROS) (Lenzen 2017) which are the major contributors of oxidative
stress – has been reported as the cardinal reasons behind a presentation of chronic kidney
disease. Both renal failure and diabetes together can cause a severe oxidative stress (Sies,
Berndt and Jones 2017). Certain defects found in glycolysis along with an elevated action of
xanthine oxidase, reduced nicotinamide adenine dinucleotide phosphate oxidase along with

A CASE STUDY2
nitric oxide synthase uncoupling – leads to the development of oxidative stress and diabetic
related chronic kidney disease.
Sharon is diagnosed with Type 2 Diabetes Mellitus and Metformin has been
prescribed to better her condition. Metformin as a drug is a bi- guanide class hypoglycemic
agent to be taken orally. Metformin (Rena, Hardie and Pearson 2017) lowers hyperglycemia
primarily by diminishing glycogen-o-lysis and enhances insulin sensitivity of peripheral
tissues by improving glucose uptake and glucose utilization (Xin et al. 2016). Metformin has
been physiologically shown to diminish glucose production in hepatocytes and
pharmacologically - metformin has seen to play a vital role in the human gut. Findings of
Metformin’s mechanism of action has been reported to vary when administered in acute and
chronic settings. At molecular level, Metformin acts through both AMPK-independent and
AMP-activated protein kinase mechanism. Metformin inhibits mitochondrial (cellular)
respiration by blocking the action of glycerophosphate dehydrogenase. Metformin has also
shown to alter a biological mechanism involving the lysosomes. Metformin has been seen to
accumulate 1000 folds more in mitochondria than in extracellular fluid. This is because the
drug has a positive charge and a marked difference of bioelectric potential across the cell
membrane pushes Metformin molecules into the mitochondria. Overall, metformin reduces
blood cholesterol levels (hyperlipidemia), diminishes systolic blood pressure which helpful to
trear Sharon’s high systolic pressure. Genetic studies have shown – metformin to have anti-
cancer properties and its mechanism of action also helps in prevention of dementia.
Response to Question 2:
Normal blood glucose level at fasting is 3.9 to 5.5 mmol/L which in case of Sharon
has been reported to be 7 to 8 mmol/L. Normal glucose level at post prandial state is
approximately 7.8 mmol/L which case of Sharon has benn reported to be 8 to 11 mmol/L.