ESRD secondary to CGN - Nursing Case Study
Pathophysiology
• Primary mechanism: Chronic Glomerulonephritis (CGN) leads to persistent inflammation of the glomeruli, causing structural damage and scarring (glomerulosclerosis), which progressively impairs kidney filtration function.
• Secondary mechanism: The ongoing glomerular injury triggers compensatory hyperfiltration in remaining nephrons, accelerating their damage and loss, ultimately reducing total renal function.
• Key complication: As glomerular filtration rate declines, waste products accumulate in the blood, leading to uremia and the systemic complications characteristic of End-Stage Renal Disease (ESRD), necessitating renal replacement therapy.
Patient Profile
Demographics:
52-year-old male, construction worker
History:
• Key past medical history: Chronic Glomerulonephritis (CGN) diagnosed 10 years ago, hypertension, type 2 diabetes
• Current medications: Lisinopril, Metformin, Furosemide, Erythropoietin injections
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Increasing fatigue and shortness of breath
• Key symptoms: Edema in lower extremities, decreased urine output, nausea, muscle cramps
• Vital signs: Blood pressure 160/95 mmHg, heart rate 92 bpm, respiratory rate 22 breaths per minute, temperature 98.6°F, oxygen saturation 94% on room air
Section 1
New Diagnostic Results:
Upon admission, the patient underwent a series of diagnostic tests to assess the progression of his kidney disease and related complications. Laboratory results revealed a serum creatinine level of 6.5 mg/dL and a blood urea nitrogen (BUN) of 75 mg/dL, indicating significant renal impairment. The patient's estimated glomerular filtration rate (eGFR) was calculated at 12 mL/min/1.73 m², confirming the diagnosis of End-Stage Renal Disease (ESRD). Electrolyte imbalances were also noted, with hyperkalemia showing a potassium level of 5.8 mEq/L, posing an immediate risk for cardiac complications. Additionally, a complete blood count showed anemia with a hemoglobin level of 9.0 g/dL, likely secondary to decreased erythropoietin production and chronic disease.
Further diagnostic imaging, including a renal ultrasound, demonstrated bilateral kidney atrophy with increased echogenicity, consistent with chronic parenchymal disease. An echocardiogram was performed to assess the cause of the patient's shortness of breath and revealed mild left ventricular hypertrophy, a common sequela of long-standing hypertension and chronic kidney disease. This finding suggests that the patient's cardiac symptoms may be exacerbated by volume overload due to impaired renal function.
These diagnostic results emphasize the critical nature of the patient's condition and highlight the need for urgent intervention to address the metabolic derangements and prevent further complications. With the confirmation of ESRD, discussions regarding the initiation of renal replacement therapy, such as hemodialysis, are imperative. This stage of the patient's journey will require careful consideration of his cardiovascular status and management of electrolyte imbalances to ensure a safe transition to dialysis. The clinical team must also address the patient's anemia, potentially adjusting erythropoietin therapy and considering iron supplementation.
Section 2
Change in Patient Status:
Following the initial assessment and diagnostic findings, the clinical team initiated a series of interventions to address the patient's critical condition. Despite efforts to manage his electrolyte imbalances and stabilize his cardiovascular status, the patient began exhibiting signs of worsening hyperkalemia. His potassium level increased to 6.2 mEq/L, accompanied by ECG changes, including peaked T waves and a widened QRS complex, indicating an increased risk for life-threatening arrhythmias. The patient also reported new episodes of palpitations and dizziness, heightening concerns about his cardiac stability.
In response to these developments, the healthcare team promptly administered calcium gluconate to stabilize the cardiac membrane, alongside insulin and glucose to facilitate the intracellular shift of potassium. Concurrently, sodium polystyrene sulfonate was given to enhance potassium excretion through the gastrointestinal tract. Despite these measures, the patient's heart rate remained irregular, with episodes of tachycardia observed on telemetry, underscoring the need for more aggressive intervention.
Recognizing the urgent need for renal replacement therapy, the decision was made to initiate emergent hemodialysis. This intervention aimed not only to correct the severe hyperkalemia but also to address the patient's worsening volume overload, which was contributing to his dyspnea and peripheral edema. The initiation of dialysis brought about a noticeable improvement in the patient's clinical status, as his potassium levels normalized, and his cardiac rhythm stabilized. However, the team remained vigilant, aware of the potential for additional complications such as dialysis disequilibrium syndrome or hypotension. As the patient transitioned to regular dialysis sessions, ongoing assessment and adjustment of his treatment plan became crucial to managing his complex and evolving clinical needs.
Section 3
New Complications:
Following the initiation of hemodialysis, the patient's potassium levels stabilized, and his cardiac rhythm returned to a more regular pattern. However, during the second dialysis session, the patient began experiencing symptoms of dialysis disequilibrium syndrome, including restlessness, headache, and mild confusion. These symptoms were indicative of a rapid change in fluid and electrolyte balance, leading to cerebral edema. The healthcare team closely monitored his neurological status, noting that his Glasgow Coma Scale (GCS) score had decreased from 15 to 13.
Vital signs taken during this period revealed a blood pressure of 98/60 mmHg, heart rate of 94 bpm, respiratory rate of 22 breaths per minute, and oxygen saturation at 94% on room air. Laboratory results showed a slight decrease in serum sodium to 132 mEq/L, suggesting a potential contributing factor to his altered mental status. Recognizing the need for careful management, the team adjusted the dialysis parameters to slow the rate of fluid removal and provided supportive care to address the patient's symptoms.
Despite these efforts, the patient's condition remained precarious, necessitating ongoing assessment and intervention. The team discussed the potential need for additional diagnostic imaging, such as a CT scan of the brain, to rule out other causes of his neurological symptoms. As the patient continued under close observation, the importance of balancing electrolyte correction with the prevention of rapid shifts became a focal point in his treatment plan. This highlighted the complexity of managing end-stage renal disease with concurrent complications, underscoring the need for a multidisciplinary approach to ensure optimal patient outcomes.
Section 4
Change in Patient Status
Following the adjustment in dialysis parameters and supportive care, the patient's condition seemed to stabilize temporarily. His restlessness diminished, and he reported a slight reduction in headache intensity. However, over the next few hours, the patient's mental status began to deteriorate further. Nursing staff observed increased lethargy, and his GCS score fell to 11, raising concerns about his neurological function. The patient was now responding to verbal stimuli but was slower to answer questions and was unable to recall recent events.
Vital signs indicated a concerning trend: his blood pressure had decreased further to 92/58 mmHg, while his heart rate increased to 102 bpm, suggesting compensatory tachycardia possibly due to hypovolemia or worsening cerebral edema. Oxygen saturation remained stable at 95% on room air, but his respiratory rate increased to 24 breaths per minute. Repeat laboratory tests showed a continued decrease in serum sodium to 130 mEq/L, raising the suspicion of hyponatremia contributing to his altered mental status.
Given the patient's deteriorating condition, the healthcare team decided to proceed with a CT scan of the brain to assess for any acute intracranial pathology such as hemorrhage or severe cerebral edema. The team also considered the possibility of introducing hypertonic saline cautiously to correct the hyponatremia while avoiding rapid shifts that could exacerbate cerebral edema. The critical balance between managing electrolyte imbalances and preventing further neurological deterioration was emphasized. This unfolding scenario required the healthcare team to apply clinical reasoning to prioritize interventions and coordinate care effectively, reflecting the dynamic nature of managing complex cases in end-stage renal disease.
Section 5
New Diagnostic Results
The CT scan of the brain revealed mild cerebral edema, but no evidence of acute intracranial hemorrhage. This finding corroborated the suspicion that the patient's neurological decline was likely exacerbated by the electrolyte imbalance rather than any acute structural damage. Given the mild nature of the edema, the clinical team decided to proceed cautiously with hypertonic saline infusion to address the hyponatremia, aiming for a gradual increase in serum sodium levels rather than rapid correction to avoid the risk of osmotic demyelination syndrome.
In addition to the CT findings, further laboratory tests provided additional insights. The patient's serum creatinine remained elevated at 9.5 mg/dL, consistent with his ESRD status, while his potassium level had decreased slightly to 4.8 mEq/L following dialysis adjustments. However, his blood urea nitrogen (BUN) was notably elevated at 68 mg/dL, indicating poor clearance and potential contribution to his altered mental status. The patient's calcium levels were low at 8.0 mg/dL, suggesting a need for careful management to prevent further neuromuscular irritability.
The healthcare team, integrating these diagnostic results, emphasized the importance of a multidisciplinary approach to monitor the patient's response to the hypertonic saline infusion. They planned frequent neurological assessments and close monitoring of electrolyte levels to ensure gradual correction and stabilization. The team also discussed the potential need for adjusting dialysis parameters further if the patient's condition did not improve, reflecting the complexities of managing a patient with ESRD and concurrent neurological complications. This careful balancing of interventions and monitoring laid the groundwork for the next steps in the patient's care journey, requiring continual reassessment and adaptation of the care plan.