Chronic kidney disease - Nursing Case Study

Pathophysiology

• Primary mechanism: Chronic kidney disease (CKD) primarily involves the progressive loss of nephrons due to sustained injury, often from diabetes or hypertension. This leads to glomerular sclerosis and reduced filtration capacity, impairing waste and fluid removal.

• Secondary mechanism: As nephron loss continues, surviving nephrons undergo hypertrophy and hyperfiltration to compensate. This adaptive response increases pressure and strain, accelerating nephron damage and further diminishing renal function.

• Key complication: The decline in kidney function leads to the accumulation of uremic toxins, fluid overload, and electrolyte imbalances, which can result in complications like cardiovascular disease, anemia, and bone mineral disorders.

Patient Profile

Demographics:

56-year-old male, construction worker

History:

• Key past medical history: Hypertension for 10 years, Type 2 Diabetes for 8 years

• Current medications: Lisinopril, Metformin, Amlodipine

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increasing fatigue and swelling in legs

• Key symptoms: Shortness of breath, foamy urine, muscle cramps, persistent nausea

• Vital signs: Blood pressure 150/95 mmHg, heart rate 92 bpm, respiratory rate 20 breaths per minute, temperature 98.6°F

Section 1

New Diagnostic Results:

In light of the patient's presenting symptoms, his healthcare team ordered a series of diagnostic tests to evaluate the extent of his kidney dysfunction and identify any complications. Key results from the laboratory tests revealed a serum creatinine level of 3.2 mg/dL and a blood urea nitrogen (BUN) level of 45 mg/dL, both indicative of impaired renal function. The patient's estimated glomerular filtration rate (eGFR) was calculated to be 29 mL/min/1.73m², confirming stage 4 chronic kidney disease. Additionally, urinalysis showed significant proteinuria with a protein level of 2.5 g/day, further evidence of nephron damage and glomerular filtration barrier compromise.

Electrolyte analysis indicated hyperkalemia, with serum potassium levels elevated at 5.8 mEq/L, raising concerns about cardiac stability, given the patient's history of hypertension. Anemia was also noted, with a hemoglobin level of 9.8 g/dL, likely due to decreased erythropoietin production by the failing kidneys. Imaging studies, including renal ultrasound, showed bilateral renal atrophy with no evidence of acute obstruction, corroborating the chronic nature of the disease.

These findings necessitate a comprehensive review of the patient's medication regimen and potential adjustments to prevent further deterioration. The healthcare team is considering the initiation of a renal-friendly diet to manage electrolyte imbalances and protein intake, alongside exploring erythropoiesis-stimulating agents to address anemia. The results also prompt the need for closer cardiovascular monitoring due to the increased risk of complications such as arrhythmias and exacerbation of heart failure symptoms. This diagnostic information sets the stage for discussing potential interventions such as adjusting antihypertensive therapy, considering diuretics for fluid management, and possibly discussing the long-term need for renal replacement therapy options.

Section 2

Change in Patient Status:

A week following the initial diagnostic assessment, the patient, Mr. Thompson, returned to the clinic for a follow-up evaluation. He reported increased fatigue and mild shortness of breath on exertion, symptoms he attributed to his daily activities but which were concerning given his current medical condition. Upon examination, his blood pressure was elevated at 160/95 mmHg, and his heart rate was noted to be irregular with a rate of 98 beats per minute, findings that heightened concerns about cardiac stability. A repeat electrolyte panel showed persistent hyperkalemia with a slightly elevated potassium level of 6.0 mEq/L, despite initial dietary modifications aimed at reducing potassium intake.

In addition to exacerbated electrolyte imbalances, Mr. Thompson's hemoglobin level had decreased further to 9.2 g/dL, warranting an escalation in management of his anemia. Given these developments, the healthcare team initiated a low-dose erythropoiesis-stimulating agent to stimulate red blood cell production and improve his energy levels. They also discussed potential adjustments to his antihypertensive regimen, considering the addition of a diuretic to manage fluid retention and control blood pressure more effectively. The irregular heartbeat raised the potential for arrhythmias, prompting a referral to cardiology for further assessment and possible Holter monitoring.

These changes in Mr. Thompson's status underscore the progressive nature of his chronic kidney disease and the need for integrated management strategies. The healthcare team emphasized the importance of regular monitoring and patient education on recognizing symptoms of electrolyte imbalances and cardiovascular instability. Mr. Thompson's evolving clinical picture highlighted the delicate balance required in managing chronic kidney disease complications while maintaining quality of life, setting the stage for an ongoing dialogue about future treatment options, including potential dialysis.

Section 3

Two weeks after Mr. Thompson's antihypertensive regimen was adjusted and a low-dose erythropoiesis-stimulating agent was initiated, he returned for another follow-up appointment. He reported a slight improvement in energy levels, but his shortness of breath had worsened, now occurring even with minimal exertion. His vital signs revealed a blood pressure of 150/92 mmHg, slightly improved but still elevated, and a heart rate that remained irregular at 96 beats per minute. Notably, his respiratory rate was increased to 24 breaths per minute, and there was mild peripheral edema in his lower extremities.

A comprehensive metabolic panel indicated that Mr. Thompson's potassium level had slightly decreased to 5.8 mEq/L, but it remained above the normal range, necessitating continued vigilance. His renal function had further declined, with a creatinine level of 3.2 mg/dL and an estimated glomerular filtration rate (eGFR) of 28 mL/min/1.73m², signaling a progression to stage 4 chronic kidney disease. Hemoglobin levels showed a marginal increase to 9.5 g/dL, suggesting a partial response to the erythropoiesis-stimulating agent, though anemia management remained a priority.

In light of these findings, the healthcare team deliberated on further intervention strategies. The addition of a loop diuretic was considered to address fluid overload, contributing to both his hypertension and dyspnea. The cardiology referral was expedited due to the persistence of an irregular heartbeat, raising concerns about the potential for atrial fibrillation or other arrhythmias. Mr. Thompson's case continued to highlight the intricacies of managing chronic kidney disease with coexisting cardiovascular issues, reinforcing the need for a multidisciplinary approach and close monitoring to prevent further complications. As his condition evolved, discussions about future plans, including the possibility of dialysis or renal transplantation, became increasingly pertinent.

Section 4

In the weeks following the adjustment to Mr. Thompson's treatment plan, his condition took a concerning turn. During a routine check-up, it was noted that he had developed an increased frequency of nocturnal dyspnea, and his peripheral edema had progressed from mild to moderate, now extending to his hands. His blood pressure remained stubbornly elevated at 152/94 mmHg, despite adherence to his antihypertensive regimen. His heart rate was recorded at 102 beats per minute, and the irregular rhythm persisted. His respiratory rate increased further to 26 breaths per minute, indicating worsening respiratory distress.

A repeat comprehensive metabolic panel revealed that Mr. Thompson's potassium level had stabilized at 5.4 mEq/L, but his renal function continued to decline, with a creatinine level now at 3.5 mg/dL and an eGFR reduced to 25 mL/min/1.73m², confirming the progression within stage 4 chronic kidney disease. Alarmingly, his hemoglobin level had plateaued at 9.3 g/dL, suggesting a suboptimal response to the erythropoiesis-stimulating agent, potentially exacerbated by the fluid overload. The cardiology team confirmed atrial fibrillation through an ECG, necessitating immediate consideration of anticoagulation therapy to mitigate stroke risk, while balancing the potential for bleeding complications given his renal impairment.

These developments prompted the healthcare team to intensify the management plan. The loop diuretic dosage was increased to more aggressively manage fluid retention, and discussions were initiated regarding the initiation of anticoagulant therapy, carefully weighing the risks and benefits in the context of his kidney function. Mr. Thompson was counseled on the importance of dietary modifications to further control potassium levels and was educated on recognizing signs and symptoms of worsening heart failure. The exploration of dialysis options was accelerated, with an emphasis on preparing Mr. Thompson psychologically and logistically for this possible next step in his treatment journey. The multidisciplinary approach remained crucial, as the team worked collaboratively to stabilize Mr. Thompson's condition and prevent further complications.

Section 5

In the subsequent weeks, Mr. Thompson's response to the intensified management plan demonstrated mixed outcomes. His increased loop diuretic regimen initially led to a modest reduction in peripheral edema, particularly in the lower extremities, though the swelling in his hands persisted. His blood pressure showed slight improvement, averaging 146/90 mmHg, but his heart rate remained elevated at around 100 beats per minute with continued irregular rhythms. Despite these changes, Mr. Thompson began experiencing more frequent episodes of dizziness and fatigue, raising concerns about the balance of his fluid and electrolyte status.

A follow-up comprehensive metabolic panel showed a slight improvement in creatinine levels, now at 3.3 mg/dL, yet his eGFR remained at 25 mL/min/1.73m², indicating that while some aspects of his renal function stabilized, the overall kidney disease progression was unhalted. His potassium levels stayed at the higher end, recorded at 5.3 mEq/L, reinforcing the need for sustained dietary vigilance. The most concerning development was a drop in his hemoglobin level to 8.9 g/dL, suggesting worsening anemia that could be linked to both his chronic kidney disease and possible inadequate response to erythropoiesis-stimulating agents.

Clinically, Mr. Thompson's nocturnal dyspnea persisted, albeit with reduced intensity, yet his respiratory rate remained elevated at 24 breaths per minute, indicating ongoing respiratory compromise. The healthcare team was prompted to reassess the anticoagulation strategy, considering his increased fall risk due to dizziness. The cardiology and nephrology teams revisited the possibility of early dialysis initiation to better manage his fluid overload and reduce the burden on his cardiovascular system. This intersection of symptoms and lab results required the team to engage in further clinical reasoning, focusing on the delicate equilibrium between managing Mr. Thompson's heart failure symptoms and the progression of his chronic kidney disease. The next steps involved close monitoring, continued patient education, and a refined interdisciplinary approach to adjust his care plan effectively.