nephrotic syndrome - Nursing Case Study

Pathophysiology

• Primary mechanism: Increased glomerular permeability leads to significant proteinuria. Damage to the glomerular filtration barrier, often due to podocyte injury, allows large proteins like albumin to leak into the urine, resulting in hypoalbuminemia.

• Secondary mechanism: Hypoalbuminemia reduces plasma oncotic pressure, causing fluid to shift from the vascular space to interstitial tissues, resulting in edema. This fluid imbalance also triggers the renin-angiotensin-aldosterone system, exacerbating fluid retention.

• Key complication: The loss of proteins, including immunoglobulins, increases susceptibility to infections. Additionally, hyperlipidemia often occurs as the liver compensates by increasing lipoprotein synthesis, heightening the risk of cardiovascular issues.

Patient Profile

Demographics:

43-year-old female, office administrator

History:

• Key past medical history: Hypertension, Type 2 Diabetes, Hyperlipidemia

• Current medications: Lisinopril, Metformin, Atorvastatin, Prednisone

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Swelling in legs and abdomen

• Key symptoms: Edema, frothy urine, fatigue, decreased urine output

• Vital signs: Blood pressure 150/95 mmHg, heart rate 88 bpm, respiratory rate 20 breaths per minute, temperature 98.6°F, oxygen saturation 97% on room air

Section 1

Two days following the initial presentation, the patient experiences a noticeable change in her condition. She reports increasing fatigue and breathlessness. Upon assessment, the nurse notes that her edema has progressed, now extending to her arms and hands. Additionally, her abdominal distension appears more pronounced. Her vital signs reveal a blood pressure of 160/100 mmHg, heart rate of 92 bpm, respiratory rate of 24 breaths per minute, and oxygen saturation of 95% on room air. Auscultation of her lungs reveals bilateral crackles at the bases, suggestive of fluid overload and potential pulmonary edema.

New laboratory results show worsening proteinuria with a urine protein-to-creatinine ratio of 6.5 g/g, indicating significant protein loss. Serum albumin levels have further decreased to 2.1 g/dL, exacerbating her hypoalbuminemia. Her lipid profile reveals an increase in total cholesterol to 280 mg/dL, with elevated LDL and triglycerides, signifying worsening hyperlipidemia. Renal function tests show a slight increase in serum creatinine to 1.5 mg/dL, suggesting a decline in kidney function. These findings reflect the progression of her nephrotic syndrome and the need for more aggressive management to prevent further complications.

The healthcare team considers adjusting her medication regimen, particularly addressing her fluid overload and hypertension, which are contributing to her symptoms. Diuretic therapy is initiated with cautious titration to manage edema and improve her respiratory status. Additionally, the team discusses the potential need for anticoagulation therapy, given her increased risk of thromboembolic events due to significant protein loss. These interventions aim to stabilize her condition and prevent further deterioration, while the team continues to monitor her response closely and evaluates the need for additional diagnostic procedures or specialty consultations.

Section 2

Two days after the initiation of diuretic therapy, the patient exhibits a mixed response. She reports a slight improvement in breathlessness, although fatigue persists. The nurse notes a modest reduction in peripheral edema, particularly in the lower extremities, but swelling remains significant in her arms and hands. Her abdominal distension shows little change, indicating persistent ascites. During assessment, vital signs reveal a blood pressure of 150/95 mmHg, heart rate of 88 bpm, respiratory rate of 22 breaths per minute, and oxygen saturation of 96% on room air. Auscultation continues to reveal bilateral crackles at the lung bases, although slightly diminished from the previous assessment.

New laboratory results show a slight improvement in serum creatinine, now at 1.4 mg/dL, suggesting a mild recovery in renal function. However, proteinuria remains severe, with a urine protein-to-creatinine ratio of 6.0 g/g, and serum albumin remains critically low at 2.0 g/dL. Her lipid profile remains elevated, with total cholesterol at 275 mg/dL. A recent coagulation profile indicates a normal INR but a slightly elevated D-dimer level, raising the clinical suspicion of a hypercoagulable state. The healthcare team deliberates on the balance between managing fluid overload and preventing potential thromboembolic complications, carefully considering the benefits and risks of anticoagulation therapy.

Despite initial therapeutic adjustments, the patient's condition underscores the complexity of managing nephrotic syndrome with concurrent fluid overload and the risk of thrombosis. The team decides to consult with a nephrologist to explore additional treatment options, including potential immunosuppressive therapy if indicated, and to reassess the need for further diagnostic imaging to evaluate for any underlying thromboembolic events. The ongoing monitoring of her response to treatment and the anticipation of possible complications guide the next steps in her care, emphasizing the importance of a multidisciplinary approach in managing her condition.

Section 3

The healthcare team decides to focus on the new complications emerging from the patient's condition, particularly the risk of thromboembolic events given her elevated D-dimer level. As part of a comprehensive evaluation, a Doppler ultrasound of the lower extremities is ordered to assess for deep vein thrombosis (DVT), which could explain her persistent edema and fatigue. The ultrasound reveals a non-occlusive thrombus in the left popliteal vein, confirming the presence of a DVT. This finding necessitates the initiation of anticoagulation therapy to prevent further thromboembolic complications. Given her nephrotic syndrome and the potential for bleeding, the team opts for a cautious approach, starting with low-molecular-weight heparin while closely monitoring her coagulation profile and renal function.

Meanwhile, the nephrologist reviews the patient's case, noting the persistently severe proteinuria and hypoalbuminemia, which contribute to her hypercoagulable state and fluid retention. The nephrologist recommends initiating corticosteroid therapy to address the underlying inflammation and potentially reduce proteinuria. The team discusses the potential side effects of steroids, such as increased blood pressure and risk of infection, and plans to monitor her closely for any adverse reactions.

In the following days, the patient's condition requires careful monitoring. Her blood pressure stabilizes slightly with the addition of antihypertensive medication, and her edema shows some improvement with the combination of diuretics and anticoagulation therapy. However, her fatigue remains a significant issue, likely exacerbated by her low albumin levels and ongoing inflammation. The healthcare team remains vigilant in assessing her response to the new interventions, ready to adjust her treatment plan as necessary to manage the complexities of her nephrotic syndrome while preventing further complications.

Section 4

In the subsequent days, the patient's condition reveals a mixed response to the ongoing treatment. Her response to the corticosteroid therapy is initially positive, as evidenced by a slight reduction in proteinuria from 8g/day to 6g/day, indicating a partial but promising response to the intervention. However, a new complication emerges as the patient begins to experience increasing hypertension, with her blood pressure readings averaging 160/100 mmHg, likely a side effect of the corticosteroids. This necessitates an adjustment in her antihypertensive regimen, adding an ACE inhibitor to better control her blood pressure and protect renal function.

Concurrent laboratory evaluations show a concerning trend in her renal profile, with serum creatinine levels rising from 1.2 mg/dL to 1.5 mg/dL. This change raises suspicion of potential steroid-induced nephrotoxicity or worsening of her nephrotic syndrome. Additionally, her albumin levels remain low at 2.0 g/dL, contributing to persistent fatigue and delayed improvement in edema. The healthcare team deliberates the benefit-risk ratio of continuing corticosteroids versus potential renal deterioration, weighing the necessity of maintaining adequate immunosuppression to manage her nephrotic state.

The patient also exhibits signs suggestive of new complications, with increased bruising noted on her extremities during physical examination, raising concerns about over-anticoagulation. The team promptly reviews her coagulation profile, finding her INR slightly elevated at 1.5, prompting a reassessment of her anticoagulation therapy. Careful titration of her medication is planned to balance the prevention of further thromboembolic events with the risk of bleeding. The healthcare team remains vigilant, ready to adapt her treatment plan as they continue to navigate the complexities of her condition, ensuring comprehensive management of her nephrotic syndrome and associated complications.

Section 5

In the ensuing days, the patient’s condition takes a concerning turn with the development of new complications. During routine monitoring, the nursing staff notes a sudden increase in the patient's peripheral edema, now extending to the sacral area, suggesting a worsening of her fluid retention. Her weight has increased by 3 kilograms over the last 48 hours. This exacerbation prompts the healthcare team to reassess her fluid management strategy. Currently on a sodium-restricted diet and loop diuretics, the patient’s regimen is adjusted to include a higher dose of furosemide, while closely monitoring her electrolyte levels to prevent imbalances that could lead to further complications.

Further complicating her clinical picture, the patient begins to report episodes of dyspnea and orthopnea, particularly at night, indicative of possible pulmonary congestion. An urgent chest X-ray is performed, revealing mild pulmonary edema. Her oxygen saturation has decreased to 92% on room air, necessitating supplemental oxygen therapy to maintain adequate levels. The team considers the possibility of heart failure as a result of fluid overload, warranting an echocardiogram to evaluate cardiac function and guide further management.

In response to these developments, the interdisciplinary team discusses the potential need for escalating her treatment to include more aggressive diuretic therapy or the introduction of additional medications such as aldosterone antagonists. The patient's renal function and electrolyte balance remain critical considerations, as they aim to manage her fluid status without exacerbating her nephrotic syndrome. This situation underscores the complexity of her care, requiring careful coordination and ongoing assessment to strike a balance between effective symptom management and the preservation of renal health. The team continues to monitor her closely, prepared to implement further interventions as necessary to stabilize her condition and improve her quality of life.