CKD - Nursing Case Study

Pathophysiology

• Primary mechanism: Progressive and irreversible loss of nephrons, the functional units of the kidney. This loss can be caused by various diseases such as diabetes, hypertension, or glomerulonephritis. Over time, the remaining nephrons undergo hypertrophy to compensate, leading to further damage.

• Secondary mechanism: Chronic kidney damage leads to systemic inflammation and oxidative stress. This condition promotes the formation of fibrous tissue in place of healthy kidney tissue (fibrosis), further decreasing renal function.

• Key complication: Reduced kidney function results in fluid and waste accumulation, leading to uremia. This condition can cause symptoms like nausea, fatigue, and cognitive impairment. Also, kidneys' reduced ability to produce erythropoietin can cause anemia.

Patient Profile

Demographics:

62-year-old male, retired construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes, recurrent urinary tract infections

• Current medications: Metformin, Lisinopril, Amlodipine

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Chronic fatigue, significant unintentional weight loss, and swelling in hands and feet

• Key symptoms: Persistent itching, shortness of breath, nausea, frequent urination, particularly at night

• Vital signs: Blood pressure 150/95 mm Hg, Pulse rate 90 beats per minute, Respiratory rate 18 breaths per minute, Temperature 98.1°F, Oxygen saturation 88% on room air

Section 1

New Diagnostic Results:

The patient’s blood tests showed a creatinine level of 3.8 mg/dL and a blood urea nitrogen (BUN) level of 40 mg/dL, both of which are significantly higher than normal, indicating impaired kidney function. Additionally, his hemoglobin level was found to be 10.2 g/dL, suggesting anemia likely secondary to chronic kidney disease (CKD). Urinalysis showed proteinuria and microscopic hematuria, further supporting the diagnosis of CKD. An ultrasound of the kidneys revealed bilateral renal atrophy.

Change in Patient Status:

The patient's condition began to worsen over the next few days. His blood pressure remained elevated at 160/100 mm Hg despite antihypertensive medications. His oxygen saturation dropped to 84% on room air, and he reported increased difficulty in breathing. The swelling in his hands and feet has also worsened, suggesting worsening fluid retention. His shortness of breath and increased fluid retention may be indicative of developing congestive heart failure, a common complication in patients with advanced CKD. His persistent itching has become more severe and the patient has developed restless legs syndrome (RLS), both of which are common in CKD due to the build-up of toxins in the blood.

Section 2

New Complications:

The patient's condition continues to deteriorate. His most recent lab results revealed a potassium level of 6.0 mEq/L, significantly higher than the normal range of 3.5-5.0 mEq/L. This hyperkalemia is a common complication in CKD due to impaired renal excretion of potassium. The patient also complained of palpitations, which could be a manifestation of hyperkalemia that can affect heart rhythm. His phosphorus level was also elevated at 6.5 mg/dL, above the normal range of 2.5-4.5 mg/dL, suggesting mineral and bone disorder associated with CKD.

Additionally, the patient developed a fever of 38.5°C. He reported chills and pain during urination, suggesting a possible urinary tract infection (UTI). This is a common complication in CKD patients due to decreased immunity and structural changes in the urinary system. A urine culture has been ordered to identify the causative organism and guide antibiotic therapy. This new complication adds a layer of complexity to the patient's management, requiring careful selection of antibiotics that won't exacerbate his kidney condition. The patient's deteriorating condition calls for a comprehensive re-evaluation of his treatment plan, which may include adjustment of his medications, possible dialysis, and management of his new complications.

Section 3

New Diagnostic Results:

The results of the urine culture confirmed the presence of Escherichia coli, a common cause of urinary tract infections. The patient’s complete blood count also showed an elevated white blood cell count of 14,000 cells/mcL, indicating an ongoing infection. The patient's blood pressure was observed to be consistently high, measuring around 160/90 mmHg despite the use of antihypertensives. This could be due to the CKD, as the diseased kidneys may be releasing an excessive amount of renin, contributing to hypertension.

Change in Patient Status:

Despite being started on a course of ceftriaxone, the patient's condition did not improve significantly. He continued to experience fever and chills, and his pain during urination persisted. His potassium level remained elevated at 5.8 mEq/L, and his phosphorus levels continued to rise, reaching 7.0 mg/dL. The patient also began experiencing increased fatigue and reduced appetite, common symptoms associated with worsening CKD. His shortness of breath also worsened, suggesting a possible development of pulmonary edema secondary to fluid overload, a complication often seen in CKD patients. This necessitates an urgent re-evaluation of his fluid management strategy.

Section 4

New Complications:

The patient's condition took a turn for the worse when he started experiencing seizures, a potential sign of uremic encephalopathy, a severe complication of CKD characterized by the accumulation of toxins in the brain due to impaired kidney function. His blood urea nitrogen (BUN) level had risen to 85 mg/dL, and creatinine level was at 5.6 mg/dL, indicating worsening renal dysfunction. Electrolyte imbalance, particularly the high potassium level, could also have contributed to the seizures. Furthermore, the patient reported severe muscle cramps, which might indicate the onset of renal osteodystrophy due to the high phosphorus level and the inability of the kidneys to produce adequate amounts of active vitamin D.

Response to Interventions:

In response to these new complications, the healthcare team decided to start the patient on hemodialysis to manage the uremic symptoms, control the potassium and phosphorus levels, and alleviate the fluid overload. The patient was also given calcium supplements and vitamin D to manage the renal osteodystrophy. Additionally, the antihypertensive regimen was revised to include calcium channel blockers, which could also help lower the high phosphorus level. Despite these interventions, the patient's blood pressure remained uncontrolled, necessitating further evaluation and adjustment of his treatment plan.

Section 5

Change in Patient Status:

Despite the aggressive management, the patient's condition continued to deteriorate. He started to experience shortness of breath at rest and was having difficulty sleeping due to orthopnea. This suggested that the fluid overload was not adequately controlled, leading to pulmonary edema. His blood pressure readings remained persistently high, with systolic readings ranging between 160-180 mmHg and diastolic readings between 90-100 mmHg. The patient also reported increasing fatigue and a worsening of his muscle cramps, indicating that the renal osteodystrophy was not well controlled despite the vitamin D and calcium supplementation.

New Complications:

During a routine examination, the patient's nurse noted a rapid irregular pulse rate, prompting an immediate EKG which confirmed the presence of atrial fibrillation (AF), a new complication potentially linked to the uncontrolled hypertension and electrolyte imbalance. His potassium level had risen to 6.0 mEq/L, further increasing the risk of cardiac arrhythmias. The patient's hemoglobin level had also dropped to 8.0 g/dL, suggesting the development of anemia, a common complication in CKD due to the decreased production of erythropoietin. This new development calls for an urgent reassessment of the patient's current treatment plan and the initiation of appropriate interventions to manage the anemia and AF.