07.3 Primary glomerular disorders

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Questions and Answers

What distinguishes proliferative glomerular disorders from non-proliferative disorders?

Proliferative disorders exhibit increased cellularity in glomeruli. (correct)

Proliferative disorders cause more severe edema.

Non-proliferative disorders are always associated with systemic diseases.

Non-proliferative disorders always lead to hematuria.

Which clinical manifestation is primarily associated with nephrotic syndrome?

Hematuria

Azotemia

Oliguria

Hyperlipidemia (correct)

The mnemonic 'HELP' is used to remember the features of which syndrome?

Diabetic nephropathy

Nephrotic syndrome (correct)

Nephritic syndrome

Acute kidney injury

What is a common presentation of nephritic syndrome?

Mild-to-moderate proteinuria and hypertension Signup and view all the answers

What is the main pathophysiological mechanism involved in non-proliferative glomerular disorders?

Damage to the glomerular basement membrane Signup and view all the answers

In a child presenting with symptoms of nephrotic syndrome, which condition is most likely suspected?

Minimal change disease Signup and view all the answers

Which of the following is NOT a typical feature of nephritic syndrome?

Severe hypoalbuminemia Signup and view all the answers

What is the primary focus when distinguishing between primary and secondary glomerular diseases?

Whether associated diseases affect multiple organs Signup and view all the answers

What triggers the accumulation of IgA immune complexes in IgA nephropathy?

Respiratory or GI infections Signup and view all the answers

Which drug is primarily used to manage minimal change disease?

Prednisone Signup and view all the answers

What distinguishes Focal Segmental Glomerulosclerosis (FSGS) from minimal change disease?

Histological appearance showing segmental glomerular sclerosis Signup and view all the answers

When does IgA nephropathy typically manifest in relation to infection?

1–2 days post-infection Signup and view all the answers

Which is a common consequence of Focal Segmental Glomerulosclerosis (FSGS)?

Progression to chronic kidney disease Signup and view all the answers

What renal examination is essential for diagnosing glomerular disorders that do not respond to empirical therapy?

Renal biopsy Signup and view all the answers

In cases of IgA nephropathy, what finding supports its diagnosis?

Elevated serum IgA levels in about 50% of cases Signup and view all the answers

Which statement about ACE inhibitors like Lisinopril is accurate?

They lower intraglomerular pressure to protect kidney function. Signup and view all the answers

What is a characteristic feature observed in minimal change disease under microscopy?

Effacement of podocyte foot processes Signup and view all the answers

Which treatment is typically first-line for minimal change disease?

Steroids Signup and view all the answers

What is a common complication associated with nephrotic syndrome?

Pulmonary embolism Signup and view all the answers

Which condition is typically treated with supportive care and is usually self-limiting?

Post-streptococcal glomerulonephritis Signup and view all the answers

What microscopy finding is characteristic of membranous nephropathy?

Spike and dome appearance Signup and view all the answers

Which laboratory finding is crucial for diagnosing nephrotic syndrome?

Proteinuria Signup and view all the answers

Which pathophysiological feature is associated with post-streptococcal glomerulonephritis?

Subepithelial immune deposits Signup and view all the answers

Which of the following is NOT typically involved in the management of membranous nephropathy if it is unresponsive?

Diuretics Signup and view all the answers

Study Notes

Primary Glomerular Disorders

Primary glomerular disorders affect the glomeruli, the kidney's filtering units
Classified as proliferative (increased cellularity) or non-proliferative (no significant cellular increase)
Proliferative disorders often lead to nephritic syndrome (hematuria, hypertension)
Non-proliferative disorders usually result in nephrotic syndrome (severe proteinuria, hypoalbuminemia, edema)

Learning Objectives

Identify and describe common primary glomerular disorders (histological and clinical characteristics)
Distinguish between proliferative and non-proliferative disorders, focusing on pathophysiological mechanisms and clinical presentations
Recognize diagnostic and therapeutic approaches for nephrotic and nephritic syndromes within the context of primary glomerular disorders

Key Concepts and Definitions

Proliferative Disorders: Increased glomerular cell growth, often leading to nephritic syndrome
Non-Proliferative Disorders: No significant cellular increase, usually causing nephrotic syndrome
Nephrotic Syndrome: Characterized by severe proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia, edema
Nephritic Syndrome: Often presents with hematuria, mild-to-moderate proteinuria, hypertension, and sometimes oliguria

Clinical Applications

Case study example: 6-year-old child with facial edema, fatigue, and foamy urine (suggestive of nephrotic syndrome, possibly minimal change disease)
Diagnostic Approach (Nephrotic Syndrome): Check proteinuria (urinalysis), serum albumin, and lipid panel; empiric steroid therapy often initiated in children
Diagnostic Approach (Nephritic Syndrome): Order urine microscopy, serum creatinine levels, and consider recent infections (especially post-streptococcal glomerulonephritis)
Treatment Options (Minimal Change Disease): Steroids are the first-line treatment, often highly effective in children

Pathophysiology

Non-Proliferative Disorders (e.g., Minimal Change Disease): Loss of podocyte foot process structure (effacement) without other significant histological changes; often steroid-responsive
Membranous Nephropathy: Immune complex deposit on glomerular basement membrane, resulting in membrane thickening (spike and dome appearance on microscopy)
Proliferative Disorders (e.g., Post-Streptococcal Glomerulonephritis): Immune complexes deposit in glomeruli, causing inflammation and hypercellularity; often following group A streptococcal infection "humps" on histology
IgA Nephropathy (Berger's Disease): IgA immune complexes accumulate in the glomerular mesangium often triggered by respiratory or Gl infections; common worldwide

Pharmacology

Steroids (e.g., Prednisone): primarily used to reduce immune-mediated podocyte damage in minimal change disease; may require prolonged treatment in some cases; ACE inhibitors (e.g., Lisinopril): Reduce proteinuria and protect kidney function

Differential Diagnosis

Minimal Change Disease vs. Focal Segmental Glomerulosclerosis (FSGS): Both present with nephrotic syndrome; FSGS is less steroid responsive
IgA Nephropathy vs. Post-Streptococcal Glomerulonephritis: Both are infection-related; IgA Nephropathy typically arises 1-2 days after infection; Post-Streptococcal in 1-3 weeks
Key Clinical Distinction: IgA nephropathy often presents with elevated serum IgA levels

Investigations

Renal Biopsy: Essential for diagnosing glomerular disorders that are not responding to empirical treatment. Findings guide further treatment (especially in adults or unusual cases)
Serum IgA Levels: Used in diagnosing IgA nephropathy (elevated in ~50% of cases)
Urine Microscopy: Checks for red blood cell casts in the urine to support diagnosis of glomerulonephritis, particularly in post-streptococcal cases

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Description

This quiz focuses on primary glomerular disorders, examining their classifications into proliferative and non-proliferative types. You will learn about their clinical characteristics, diagnostic approaches, and the pathophysiological mechanisms underlying nephritic and nephrotic syndromes. Test your knowledge on the common disorders affecting the kidney's glomeruli.