A Case Study on Sharon Diabetes and Chronic Kidney Disease Interrelation

This case study explores the interrelation between diabetes and chronic kidney disease in a patient named Sharon. It discusses the stages of chronic kidney disease, the effects of diabetes on the kidneys, and the medications used to manage diabetes. It also suggests potential inventions for managing insulin resistance and slowing down the progression of chronic kidney disease.

CASE STUDY 1
A CASE STUDY ON SHARON DIABETES AND CHRONIC KIDNEY DISEASE
INTERELATION .
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Date

CASE STUDY 2
Diabetes affects the blood vessels by destroying endothelial epithelium of the blood
vessels. Diabetes contributes to microvascular and macro vascular complications. Chronic
kidney disease results due to renal artery being unable to perform ultrafiltration. High blood
sugar levels in the blood affects the glomerular endothelial cells which results in hyper filtration
(Thomas, Cooper and Zimmet,2016). This results in the loss of glucose, albumin and proteins in
the blood. Consequently, the renal angiotensin system reacts by increasing the blood pressure as
low blood volume is circulating in the body. Her blood pressure is 140/95 mm/Hg.This
contributes to the vicious cycle of high amount of body fluids due to the renal angiotensin system
yet the kidney’s glomerular filtration rate is decreased (Bansal et.al, 2015).
The kidneys are involved in glucose reabsorption which take places in the proximal
tubules through the sodium glucose transporters (Bakris, Fonseca, Sharma and Wright, 2009). In
chronic kidney disease due to the high amounts of glucose being hyper filtered the sodium
glucose transporters increase in number contributing to higher levels of glucose being absorbed.
This worsens the hyperglycemia as the blood glucose levels are already high and presence of
tissue insulin resistance.
Chronic kidney disease is classified into different stages according to the loss in
glomerular filtration rate. In stage one the glomerular filtration rate is below 90ml/mi. This can
remain undetected as the nephrons compensate for the destroyed ones maintaining an otherwise
normal state. Stage two the glomerular filtration rate is between 60 to 89 ml/min.Sharon is in
stage two. Stage three the glomerular filtration rate is now 30 to 59 ml/minute and the kidney

CASE STUDY 3
condition are deteriorating as the remaining nephrons are now overcompensating and some are
already destroyed. Stage four otherwise known as end stage renal disease the patient has a
glomerular filtration rate of below 29ml/minute. This is known as end stage renal disease and
calls for hemodialysis where the urea, excess electrolytes are exchanged in extracorporeal circuit
and returned to the body. Chronic kidney disease is a life time disease and while it cannot be
stopped it can be managed by controlling the causative factors such as diabetes. Sharon needs
urgent review by a nephrologist. While stage one and stage two exhibit in proteinuria and
albuminuria stage three and four exhibit uremia which is highly fatal if left untreated.
Sharon’s glomerular filtration is 85ml/minute. This process progresses in stages as the
nephrons are decreased then hyper compensate for the decreased glomerular filtration rate. The
decreased nephrons are then unable to perform their function resulting in a lower glomerular
filtration rate and finally end stage renal stage disease due to the effect of diabetes on the
efferent, afferent arterioles and glomerular capillaries.
Metformin is an oral antidiabetic drug in the biguanide class. It works by decreasing the
glucose hepatic output and decreasing insulin resistance of the tissue. The bioavailability of the
drug is 45 to 65 % after intestine absorption. Metformin does not bind to plasma proteins Its half-
life is 4 to 9 hours. Sharon is on metformin Sandoz 1000 mg daily. The drug is metabolized by
kidney elimination. Renal clearance of the drug is most effective in patients with normal
creatinine clearance. Type two diabetes is controlled by weight control but if it beyond control
then use of oral antidiabetic drugs is utilized.

CASE STUDY 4
Sharon’s fasting blood glucose levels are 7 to 8 mmol/litre while normal fasting blood
glucose levels are 4.0 to 6.1 mmol/litre.Sharon’s random blood sugar is 8 to 11 mmol/litre while
normal random blood sugar level should be 6.1 mmol/litre to 7.8 mmol/litre.Considering her
decreased glomerular filtration and the fact that she is on medication her fasting blood sugar
levels should be 4 to 7 mmol/litre while random blood sugar levels should be below 8.5
mmol.litre(American Diabetes Association,2017)
Her blood glucose levels are too high as they are beyond the normal range and
considering she is adhering to her medications. This means that the chronic kidney disease will
actually worsen and there needs to be review of her condition and the medications she is on. This
also requires continuous monitoring including glycated hemoglobin which measures the amount
of blood sugar levels in the red blood cells (Hayward et.al,2015).
Glucovance is a combination of glyburide and metformin drugs which is used to control
diabetes type two(Moore,2018) Glyburide is an oral antidiabetic drug in sulfonylurea class
available in 2.5 mg in the combination of glucovance whilst metformin is a biguanide available
in 500mg.Sharon has a glomerular filtration rate of 85 mls per minute while the normal
glomerular filtration rate is 125mls per minute. Glucovance is excreted through renal
elimination. Combining this medication with metformin Sandoz increases the amount of
metformin will be increased. Metformin is eliminated through tubular excretion (Thakare,
Shende, Shirure and Swami,2017). Considering Sharon’s compromised renal function there
could be a potential accumulation of metformin.

CASE STUDY 5
Accumulation of metformin causes lactic acidosis whereby the pH decreases and it is
potentially fatal(DeFronzo,Fleming,Chen and Bicsak,2016). Lactic acidosis can either be type A
or Type A is caused by loss of body fluids which results to hypoperfusion whilst type B results
from drugs such as metformin and malignancy. Lactic acidosis is treated through infusion of
bicarbonate solution or hemodialysis. Hemodialysis is the preferred option as it contributes to
fluid overload removal and elimination of glucovance in toxicity.
There is a concern of adding glucovance to the treatment regimen of Sharon as it could
potentially worsen her renal function and lead to lactic acidosis. According to Kajbaf and Lalau
(2014) mortality rate due to metformin lactic acidosis has been recorded to be 50%. This would
necessitate close monitoring of kidney function by creatinine tests and glomerular filtration rate.

CASE STUDY 6
Sharon has a weight of 120 kilograms and diabetes type two results from obesity. My
potential invention would be a drug that antagonizes the transformation of free fatty acids which
results in insulin tissue resistance. While the first options of controlling diabetes are weight loss
and diet management sometimes the adipose fat needs to be regulated as it results in insulin
tissue resistance. Her random blood glucose sugar levels are at 8 to 11 mmol/litre and this drug
would indirectly cause the tissues to be sensitive to insulin due to inactivation of free fatty acids.
According to Lucidi et.al (2010) the causative factors to insulin resistance in the signaling
pathway are free fatty acids. Sharon is obese and the drug would potentially sensitize the cells to
insulin.
Sharon has a glomerular filtration rate of 85 mls/min and has active proteinuria. She is
stage two of chronic kidney disease(Hill,Fatoba,Oke,Hirst,O’Callagan&Lasserson 2016) . The
progression of the disease involves nephron adaptation to damage to maintain the kidney
function (Webster, Nagler, Morton and Masson ,2017). The second potential drug would be one
that slows down the activity of the nephrons while monitoring the kidney function. This would
slow down the progression of the chronic kidney disease while monitoring the diabetic drugs
function for improvement or deterioration.

CASE STUDY 7
According to the Nursing and Midwifery Board of Australia (2016) the nursing standard
five for practice states that the registered nurse develops a plan for nursing practice. This
includes assessment of data for the patient so as to ensure the right care is given. This includes
taking blood glucose levels such as random blood glucose strips and hemoglobin glycated sugar
levels for the patient to assess the situation. This informs my nursing practice by ensuring that
the hyperglycemia or hypoglycemia is treated promptly. Also input output chart is recorded to
assess the glomerular filtration rate and subsequent replacement of nutrients.Assessment is also
done for macrovascular complications,microvascular complications such as diabetic foot ulcer
which the nurse should provide health education to the patient.
The second aspect includes planning outcome criteria and goals for a certain timeframe
that should have been achieved. The first nursing goal is to ensure that the blood sugar levels are
within range to avoid further complications such as hyperosmolar hyperketotic syndrome. This is
done by administration of medicines and subsequent monitoring for complications such as lactic
acidosis. The second nursing goal is to ensure the nutritional status suits the patient’s condition.
This includes low protein due to hyperemia, low salt due to fluid retention and high carbohydrate
to ensure high energy levels during the disease process.The third nursing goal is to monitor for
other diabetic complications such as retinopathy and diabetic foot ulcer.
The third aspect is coordinating the resources and planning efficiently. This means that
the registered nurse should be ready to assess a decreasing glomerular filtration and collaborate
with other healthcare professionals to plan hemodialysis. This also means inserting a catheter to
assess the urine for color and volume changes.Collaboration with the nutritionists to plan for the
patient’s diet.

CASE STUDY 8
The final aspect is planning for evaluation of the set nursing priorities. This involves
interpretation of blood sugar levels after treatment. Also, interpretation of computed tomography
on the kidneys to assess the atrophy and size. This also helps to plan for the future of the
patient.Planned patient care involves incorporating the physician’s,nutritionist,counsellor and
therapists in the nursing care plan.

CASE STUDY 9
REFERENCES
American Diabetes Association, 2017. 2. Classification and diagnosis of diabetes. Diabetes care,
40(Supplement 1), pp.S11-S24.
Bakris, G.L., Fonseca, V.A., Sharma, K. and Wright, E.M., 2009. Renal sodium–glucose
transport: role in diabetes mellitus and potential clinical implications. Kidney international,
75(12), pp.1272-1277.
Bansal, N., McCulloch, C.E., Rahman, M., Kusek, J.W., Anderson, A.H., Xie, D., Townsend,
R.R., Lora, C.M., Wright, J., Go, A.S. and Ojo, A., 2015. Blood pressure and risk of all-cause
mortality in advanced chronic kidney disease and hemodialysis: the chronic renal insufficiency
cohort study. Hypertension, 65(1), pp.93-100.
DeFronzo, R., Fleming, G.A., Chen, K. and Bicsak, T.A., 2016. Metformin-associated lactic
acidosis: Current perspectives on causes and risk. Metabolism, 65(2), pp.20-29.
Hayward, R.A., Reaven, P.D., Wiitala, W.L., Bahn, G.D., Reda, D.J., Ge, L., McCarren, M.,
Duckworth, W.C. and Emanuele, N.V., 2015. Follow-up of glycemic control and cardiovascular
outcomes in type 2 diabetes. New England journal of medicine, 372(23), pp.2197-2206.
Hill, N.R., Fatoba, S.T., Oke, J.L., Hirst, J.A., O’Callaghan, C.A., Lasserson, D.S. and Hobbs,
F.R., 2016. Global prevalence of chronic kidney disease–a systematic review and meta-analysis.
PloS one, 11(7), p.e0158765.
Kajbaf, F. and Lalau, J.D., 2014. Mortality rate in so‐called “metformin‐associated lactic
acidosis”: a review of the data since the 1960s. Pharmacoepidemiology and drug safety, 23(11),
pp.1123-1127.

CASE STUDY
10
Lucidi, P., Rossetti, P., Porcellati, F., Pampanelli, S., Candeloro, P., Andreoli, A.M., Perriello,
G., Bolli, G.B. and Fanelli, C.G., 2010. Mechanisms of insulin resistance after insulin-induced
hypoglycemia in humans: the role of lipolysis. Diabetes, 59(6), pp.1349-1357.
Moore, L.E., 2018. Oral Hypoglycemic Agents. In Diabetes in Pregnancy (pp. 103-110).
Springer, Cham.
Nursing and Midwifery Board of Australia(2016).Registered Nurse Standards of
Practice.Retrieved from https://www.nursingmidwiferyboard.gov.au/codes-guidelines
%20statements/professional-standards.aspx.
Thakare, V., Shende, S.S., Shirure, P.A. and Swami, O.C., 2017. Role of conventional oral
antidiabetic drugs in management of type 2 diabetes mellitus. International Journal of Research
in Medical Sciences, 5(3), p.749.
Thomas, M.C., Cooper, M.E. and Zimmet, P., 2016. Changing epidemiology of type 2 diabetes
mellitus and associated chronic kidney disease. Nature Reviews Nephrology, 12(2), p.73.
Webster, A.C., Nagler, E.V., Morton, R.L. and Masson, P., 2017. Chronic kidney disease. The
Lancet, 389(10075), pp.1238-1252.