Nephrotic Syndrome

by

Definition

Nephrotic Syndrome is a condition when the kidneys leak large amounts of protein into the urine. This happens because of damage to the kidney’s glomeruli, which are responsible for filtering blood.

Pathophysiology

  • Glomerular Damage:- The glomeruli are responsible for filtering blood, and retaining essential proteins while allowing waste and excess fluids to pass into the urine. In nephrotic syndrome, the glomeruli become damaged due to an immune response or other factors. This damage increases the permeability of the glomerular basement membrane, leading to the leakage of large amounts of protein, particularly albumin, into the urine (proteinuria).
  • Hypoalbuminemia:- As a result of excessive protein loss in the urine, blood albumin levels drop significantly. Albumin is crucial for maintaining oncotic pressure, which keeps fluid within the blood vessels. When albumin levels are low, fluid escapes into the interstitial spaces, leading to widespread edema.
  • Hyperlipidemia:- The liver compensates for the loss of protein by increasing the production of lipoproteins, leading to elevated levels of cholesterol and triglycerides in the blood. This condition is commonly observed in patients with nephrotic syndrome.
  • Edema Formation:- The combination of hypoalbuminemia, sodium retention by the kidneys, and fluid leakage into tissues (due to low oncotic pressure) leads to the characteristic swelling seen in nephrotic syndrome. Edema often begins in the lower extremities and can progress to generalized edema, including pleural effusion (fluid around the lungs) and ascites (fluid in the abdomen).

Causes

  • Primary Glomerular Diseases:- These are conditions that directly affect the kidneys and are the most common causes of nephrotic syndrome:-
    • Minimal Change Disease (MCD):- The most common cause of nephrotic syndrome in children, MCD is characterized by glomeruli that appear normal under a light microscope but show effacement of podocyte foot processes under an electron microscope.
      •  The exact cause of MCD is unknown, but it is thought to involve immune dysregulation leading to glomerular damage.
    • Focal Segmental Glomerulosclerosis (FSGS):- A condition where scarring (sclerosis) occurs in some parts of the glomeruli, leading to protein leakage. FSGS can be primary (idiopathic) or secondary to other conditions.
      • FSGS is often associated with hypertension, obesity, and other factors that cause increased pressure in the glomeruli.
    • Membranous Nephropathy:- A condition characterized by thickening of the glomerular basement membrane due to immune complex deposition. It is a common cause of nephrotic syndrome in adults.
      • Membranous nephropathy is often associated with autoimmune diseases, infections, and certain medications.
  • Secondary Causes:- These are conditions outside the kidneys that can lead to nephrotic syndrome:
    • Diabetes Mellitus:- Diabetic nephropathy is a leading cause of nephrotic syndrome, resulting from long-term high blood sugar levels damaging the kidneys. It often presents as nodular glomerulosclerosis (Kimmelstiel-Wilson lesions).
      • Chronic hyperglycemia leads to the thickening of the glomerular basement membrane and mesangial expansion, resulting in proteinuria.
    • Systemic Lupus Erythematosus (SLE):- An autoimmune disease that can cause inflammation and damage to multiple organs, including the kidneys. Lupus nephritis, a complication of SLE, often leads to nephrotic syndrome.
      • Immune complex deposition in the glomeruli leads to inflammation and increased glomerular permeability.
    • Infections:- Certain infections like hepatitis B, hepatitis C, HIV, and malaria can cause nephrotic syndrome. These infections may trigger an immune response that damages the glomeruli.
      • Infections can lead to immune complex deposition or direct viral injury to the kidneys.
    • Medications:- Some drugs, such as nonsteroidal anti-inflammatory drugs (NSAIDs), penicillamine, and gold salts, can cause nephrotic syndrome by inducing glomerular injury.
      • These medications can cause direct toxicity to the kidneys or trigger an immune-mediated response leading to glomerular damage.

Symptoms

  • Edema:- One of the hallmark symptoms of nephrotic syndrome, edema is most noticeable in the feet, ankles, legs, and around the eyes. In severe cases, it can extend to the abdomen (ascites) and lungs (pleural effusion).
    • Rationale:- Edema occurs due to the loss of albumin in the urine, which reduces oncotic pressure, allowing fluid to accumulate in tissues.
  • Proteinuria:- Excessive protein in the urine, usually more than 3.5 grams per day, often results in frothy or foamy urine.
    • Rationale:- Proteinuria is a direct consequence of glomerular damage that allows proteins to pass through the glomerular filter into the urine.
  • Hypoalbuminemia:- Low levels of albumin in the blood, often less than 2.5 g/dL, due to the loss of protein in the urine.
  • Hyperlipidemia:- Elevated levels of cholesterol and triglycerides in the blood are common in nephrotic syndrome due to the liver’s response to hypoalbuminemia.
    • Rationale:- The liver produces more lipoproteins to compensate for low albumin levels, leading to hyperlipidemia.
  • Fatigue:- Generalized weakness and tiredness due to the loss of essential proteins, anemia, and the effects of chronic illness.
    • Rationale:- Protein loss and anemia reduce the body’s energy levels, causing fatigue.
  • Weight Gain:- Primarily due to fluid retention rather than fat accumulation. Patients may notice rapid weight gain as edema worsens.
    • Rationale:- The retention of fluids in the body increases overall weight, particularly in areas prone to edema.

Diagnostic Tests

  • Urinalysis:-
    • Proteinuria Detection:- A urine dipstick test can detect significant amounts of protein in the urine, ( per day loss of 4 to 30 gm protein)
      • Proteinuria is a key diagnostic criterion for nephrotic syndrome.
    • Microscopic Hematuria:- The presence of red blood cells in the urine, often seen in nephrotic syndrome, especially in cases associated with glomerulonephritis.
      • Hematuria indicates glomerular injury or inflammation.
  • Blood Tests:-
    • Serum Albumin:- Low levels of albumin in the blood (hypoalbuminemia), often below 2.5 g/dL.
      • Normal Range:- 3.5-5.0 g/dL.
      • Rationale:- Hypoalbuminemia reflects the loss of protein in the urine and is a marker of nephrotic syndrome severity.
    • Lipid Profile:- Elevated levels of cholesterol and triglycerides, often exceeding 300 mg/dL, are common in nephrotic syndrome.
      • Normal Cholesterol Levels:- Less than 200 mg/dL.
      • Rationale:- Hyperlipidemia results from the liver’s compensatory response to hypoalbuminemia.
    • Serum Creatinine and Blood Urea Nitrogen (BUN):- Tests to assess kidney function and monitor for potential kidney damage.
      • Normal Serum Creatinine:- 0.6-1.2 mg/dL.
      • Normal BUN:- 7-20 mg/dL.
      • Rationale:- Elevated levels may indicate declining kidney function or an underlying cause of nephrotic syndrome.
    • Complement Levels:-
      • C3 and C4 Levels:- Low complement levels can indicate an underlying immune-mediated cause, such as lupus nephritis.
        • Rationale:- Reduced complement levels suggest immune complex-mediated glomerular injury.
    • Tumor Markers:- In cases of suspected secondary nephrotic syndrome due to malignancies, specific tumor markers like PSA (Prostate-Specific Antigen) for prostate cancer or CA-125 for ovarian cancer may be assessed.
      • Rationale:- Tumor markers help identify underlying malignancies that could cause nephrotic syndrome.
  • 24-Hour Urine Collection:- Measures the total amount of protein lost in the urine over 24 hours. Proteinuria greater than 3.5 grams per day confirms the diagnosis of nephrotic syndrome.
    • Rationale:- This test provides a quantitative assessment of proteinuria, which is essential for diagnosis and monitoring.
  • Renal Biopsy:- A procedure to obtain a small sample of kidney tissue for examination under a microscope to diagnose the underlying cause of nephrotic syndrome.
    • Purpose:- Identifies the specific type of glomerular disease and guides treatment.
    • Risks:- Includes bleeding, infection, and pain.

Management

Non-Pharmacological Management

  • Dietary Modifications:-
    • Low-Sodium Diet:- Reducing sodium intake to help control edema and hypertension. Aim for less than 2,000 mg of sodium per day.
      • Rationale:- Sodium reduction helps prevent fluid retention and manage blood pressure.
    • Moderate Protein Intake:- Balancing protein intake to avoid worsening kidney damage while ensuring adequate nutrition. Aim for 0.8-1.0 grams of protein per kilogram of body weight per day.
      • Rationale:- Adequate protein intake supports overall health while minimizing further protein loss.
    • Low-Fat Diet:- Limiting saturated fats and cholesterol to manage hyperlipidemia. Emphasize fruits, vegetables, and whole grains.
      • Rationale:- A low-fat diet helps control elevated cholesterol and triglyceride levels, reducing cardiovascular risk.
  • Fluid Restriction:-
    • Fluid Intake Monitoring:- Limiting fluid intake to manage edema and prevent fluid overload. Recommendations vary based on the severity of edema and kidney function.
      • Rationale:- Fluid restriction helps control swelling and prevents complications related to excessive fluid accumulation.
  • Rest and Activity Balance:-
    • Rest During Edema:- Encouraging rest during periods of significant edema to reduce swelling and discomfort.
      • Rationale:- Resting helps alleviate symptoms of severe edema and promotes overall well-being.
    • Gradual Increase in Activity:- Once edema is controlled, slowly increase physical activity to improve overall fitness and prevent deconditioning.
      • Rationale:- Regular exercise supports cardiovascular health and overall physical condition.

Pharmacological Management

  • Diuretics:-
    • Medications:- Furosemide (Lasix), Spironolactone (Aldactone).
    • Mechanism:- Diuretics help reduce edema by promoting urine production and sodium excretion.
      • Rationale:- Reducing fluid overload alleviates swelling and helps manage hypertension.
    • Side Effects:- May include electrolyte imbalances (e.g., hypokalemia or hyperkalemia), dehydration, and hypotension.
  • Angiotensin-Converting Enzyme (ACE) Inhibitors:-
    • Medications:- Enalapril, Lisinopril.
    • Mechanism:- Lower blood pressure and reduce proteinuria by decreasing glomerular pressure and providing kidney protection.
      • Rationale:- ACE inhibitors help reduce the strain on the kidneys and decrease protein leakage.
    • Side Effects:- Cough, hyperkalemia (high potassium levels), and hypotension.
  • Angiotensin II Receptor Blockers (ARBs):-
    • Medications:- Losartan, Valsartan.
    • Mechanism:- Similar to ACE inhibitors, these drugs reduce proteinuria and protect the kidneys by blocking the effects of angiotensin II.
      • Rationale:- ARBs help manage blood pressure and reduce glomerular damage.
    • Side Effects:- Dizziness, fatigue, and hyperkalemia.
  • Corticosteroids:-
    • Medications:-Prednisolone
    • Mechanism:- Suppress the immune system to reduce inflammation and glomerular damage, especially in conditions like minimal change disease.
      • Rationale:- Steroids help reduce the immune response causing kidney damage.
    • Side Effects:- Weight gain, high blood sugar, increased risk of infections, and osteoporosis.
  • Immunosuppressants:-
    • Medications:- Cyclophosphamide, Cyclosporine, Tacrolimus.
    • Mechanism:- Used when steroids alone are not effective; these drugs control the immune response and reduce kidney damage.
      • Rationale:- Immunosuppressants are used to treat nephrotic syndrome caused by immune-mediated diseases.
    • Side Effects:- Increased risk of infections, kidney toxicity, and liver dysfunction.
  • Statins:-
    • Medications:- Atorvastatin, Simvastatin.
    • Mechanism:- Lower cholesterol levels to manage hyperlipidemia.
      • Rationale:- Statins help reduce cardiovascular risk associated with elevated cholesterol levels.
    • Side Effects:- Muscle pain, liver enzyme abnormalities.

Surgical Management

  • Paracentesis:-
    • Procedure:- Removal of excess fluid from the abdominal cavity using a needle inserted through the abdominal wall.
    • Purpose:- To relieve discomfort and prevent complications related to severe ascites.
    • Risks:- Infection, low blood pressure, electrolyte imbalances.

Nursing Care

Assessment:-
  • Monitor Fluid Balance:-
    Accurately record fluid intake and output to assess the effectiveness of diuretics and monitor for signs of fluid overload or dehydration.
    Rationale:- Proper monitoring helps manage edema and prevent complications related to fluid imbalances.
  • Daily Weight Monitoring:-
    Weigh the patient daily at the same time, in minimal clothing, and accurately record the results.
    Rationale:- Daily weight monitoring helps detect subtle changes in fluid status, which is crucial for managing edema and preventing fluid overload.
  • Edema Assessment:-
    Regularly evaluate swelling in the legs, ankles, and face to monitor the progression of edema.
    Rationale:- Tracking changes in edema helps assess treatment efficacy and adjust management strategies.
  • Measure Abdominal Girth:-
    Measure abdominal girth regularly to monitor for ascites or worsening fluid retention.
    Rationale:- Measuring abdominal girth provides additional data on fluid retention and helps guide treatment decisions.
  • Vital Signs:-
    Monitor blood pressure, pulse, and respiratory rate, especially in patients receiving antihypertensive medications.
    Rationale:- Vital signs provide insight into cardiovascular health and potential side effects of medications.
Patient Education:-
  • Medication Adherence:-
    Educate patients on the importance of taking medications as prescribed and reporting any side effects.
  • Dietary Guidance:-
    Provide information on following a low-sodium, low-fat, and moderate-protein diet
  • Recognizing Symptoms:-
    Teach patients to recognize symptoms of complications, such as increased swelling, shortness of breath, or signs of infection.
    Early recognition of symptoms allows for timely intervention and management.

Complications

  • Acute Kidney Injury (AKI):- Sudden loss of kidney function, often due to severe dehydration, infection, or progression of the underlying kidney disease.
    • Rationale:- Damage to the glomeruli reduces the kidneys’ ability to filter blood, leading to an accumulation of waste products.
  • Infections:- Increased risk of infections, including urinary tract infections (UTIs), pneumonia, and peritonitis.
    • Rationale:- The loss of protective proteins and the effects of immunosuppressive treatments increase susceptibility to infections.
  • Thromboembolism:- Increased risk of blood clots, including deep vein thrombosis (DVT) and pulmonary embolism (PE).
    • Rationale:- Nephrotic syndrome causes hypercoagulability, increasing the risk of clot formation.
  • Chronic Kidney Disease (CKD):- Progressive loss of kidney function over time, potentially leading to end-stage renal disease (ESRD).
    • Rationale:- Persistent glomerular damage and proteinuria result in scarring of the kidneys and reduced filtration capacity.
  • Malnutrition:- Loss of essential proteins in the urine can lead to malnutrition, muscle wasting, and weakness.
    • Rationale:- The depletion of proteins affects overall health and nutrition status.
  • Cardiovascular Disease:- Increased risk of heart disease and stroke due to hyperlipidemia, hypertension, and chronic inflammation.
    • Rationale:- Elevated cholesterol levels and persistent inflammation contribute to the development of cardiovascular complications.
  • Electrolyte Imbalances:-Diuretics and kidney dysfunction can disrupt electrolyte balance, leading to conditions like hyponatremia or hyperkalemia.

Leave a Comment