Question

Patient Profile

Natalia Battong, a 42-year-old schoolteacher, has been treated for type 2 diabetes mellitus since the age of 25. Her nephrologist has observed her for the past several years for manifestations of progressive chronic kidney disease. Eight weeks ago, she had an arteriovenous fistula created in preparation for starting hemodialysis. Over the past week, she has experienced anorexia, nausea, vomiting, problems with concentration, and pruritus.

Subjective Data

• • Complains of swelling in her feet and hands
• • Has gained 4.5 kg in the past 2 weeks
• • Complains of dyspnea and weakness when walking

Objective Data

Laboratory Data

• • Estimated glomerular filtration rate (eGFR): 8.0 mL/min/1.73 m²
• • Serum creatinine: 560 mmol/L
• • Blood urea nitrogen (BUN): 32 mmol/L
• • Potassium: 6 mmol/L
• • Hemoglobin: 95 g/L

Chest Radiograph

• • Pulmonary edema

Discussion Questions

1. 1. Explain the basic pathophysiological changes that resulted in the development of Mrs. Battong's diabetic nephropathy.
2. 2. What are the indications for dialysis in this patient?
3. 3. Identify the abnormal diagnostic study results, and explain why each would occur.
4. 4. Explain why Mrs. Battong developed each of the clinical manifestations she shows.
5. 5. Priority decision: What are the priority nursing interventions for Mrs. Battong and her family?
6. 6. Priority decision: Based on the assessment data provided, what are the priority nursing diagnoses? Are there any collaborative problems?

Answer 1

ANSWERS

1. Pathophysiology of diabetic nephropathy

  

Diabetes is the major cause in the end stage renal disease.  

Diabetic nephropathy is occured as the result of interaction between hemodynamic and metabolic changes.

Hemodynamic changes includes increase in the systemic and intraglomerular pressure as well as the overaction of the RAAS. Glomerular hyper filteration and increased activation of RAAS lead to stress on the endothelial cells, the mesoangial cells and podocytes

Metabolic factors include formation of AGES(advanced glycation end products). The glycasilation products accumulate on the proteins of vessel wall collagen, forming an irreversible complex of cross-linked AGEs. RAGE is a signal transduction receptor found on a number of cell types including macrophages, endothelial cells, renal mesangial cells and podocytes in the glomerulus. Bindinng of AGEs with RAGE results in production of cytosolic Reactive Oxygen Species (ROS) as well as intracellular molecules such as protein kinace C, NF-kB and the activation of growth factors TGF-B and vascular endothelial growth factor (VEGF). These factors together with the hemodynamic changes results in podocyte injury, oxidative stress,infalmmation and fibrosis. Eventually kidney fuction is declined by more permeable glomerular membrane and less efficient filtration.

2. Indications of dialysis

* complaints of swelling on her hands and legs, Increased body weight over a short period( these are due to the decreased excreation of water by kidney. water retention results in weight gain)

* Breathing difficulty as a result of pulmonary edema due to the collection of fluids in the lungs.

* Estimated glomerular filtration rate (eGFR): 8.0 mL/min/1.73 meter square, serumcreatinine: 560 mmol/L, Blood urea nitrogen (BUN): 32 mmol/L, Potassium: 6 mmol/L

• Hemoglobin: 95 g/L

3. abnormal findings includes

Decreased glomerular filtration rate (eGFR): 8.0 mL/min/1.73 meter square, it resulted from the abnormal thckening of the vessels in the kidney

serumcreatinine: 560 mmol/L, Blood urea nitrogen (BUN): 32 mmol/L, Potassium: 6 mmol/L As a result of damaged renal tubules creatinine and blood urea nitrogen is not excreated by kidney and thus increased in the circulation. potassium also reabsorbed in to the circulation due to the thickening and high permeability of membranes in the tubules.

• Hemoglobin: 95 g/L due to the hypoxic changes in the kidney it results in the excess production of hemoglobin in the blood.

4. Due to hyperglycemia intially kidneys are excreating the excess glucose through urine and later on uncontrolled DM causes damages to the vascular and cellular level in the kidney. I t results in the thickening and fibrosis of the small vessels in the kidney. These vessels are permeable to water and reabsorbs certain elements in the tubules. as a result of decreased glomerular filtration the amout of urine is decreaed. Body retains the excess water in the tissues, results in swelling in the legs and arms, leads to weight gain in the patient. as well as pulmonary edema . Due to the pulmonary edema patient experiences the breathing difficulty while walking. Decreased glomerular filteration leads to retaining of BUN, potassium, creatinine in the circulation it results in the increased serum level of these.As a result of elevated levels of BUN, creatinine and potassium she experiences nausea,vomiting, pruritis and problems with concentration.