kidney transplant - Nursing Case Study

Pathophysiology

• Primary mechanism: Chronic renal dysfunction necessitates a kidney transplant. Post-transplant, the immune system recognizes the new kidney as foreign, triggering an immune response. Immunosuppressive drugs are used to inhibit this response, but they risk serious infections and malignancies.

• Secondary mechanism: Ischemia-reperfusion injury occurs during transplantation, where the kidney is deprived of blood supply then reperfused. This can cause acute kidney injury by producing reactive oxygen species damaging cells, leading to inflammation, cell death, and fibrosis.

• Key complication: Chronic allograft nephropathy, a progressive loss of kidney function post-transplant, is a common complication. It results from a mix of immunological (rejection episodes) and non-immunological factors (hypertension, infections), leading to fibrosis and graft loss.

Patient Profile

Demographics:

57-year-old male, former construction worker

History:

• Key past medical history: Diagnosed with Hypertension in 2005, Chronic Kidney Disease (stage 5) in 2012, Diabetes Mellitus type 2 in 2014, and Coronary Artery Disease in 2016; underwent coronary artery bypass graft in 2017

• Current medications: Metformin, Lisinopril, Amlodipine, Warfarin, Lasix, and Multivitamins

• Allergies: Penicillin, Sulfa drugs

Current Presentation:

• Chief complaint: Shortness of breath, severe fatigue, and swelling in the legs and feet

• Key symptoms: Persistent high blood pressure, frequent urination especially at night, foamy or bloody urine, puffy eyes, reduced appetite, unexplained weight loss, and persistent itchiness

• Vital signs: Blood Pressure: 170/110 mmHg, Pulse: 110 bpm, Respiratory rate: 22 breaths per minute, Temperature: 98.6°F, Oxygen saturation: 88% on room air

Section 1

Change in Patient Status:

Over the next 72 hours, the patient's condition deteriorated significantly. His BP increased to 190/120 mmHg, and his pulse quickened to 130 bpm. Furthermore, his respiratory rate escalated to 28 breaths per minute, and his oxygen saturation dropped to 82% on room air. His symptoms also worsened, with the patient complaining of severe nausea, vomiting, and a decrease in urine output. His weight increased by 3 kg, suggesting fluid retention, and his fatigue intensified, making it nearly impossible for him to perform simple tasks.

Laboratory tests revealed a marked increase in serum creatinine levels from 1.5 mg/dL to 3.7 mg/dL, blood urea nitrogen (BUN) from 20 mg/dL to 50 mg/dL, and potassium levels from 4.5 mEq/L to 6.2 mEq/L. Urinalysis showed proteinuria and hematuria. A decrease in urine sodium concentration was also evident. Furthermore, an echocardiogram revealed an ejection fraction of 45% indicating that his heart was not pumping blood efficiently. These findings raised concerns about the progression of chronic allograft nephropathy and the possibility of acute kidney injury and heart failure. The patient was closely monitored and prepared for further diagnostic tests to evaluate the functioning of the transplanted kidney and heart.

Section 2

New Diagnostic Results:

Further diagnostic tests were performed to evaluate the decline in the patient's renal function and cardiac status. A renal biopsy of the transplanted kidney revealed significant interstitial fibrosis and tubular atrophy, consistent with chronic allograft nephropathy. The degree of fibrosis suggested irreversible damage to the kidney. A 24-hour urine protein was elevated at 3.5 g/day, indicative of significant proteinuria and further pointing towards the progression of renal disease.

A cardiac catheterization was performed to assess the patient's cardiac function, given his elevated blood pressure and decreased ejection fraction. The test revealed severe concentric left ventricular hypertrophy and a significantly increased left ventricular end-diastolic pressure of 22 mmHg, indicative of diastolic heart failure. These findings, combined with the patient's worsening clinical status, suggested a possible connection between the patient's worsening renal function and his cardiac status. The team was faced with the complex task of managing the dual challenges of chronic allograft nephropathy and diastolic heart failure, requiring advanced critical thinking and clinical judgment.

Section 3

Change in Patient Status:

Despite the team's aggressive therapeutic approach, the patient's status continued to deteriorate. The patient's blood pressure remained persistently elevated at 170/95 mmHg, despite the addition of a second antihypertensive agent. His serum creatinine level increased to 4.2 mg/dL, further confirming the progression of renal disease. In addition, the patient developed anasarca, with significant peripheral edema and ascites, suggesting worsening renal and cardiac function. The patient also complained of increasing dyspnea and fatigue, likely related to the combined effects of fluid overload and decreased oxygenation due to the diastolic heart failure.

In light of these developments, the team had to reconsider the therapeutic strategy. The patient's escalating blood pressure, worsening renal function, and the development of fluid overload indicated the need for more aggressive interventions, such as adding a third antihypertensive agent or considering dialysis. The team was also confronted with the difficult decision of whether or not to pursue a second kidney transplant, given the high risk associated with his cardiac status. In the midst of these challenges, the team had to balance the urgency of addressing the patient's deteriorating condition with the potential risks of more aggressive interventions.

Section 4

New Diagnostic Results:

Despite the team's aggressive approach, the latest diagnostic tests painted a grim picture. The patient's hemoglobin level had dropped to 8.2 g/dL, indicating a significant progression in anemia. His B-type natriuretic peptide (BNP) level was now at 1500 pg/mL, suggesting a decompensated heart failure. A chest radiograph showed signs of pulmonary edema, further corroborating the diagnosis. Additionally, an echocardiogram revealed a decrease in ejection fraction to 35%, pointing to a worsening cardiac function.

The patient's renal function tests had also taken a hit. His estimated glomerular filtration rate (eGFR) had fallen to 20 mL/min/1.73 m2, indicating stage 4 chronic kidney disease. His urine albumin-to-creatinine ratio (ACR) was now 350 mg/g, suggesting heavy proteinuria. The presence of red and white blood cell casts in his urine sample further confirmed the diagnosis of rapidly progressive glomerulonephritis. These findings necessitated an urgent revision of the therapeutic plan. The team had to decide whether to initiate dialysis immediately or opt for aggressive immunosuppression, considering the patient's compromised cardiac status. The dilemma of pursuing a second kidney transplant loomed large, with the patient's deteriorating condition adding to the complexity.

Section 5

Change in Patient Status:

The patient's condition continued to deteriorate over the next 24 hours. He started to experience increased dyspnea and orthopnea, which was indicative of worsening heart failure. The patient's blood pressure dropped to 90/60 mmHg with a heart rate of 105 beats per minute, pointing towards a state of shock. Furthermore, he developed a decrease in urine output to less than 0.5 mL/kg/hr, indicating worsening renal failure.

New Complications:

The situation escalated when the patient started to show confusion and disorientation, suggestive of uremic encephalopathy. A repeat blood test showed a significant increase in his serum creatinine to 6.0 mg/dL and blood urea nitrogen (BUN) to 80 mg/dL. His serum potassium had risen to 6.5 mEq/L, posing a risk for life-threatening cardiac arrhythmias. An electrocardiogram (ECG) showed tall, peaked T-waves, a sign of hyperkalemia. His worsening renal and cardiac status, coupled with the development of uremic encephalopathy and hyperkalemia, necessitated an immediate reevaluation of the therapeutic approach and complex decision-making regarding the possibility of immediate dialysis.