Reflections on Medical Education: Understanding Glomerulonephritis: ( Part 2- Clinical Patterns and Cases)

Glomerulonephritis (GN) can be a quiet intruder or a dramatic disruptor. It may first present as an incidental finding on urinalysis — microscopic haematuria or mild proteinuria — or arrive with oedema, dark-coloured urine, rising blood pressure, or even renal failure. For clinicians, GN is a diagnostic challenge and a physiologic puzzle. What unites its many forms is a common battleground: the glomerulus. In this post, we explore how glomerular injury arises, how it disturbs the kidney’s delicate filtration barrier, and how two classic clinical patterns — nephritic and nephrotic syndromes — help us make sense of the chaos.

In this post, we’ll walk through what glomerulonephritis is, how it disrupts the kidney’s filtration barrier, and why understanding its immune mechanisms matters for recognising—and reasoning through—renal disease.

🩸 Nephritic vs Nephrotic Syndrome: Clinical Clues from a Leaky Filter

Nephritic syndrome is driven by inflammation — red cell casts, haematuria, and oliguria often dominate.

Nephrotic syndrome is driven by barrier dysfunction — marked proteinuria, hypoalbuminemia, and oedema take centre stage.

We’ll discuss:

The pathophysiologic logic behind each
How different GN types map onto this spectrum
Real cases with investigation findings and reasoning prompts

🔍 1: What Is Nephritic Syndrome?

Mechanism: Immune-mediated inflammation → capillary wall damage → haematuria ± mild proteinuria
Key features: Haematuria, red cell casts, hypertension, oliguria, mild-moderate proteinuria
Examples: PSGN, IgA nephropathy, lupus nephritis (Class III/IV), anti-GBM disease

🧠 Clinical analogy: The filter is red, swollen, and angry — it still filters, but leaks blood and resists flow.

🩸 Nephritic Syndrome: When the Filter Is Angry

Nephritic syndrome refers to a clinical picture caused by inflammatory damage to the glomerular capillary wall. The injury typically affects the endothelium and mesangium, triggering a brisk immune response that impairs filtration and allows red blood cells and some protein to leak into the urine.

🔍 Core Mechanism

At the root is immune-mediated inflammation — often with neutrophil recruitment — which:

Narrows or obstructs glomerular capillaries → reduced glomerular filtration rate (GFR)
Damages the filtration barrier → haematuria, often with red cell casts
Disrupts vascular autoregulation → salt and water retention, contributing to hypertension and oedema

This inflammation may be triggered by:

Immune complex deposition (e.g. PSGN, IgA nephropathy)
Autoantibodies (e.g. anti-GBM)
Neutrophil activation (e.g. ANCA vasculitis)

🔑 Key Clinical Features

Haematuria: often visible ("tea-coloured" or "cola-coloured" urine)
Red cell casts: shaped by tubules, indicating glomerular bleeding
Proteinuria: usually mild to moderate
Hypertension: due to salt retention and RAAS activation
Oliguria: reflecting reduced GFR
± Oedema: often periorbital or dependent

🧠 What’s Happening in the Filter?

Think of the glomerulus as a sieve. In nephritic syndrome, the sieve is inflamed, swollen, and clogged — so it filters poorly and leaks blood. It’s like trying to force water through a sponge: pressure builds, flow slows, and what's coming out isn’t clean.

🩺 Case Example: Nephritic Syndrome (Post-Infectious GN)

History:
A 9-year-old boy presents with facial puffiness and dark brown urine for the past two days. His parents report that he had a sore throat about two weeks ago but didn’t see a doctor. He now appears slightly lethargic and complains of vague abdominal discomfort.

Examination findings:

Mild periorbital and pedal oedema
Blood pressure: 135/90 mmHg
No rash, joint pain, or lung findings

Investigations:

Urinalysis: red cell casts, mild proteinuria
Serum creatinine: mildly elevated
C3: low
ASO titre: elevated

🧠 Clinical Reasoning Prompts:

What syndrome does this presentation suggest?
How does the timing of the sore throat relate to the current symptoms?
Which features help you distinguish this from nephrotic syndrome?

🧪 Diagnosis: Post-streptococcal glomerulonephritis (a classic nephritic syndrome)

This case illustrates immune complex–mediated inflammation of the glomerulus, with low complement, haematuria, and mild proteinuria, all emerging days to weeks after streptococcal infection.

🤓 Why These Findings?

In post-streptococcal glomerulonephritis, circulating immune complexes deposit in the glomeruli and activate complement, particularly the alternative pathway. This leads to an influx of neutrophils and inflammation, damaging the glomerular capillary walls.

Haematuria occurs because red blood cells escape through the compromised filtration barrier, often forming red cell casts as they mould in the tubules.
Mild proteinuria reflects limited podocyte injury — enough to leak some protein, but not to the degree seen in nephrotic syndrome.
Low C3 levels reflect complement consumption during immune activation,
raised ASO titre confirms recent streptococcal exposure.

Clinically, the reduced glomerular filtration rate contributes to oliguria, salt and water retention, and hypertension. The resulting volume overload leads to the facial and peripheral oedema seen on examination.

💧 2: What Is Nephrotic Syndrome?

Mechanism: Podocyte and slit diaphragm dysfunction → massive protein leak
Key features: Proteinuria >3.5g/day, hypoalbuminemia, edema, hyperlipidemia
Examples: Minimal change disease, membranous nephropathy, FSGS, lupus nephritis (Class V)

🧠 Clinical analogy: The filter is punched full of holes — blood cells may stay in, but protein pours out.

💧 Nephrotic Syndrome: When the Filter Becomes a Sieve

Nephrotic syndrome refers to a constellation of signs driven by excessive protein loss in the urine, typically due to damage to podocytes and the glomerular filtration barrier. Unlike nephritic syndrome, the process here is usually non-inflammatory — the capillary wall isn’t inflamed, it’s structurally compromised.