Case Study: Mr. Brian CKD

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Q1. Mr. Brian is suffering from stage 4 chronic kidney disease (CKD) which occurs when the kidneys of an individual are damaged gradually and the waste gets accumulated in the body. The role of the kidney is to filter the body waste where they fail to perform their function causing CKD that can give rise to tremendous health problems. Gradual loss of kidney function benchmarks the chronic kidney disease that is also known as chronic kidney failure (National Institute of Diabetes and Digestive and Kidney Diseases, 2021). Different stages of chronic kidney disease depend upon the potential of the kidney to filter waste and extra fluid, beginning from the mild stage and ending to the kidney failure described by stage 5. Symptoms include itching, nausea, frequent urination, and in extreme cases, it may cause abdominal pain, rashes, and fever (The American Kidney Fund, 2021). A loss of functioning nephrons is indicated by persistent urine abnormalities, anatomical abnormalities, or decreased excretory renal function. The majority of CKD patients face an increased risk of cardiovascular disease and death. End-stage renal disease (ESRD) is a term used to describe patients who have reached the end of their treatment options. Low nephron number at birth, nephron loss due to aging, and acute or chronic kidney damage caused by toxic exposures or illnesses are all risk factors for the development of CKD (Romagnani, Remuzzi, Glassock, et al., 2017).

Q2. The pathophysiology of renal failure is characterized by the production of certain cytokines and the growth factors that halt the functioning of the glomeruli. The reduced glomerular functioning alters and adapts with time and letting the kidneys perform their function. As a consequence of hyperfiltration, the remaining glomeruli undergo a surge in pressure. This release in cytokine and the GFs attributes to hypertrophy as well as hyperplasia demanding excessive glomerulus function constraining them. This escalates the permeability and proteinuria consequencing in impaired reabsorption by the epithelial cells followed by abnormal transglomerular passage of protein (Cance & Huether, 2018).

A variety of conditions are responsible for causing structural and functional kidney decline due to the existing conditions in the patient. This includes diabetes and hypertension that have a detrimental impact on the kidney structure and its function (National Kidney Foundation, 2021). This is determined by four phases that eventually cause chronic kidney failure. Beginning with the reduction in the excretory function, the aggregation of endogenous and exogenous chemicals leads to the collapse of excretory function. This results in pharmacokinetic alterations, in addition, to a rise in the concentration of certain toxic substances. When the left glomeruli are confronted with a surplus of waste products, breakdown begins, ending in osmotic diuresis. The maximum focusing capacity of the kidney decreases. Additionally, de-escalation in incretory renal function occurs with no time since kidneys play a vital role in regulating the hormonal cycles that get disrupted leading to uremia or renal anemia (Sulaiman, 2019). Thirdly, over-hydration plus electrolyte imbalances evoke protein impairment as the glomerulus fails to manage the adequate tubular transport imbalance sodium-water balance. It also interferes with the intrarenal participation of calcium phosphate. Retention of the urinary metabolites thus damages the organ that represents the last phase of chronic kidney disease. The integrated term “uremic syndrome” is employed to explain toxic organ damage. azotemia is defined as a rise in urine excretion metabolites in the blood. Parathyroid hormones, urea, creatinine, beta-2 microglobulin, a few of the metabolites that are engaged in the process of damaged kidneys. Uremia (uremic syndrome) is a term that refers to a systemic disturbance of all organ functioning, particularly the circulatory system and central nervous system (Barnett & Cummings, 2018).

Q3. The patient has a medical history of diabetes, polycystic kidney disease as well as hypertension that complicates the circumstances signifying intense symptoms. High blood pressure causes blood vessels to shrieked and widened, causing damage and weakness all over the body, especially in the kidneys. Blood flow is decreased as a consequence of constriction. Diabetes can impair the kidneys by causing damage to the following blood vessels: The kidney’s filtration units are lined with microscopic blood veins disrupts. High blood sugar levels might cause these arteries to become narrow and blocked over time (Nistala & Savin, 2017). The signs include loss of appetite, tiredness, a headache that is common to early stage. Increased weariness, colorlessness, headaches, vision problems, and a noticeable decrease of renal capacity develop into obvious as the condition develops. Pruritus evolves, and muscular fibrillations are noticed. Renal failure leads to oliguria or metabolic acidosis, fatigue, vomiting, uremic encephalopathy with a significant loss of vigilance, and heightened bleeding vulnerability (Webster, Nagler, Morton, et al., 2017).

The persistence of the symptoms due to diabetes and hypertension are undoubtedly long-term impacts since it may interfere with the filtration mechanism evoking and giving rise to cardiovascular disease which takes time. Whereas, on the other hand, swelling in the feet, poor sleeping patterns, and fatigue are the short-term symptoms that may be relieved after treatment (Nuhu & Bhandari, 2018).

Q4. Diagnosis of chronic kidney disease can be done by blood and urine tests. Creatinine is the biomarker of CKD which can be measured to identify the intensity of waste products in the blood. The urine tests outline the levels of albumin and creatinine in the urine. Urinalysis is important to know the ratio of the albumin to creatinine to analyze the severity of disease, to interpret the protein levels in the urine along with the estimation of glomerular filtration rate to frame-accurate results (Rysz, Brzózka & Franczyk et al., 2017). Dipstick tests for albumin using a chemically treated paper called a dipstick and urine albumin to creatinine ratio comparing amounts are also done (Park, Baek, Kim, et al., 2017). To acknowledge the depth of kidney damage and deeply infer the structural changes in the kidney, CT scans, MRI scans, as well as ultrasounds, are preferred. Moreover, a detailed report can be attained by undergoing a kidney biopsy that infers to a small kidney sample that will be analyzed under a microscope gaining views of the damaged part (Aigbogun, Stellhorn, Pao, et al., 2021).

Q5. Acute kidney disease occurs unexpectedly, and it is often reversible whereas chronic kidney disease occurs over some time (>3 months) and cannot be reversed. Acute kidney disease can be caused by acute tubular necrosis, urinary tract obstruction, pre-renal disease, accident, dehydration, shock. On the other hand, chronic kidney disease can be caused by Glomerulonephritis, Polycystic kidney disease, Diabetic nephropathy, Hypertension, Nephrotoxin exposure, immune system disease. The acute disease can be diagnosed by an increase in serum creatinine (SCr) within 48 hours, decreased urine volume over 6 hours (Yu & Bonventre, 2018). Chronic disease can be diagnosed by damaged kidneys, reduced glomerular filtration rate (GFR). The acute disease can be observed by Hematuria, edema, disorientation, and SOB decreased or insignificant urine volume. Signs are frequently linked to the causing, frequent thirst. Many patients face no such signs. Chronic disease can be observed by Weakness, weariness, anorexia, edema, nausea/vomiting, and reduced urine production are all symptoms that might occur. Many patients have no symptoms until their CKD has progressed. The acute disease can be treated by treating the patient with reversible causes. Chronic disease can be managed by identifying the underlying disease. Monitoring fluids is necessary for both types of disease (Romagnani, Remuzzi, Glassock, et al., 2017).

Q6. Chronic kidney disease although has no cure but patients can be treated to decrease the pain and relieve their symptoms to increase the life expectancy. The treatment for the chronic disease aims at relieving the patient’s symptoms by providing emotional support. Treatment for end-stage renal disease is required if kidneys become badly damaged. The medications to treat the complications include high blood pressure medications or beta-blockers that initially decrease the kidney function but later restore it through maintaining electrolyte balance. Metoprolol is an antihypertensive agent that acts as an effective β-blockers. They slow the succession of renal disease, albeit to a smaller extent than renin-angiotensin system blockers -the renin-angiotensin-aldosterone (Tieu, Velensoi, Andrew, et al., 2018). Lasix is another medication that belongs to the class of diuretics and is usually prescribed to hypertensive patients to prompt the working of kidneys (Khan, Sarriff, Adnan, et al., 2016).

Dialysis is used to eliminate waste products and excess fluid from your blood. A machine separates waste and extra fluids from blood during hemodialysis. A narrow tube (catheter) put into the belly fills the abdominal cavity with a dialysis solution that soaks up waste and surplus fluids during peritoneal dialysis. A kidney transplant is a surgical way to get rid of the dialysis treatment and relieve the symptoms (Morishita, Tsubaki & Shirai, 2017). Nurses as well as allied professionals including renal nutritionists, nephrologists as well as patient care technicians play an important role. The nurse interventions integrate the monitoring of fluid status with boosting the independent feelings. Along with the administration of prescribed medications and promoting low-calorie food with high fluid uptake is important. The dietician will formulate the diet plan inclusive of low-calorie food as well as increased protein uptake is promoted (Havas, Douglas & Bonner, 2018).


Barnett, L.M., & Cummings, B.S. (2018). Nephrotoxicity and renal pathophysiology: A contemporary perspective. Toxicological Sciences164(2), 379-390.

Havas, K., Douglas, C., & Bonner, A. (2018). Meeting patients where they are: improving outcomes in early chronic kidney disease with tailored self-management support (the CKD-SMS study). BMC Nephrology19(1), 1-13.

Khan, Y.H., Sarriff, A., Adnan, A.S., Khan, A.H., & Mallhi, T.H. (2016). Chronic kidney disease, fluid overload, and diuretics: A complicated triangle. PloS One11(7), e0159335.

McCance, K.L., & Huether, S.E. (2018). Pathophysiology-E-book: The Biologic Basis for Disease in Adults and Children. Elsevier Health Sciences. 8. 38-40.

Morishita, S., Tsubaki, A., & Shirai, N. (2017). Physical function was related to mortality in patients with chronic kidney disease and dialysis. Hemodialysis International21(4), 483-489.

National Institute of Diabetes and Digestive and Kidney Diseases. (2021). What is chronic kidney disease? Retrieved from

National Kidney Foundation. (2021). Chronic Kidney Disease (CKD) Symptoms and causes. Retrieved from

Nistala, R., & Savin, V. (2017). Diabetes, hypertension, and chronic kidney disease progression: role of DPP4. American Journal of Physiology-Renal Physiology312(4), F661-F670.

Nuhu, F., & Bhandari, S. (2018). Oxidative stress and cardiovascular complications in chronic kidney disease, the impact of anemia. Pharmaceuticals11(4), 103.

Park, J.I., Baek, H., Kim, B.R., & Jung, H.H. (2017). Comparison of urine dipstick and albumin: creatinine ratio for chronic kidney disease screening: A population-based study. PloS One12(2), e0171106.

Romagnani, P., Remuzzi, G., Glassock, R., Levin, A., Jager, K.J., Tonelli, M., … & Anders, H.J. (2017). Chronic kidney disease. Nature Reviews Disease Primers3(1), 1-24.

Rysz, J., Gluba-Brzózka, A., Franczyk, B., Jabłonowski, Z., & Ciałkowska-Rysz, A. (2017). Novel biomarkers in the diagnosis of chronic kidney disease and the prediction of its outcome. International Journal of Molecular Sciences18(8), 1702.

Sanon Aigbogun, M., Stellhorn, R.A., Pao, C.S., & Seliger, S.L. (2021). Radiographic Imaging in Autosomal Dominant Polycystic Kidney Disease: A Claims Analysis. International Journal of Nephrology and Renovascular Disease14, 133–142.

Sulaiman, M.K. (2019). Diabetic nephropathy: recent advances in pathophysiology and challenges in dietary management. Diabetology & Metabolic Syndrome11(1), 1-5.

The American Kidney Fund. (2021). Chronic kidney disease (CKD). Retrieved from

Tieu, A., Velenosi, T.J., Kucey, A.S., Weir, M.A., & Urquhart, B.L. (2018). β-Blocker realizability in maintenance hemodialysis patients: a randomized clinical trial. Clinical Journal of the American Society of Nephrology13(4), 604-611.

Webster, A.C., Nagler, E.V., Morton, R.L., & Masson, P. (2017). Chronic kidney disease. The Lancet389(10075), 1238-1252.

Yu, S. M.W., & Bonventre, J.V. (2018). Acute kidney injury and progression of diabetic kidney disease. Advances in chronic kidney disease25(2), 166-180.


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