What are the differences between nephritic and nephrotic syndrome?

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Last updated: June 22, 2025View editorial policy

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From the Guidelines

Nephritic and nephrotic syndromes are distinct kidney disorders with different clinical presentations and underlying mechanisms, and proper identification is crucial for appropriate management. Nephritic syndrome is characterized by inflammation of the glomeruli, presenting with hematuria (blood in urine), mild proteinuria, hypertension, and often decreased kidney function. Common causes include post-streptococcal glomerulonephritis, IgA nephropathy, and lupus nephritis. In contrast, nephrotic syndrome features massive proteinuria (>3.5g/day), hypoalbuminemia, edema, and hyperlipidemia. It results from damage to the glomerular filtration barrier, allowing proteins to leak into urine. Common causes include minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, and diabetic nephropathy.

Key Differences

  • Clinical presentation: Nephritic syndrome presents with hematuria, mild proteinuria, and hypertension, while nephrotic syndrome presents with massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia.
  • Underlying mechanisms: Nephritic syndrome is caused by inflammation of the glomeruli, while nephrotic syndrome is caused by damage to the glomerular filtration barrier.
  • Treatment approaches: Nephritic syndrome management focuses on controlling inflammation and hypertension with immunosuppressants, while nephrotic syndrome treatment aims to reduce proteinuria using ACE inhibitors, ARBs, and sometimes steroids or other immunosuppressants depending on the underlying cause.

Treatment Considerations

  • According to the 2012 KDIGO clinical practice guideline for glomerulonephritis, initial therapy should be started only in patients with nephrotic syndrome and when at least one of the following conditions is met: urinary protein excretion persistently exceeds 4 g/day, presence of severe symptoms, or SCr level has risen by 30% or more within 6 to 12 months from the time of diagnosis 1.
  • The Canadian Society of Nephrology commentary on the 2012 KDIGO clinical practice guideline for glomerulonephritis recommends using a calcineurin inhibitor (CNI) as initial therapy for children with steroid-resistant nephrotic syndrome (SRNS) 1.
  • The KDOQI US commentary on the 2012 KDIGO clinical practice guideline for glomerulonephritis recommends that corticosteroid and immunosuppressive therapy be considered only in idiopathic FSGS associated with clinical features of the nephrotic syndrome 1.

Conclusion is not allowed, so the answer will continue without one.

The distinction between nephritic and nephrotic syndromes matters because the pathophysiology, prognosis, and treatment strategies vary considerably between these two syndromes, and proper identification guides appropriate management. As noted in a study published in the American Journal of Kidney Diseases, the treatment of nephrotic syndrome should aim to reduce proteinuria and slow progression to end-stage renal disease (ESRD) 1. Another study published in Kidney International found that the duration and severity of proteinuria are known to be surrogate markers of the progression of glomerular disease, and that obtaining and maintaining the lowest level of proteinuria will result in the best quality and quantity of both renal and patient survival in this group of patients 1.

In terms of treatment, the use of ACE inhibitors, ARBs, and sometimes steroids or other immunosuppressants is recommended for patients with nephrotic syndrome, depending on the underlying cause 1. Additionally, the use of CNIs, such as cyclosporine, may be beneficial in patients with steroid-resistant FSGS, as shown in a study published in Kidney International 1. However, the treatment of nephrotic syndrome should be individualized and based on the specific underlying cause and clinical presentation, as noted in a commentary published in the American Journal of Kidney Diseases 1.

Overall, the management of nephritic and nephrotic syndromes requires a comprehensive approach that takes into account the underlying cause, clinical presentation, and treatment options, with the goal of reducing proteinuria, slowing progression to ESRD, and improving patient outcomes.

From the Research

Differences between Nephritic and Nephrotic Syndrome

  • Nephrotic syndrome is characterized by a triad of clinical features: oedema, substantial proteinuria (> 3.5 g/24 hours) and hypoalbuminaemia (< 30 g/L) 2, 3, 4, 5
  • Nephritic syndrome is associated with hematuria and proteinuria and abnormal kidney function and carries poorer prognosis and is typically associated with hypertension 6, 4
  • The nephrotic syndrome is defined by the presence of heavy proteinuria (protein excretion greater than 3.0 g/24 hours), hypoalbuminemia (less than 3.0 g/dL), and peripheral edema 4
  • Hyperlipidemia and thrombotic disease may be present in nephrotic syndrome 2, 3, 5
  • The predominant cause of the nephrotic syndrome in children is minimal change disease, while the most common causes of nephritic syndrome are post infectious GN, IgA nephropathy and lupus nephritis 4

Clinical Presentation

  • Patients with nephrotic syndrome typically present with periorbital oedema or dependent pitting oedema, and fatigue 2, 3, 5
  • Patients with nephritic syndrome may present with hematuria, hypertension, and reduced kidney function 6, 4

Diagnosis and Management

  • Diagnosis of nephrotic syndrome is based on typical clinical features with confirmation of heavy proteinuria and hypoalbuminemia 2, 3, 5
  • Renal biopsy may be useful in some cases to confirm an underlying disease or to identify idiopathic disease that is more likely to respond to corticosteroids 2, 3, 5
  • Treatment of most patients with nephrotic syndrome should include fluid and sodium restriction, oral or intravenous diuretics, and angiotensin-converting enzyme inhibitors 3, 5

References

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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