Glomerulonephritis is inflammation of the kidney's filtering units (glomeruli). It ranges from acute forms in children that heal completely to silent chronic forms that can lead to kidney failure if not caught early.
Glomerulonephritis is an inflammation of the glomeruli, the microscopic filtering structures that make up the functional unit of the kidney. It is not a single disease: it is a group of conditions that share the same anatomical target but differ profoundly in their causes, mechanisms, course, and prognosis. There are acute forms that mainly affect children and almost always heal completely, and chronic forms in adults that can progress silently for years toward chronic kidney failure.
Understanding which type of glomerulonephritis you have is essential, because the prognosis and the treatment change radically from one form to another.
What Is the Glomerulus and How Does It Work?
Each kidney contains about one million nephrons, each equipped with a glomerulus: a tuft of capillaries wrapped in a capsule. Blood enters the glomerulus under pressure and is filtered through a selective membrane: water, salts, and waste products (urea, creatinine) pass into the pre-urine, while proteins and blood cells remain in the circulation.
When the glomerulus becomes inflamed, this membrane is damaged and loses its selectivity. The filter "breaks": proteins — which should not pass through — appear in the urine (proteinuria), and red blood cells leak where they should not (hematuria). This is why dark or foamy urine is often the first sign that something is wrong with the kidney.
What Are the Types of Glomerulonephritis?
Acute Glomerulonephritis
The onset is rapid, often within days. The most classic form is acute post-streptococcal glomerulonephritis: it appears one to three weeks after streptococcal pharyngitis or a skin infection caused by group A beta-hemolytic streptococcus. It mainly affects children between 2 and 10 years of age, and the prognosis in childhood is excellent — more than 95% of cases recover completely without permanent damage.
The typical presentation of this syndrome is often seen in the emergency department: I have seen young patients more than once present with facial swelling that appeared within a few hours and cola-colored urine. This is the classic presentation of acute post-streptococcal glomerulonephritis, and recognizing it quickly allows the right work-up to be started immediately, avoiding needless anxiety. In most cases, especially in children, the prognosis is excellent.
Chronic Glomerulonephritis
It has a slow course, often silent for years or decades. It may result from an unresolved acute form or arise without an obvious triggering event. It includes a heterogeneous group of histologically distinct conditions:
IgA nephropathy is the most common primary form in the world — the immune system produces abnormal IgA antibodies that deposit in the glomerulus and trigger inflammation. Focal segmental glomerulosclerosis is characterized by scarring that affects some — but not all — of the glomeruli, with a high risk of progression. Membranous glomerulonephritis and membranoproliferative glomerulonephritis complete the picture of the main chronic forms.
Rapidly Progressive Glomerulonephritis
This is the most aggressive form: it can lead to loss of kidney function within weeks or a few months. It is rare, but early recognition is decisive — a delay in diagnosis can mean the difference between a recoverable kidney and permanent dialysis. It requires immediate, intensive immunosuppressive treatment.
Primary vs. Secondary
Glomerulonephritis is primary when the damage originates directly in the kidney, without an identifiable systemic cause. It is secondary when the kidney is involved as part of a systemic disease: systemic lupus erythematosus, diabetes, vasculitis, chronic uncontrolled high blood pressure (hypertension), or rheumatoid arthritis.
What Causes Glomerulonephritis?
The most frequent mechanism is that of immune complexes: antibodies produced by the immune system bind to antigens (bacterial, viral, or the body's own in autoimmune diseases), forming complexes that circulate in the blood and deposit in the glomerular membrane. The deposit triggers a local inflammatory response that progressively damages the filter. This mechanism underlies post-streptococcal glomerulonephritis, the form associated with hepatitis B and C, bacterial endocarditis, lupus nephritis, and IgA nephropathy.
A second mechanism, rarer but more aggressive, is that of anti-glomerular basement membrane antibodies: the immune system produces antibodies directed against the very structure of the kidney filter. The best-known form is Goodpasture syndrome, which simultaneously affects the kidney and the lung through an autoimmune mechanism.
Metabolic and vascular causes — diabetic nephropathy and hypertensive nephrosclerosis — produce chronic glomerular damage through different mechanisms (glycation of basement membrane proteins, mechanical stress from elevated pressure) but with the same end result: progressive fibrosis of the glomerulus.
Some drugs used chronically can also damage the glomerulus: nonsteroidal anti-inflammatory drugs (NSAIDs), lithium, and certain chemotherapy agents are the best documented. Genetic causes (Alport syndrome, Fabry disease) are rare but important, because identifying them completely changes the therapeutic approach and family counseling.
What Are the Symptoms of Glomerulonephritis?
Symptoms vary widely depending on the clinical form.
Nephritic syndrome — typical of acute forms — presents with gross hematuria (cola-colored or dark-tea-colored urine), edema especially of the face and periorbital area (characteristically more pronounced in the morning), new-onset high blood pressure, and oliguria. The combination of dark urine and facial swelling is almost pathognomonic and should quickly prompt medical evaluation.
Chronic forms, on the other hand, present with much more subtle and insidious symptoms: persistent proteinuria that makes the urine foamy, microscopic hematuria visible only on examination of the urinary sediment, progressive hypertension, dependent edema with positive pitting sign, and chronic fatigue. The decline in kidney function can progress for years without obvious symptoms — which is why many chronic glomerulonephritides are diagnosed incidentally during routine tests.
Nephrotic syndrome — which can accompany some forms of glomerulonephritis — is distinguished by massive protein loss in the urine (over 3.5 g per day), with consequent hypoalbuminemia (low serum albumin), generalized edema, and hyperlipidemia. Some glomerulonephritides present with a predominantly nephritic picture, others predominantly nephrotic, and others with features of both.
Warning sign: suddenly dark urine combined with facial swelling — go to the emergency department, without waiting until the next day.
How Is Glomerulonephritis Diagnosed?
Blood Tests
The initial evaluation includes: serum creatinine and estimated glomerular filtration rate (eGFR, which measures residual kidney function), serum albumin, complement C3 and C4 (their consumption indicates activation of the immune system), Erythrocyte Sedimentation Rate (ESR), and C-Reactive Protein (CRP). The immunological profile is completed with antinuclear antibodies (ANA) and anti-dsDNA (suspected lupus), antineutrophil cytoplasmic antibodies (ANCA, suspected vasculitis), anti-glomerular basement membrane antibodies (suspected Goodpasture), and Antistreptolysin O titer (ASO titer, suspected post-streptococcal form).
Urinalysis
Examination of the urinary sediment is often diagnostic. The presence of red blood cell casts — red blood cells trapped in a protein matrix that mirrors the shape of the tubule — is an almost pathognomonic marker of glomerular damage: it makes it possible to distinguish hematuria of glomerular origin from that of urological origin (stones, bladder tumors). The urine albumin-to-creatinine ratio quantifies proteinuria without resorting to a 24-hour collection.
Imaging
Renal ultrasound assesses the size, echogenicity, and symmetry of the kidneys. In acute glomerulonephritis the kidneys are of normal or increased size; in the advanced chronic form, small and hyperechoic kidneys are found, a sign of irreversible fibrosis.
Kidney Biopsy
This is the diagnostic gold standard. The needle, guided by ultrasound, takes a fragment of kidney tissue that is analyzed under light microscopy, with immunofluorescence (to identify immune-complex deposits), and under electron microscopy (to assess the ultrastructural morphology of the membrane). A biopsy is not necessary in all cases — typical post-streptococcal glomerulonephritis in children, for example, does not require it — but it is indispensable when the histological type changes the choice of treatment.
How Is Glomerulonephritis Treated?
Supportive Therapy
Common to all forms. Control of high blood pressure with ACE inhibitors or angiotensin receptor blockers (ARBs) is a priority: these drugs not only lower blood pressure but directly reduce proteinuria by lowering intraglomerular pressure, slowing the progression of kidney damage. To these are added dietary sodium restriction, diuretics for edema, and control of hyperlipidemia when present.
Immunosuppressive Therapy
Indicated in autoimmune or rapidly progressive forms. The choice among corticosteroids, cyclophosphamide, mycophenolate mofetil, and rituximab depends on the histological type identified at biopsy and on the severity of the clinical presentation. Not all glomerulonephritides require immunosuppression: in stable forms with mild proteinuria, supportive therapy is sufficient.
Treatment of the Underlying Cause
In the post-streptococcal form, the infection has typically already resolved by the time of the kidney diagnosis, and treatment is purely supportive. In diabetes, strict glycemic control slows the progression of nephropathy. In lupus, treatment of the kidney is an integral part of managing the systemic disease.
Dialysis and Transplant
In forms that progress toward end-stage chronic kidney failure, dialysis — in particular hemodiafiltration — replaces the lost kidney function and represents the bridge to kidney transplant.
In my experience as an anesthesiologist, patients with chronic glomerulonephritis and reduced kidney function require particularly careful preoperative management: the slowed clearance of drugs, the risk of fluid overload during intravenous infusion, and possible coagulation abnormalities are aspects that I systematically assess before every procedure. For this reason, when my patients are diagnosed with chronic glomerulonephritis, I always recommend that they report it to the anesthesiologist during pre-admission.
When Should You Be Concerned?
Go to the emergency department immediately if:
urine suddenly turns dark (cola- or tea-colored) combined with facial swelling; the amount of urine drops drastically over 24 hours; severe new-onset high blood pressure with headache or visual disturbances.
See a doctor within a few days if:
urine is persistently foamy; ankle edema progressively worsens; proteinuria or hematuria is found on a routine urine test; creatinine is high compared with previous check-ups with no apparent cause.
Screening is recommended for:
people with diabetes and high blood pressure (a urine test with albumin-to-creatinine ratio once a year); patients with lupus or other systemic autoimmune diseases; first-degree relatives of patients with hereditary kidney diseases.
Frequently Asked Questions (FAQ)
Can glomerulonephritis be cured?
It depends on the form. Acute post-streptococcal glomerulonephritis heals completely in more than 95% of children without leaving permanent damage. Chronic forms do not always resolve, but with the right treatment progression can be significantly slowed and kidney function preserved for many years.
Which urine changes should be a concern?
Cola-colored or dark-tea-colored urine indicates gross hematuria and requires urgent medical evaluation. Persistently foamy urine — as if it contained soap — suggests proteinuria and should be investigated even in the absence of other symptoms.
Is glomerulonephritis contagious?
No. The disease itself is not transmissible. The post-streptococcal form follows a contagious bacterial infection (streptococcal pharyngitis), but glomerulonephritis is the individual patient's immune reaction to that infection — it does not pass from one person to another.
Is a special diet needed?
In forms with high blood pressure or edema, it is important to reduce sodium (salt). In forms with reduced kidney function, the nephrologist may advise restricting protein and potassium. There is no universal diet, however: the recommendations depend on the type and stage of the disease.
How often are check-ups needed?
In the active phase, check-ups may be monthly. In stable chronic forms, nephrology follow-up is typically every 3-6 months with a urine test, creatinine, and blood pressure. The goal is to catch any change in kidney function early.
Key Takeaways
Glomerulonephritis is not a single disease but a group of conditions that share inflammation of the kidney's glomerulus. Acute post-infectious forms, especially in children, have an excellent prognosis and almost always heal completely. Chronic forms require a precise diagnosis — often through kidney biopsy — and long-term nephrology follow-up. Early diagnosis, possible through a simple urine test, can make the difference between a manageable disease and irreversible acute or chronic kidney damage.
References
Kidney Disease: Improving Global Outcomes (KDIGO). Clinical Practice Guideline for Glomerulonephritis. Kidney Int Suppl. 2012;2(2):139–274.
Couser WG. Primary membranous nephropathy. Clin J Am Soc Nephrol. 2017;12(6):983–997. PubMed
Rovin BH et al. KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney Int. 2021;100(4S):S1–S276. PubMed
Dr. Marco De Nardin
Medical Doctor, Specialist in Anesthesiology, Intensive Care and Pain Management
Dr. Marco De Nardin is a physician specializing in Anesthesiology, Intensive Care, and Pain Management. He completed his medical degree and specialty training in Italy, where he continues to practice at his private clinics in Mestre (Venice) and Milan. With extensive clinical experience spanning operating rooms, intensive care units, and pain management clinics, Dr. De Nardin brings a unique perspective that bridges acute-care medicine with chronic disease management. His clinical practice focuses on regional anesthesia, ozone therapy, intravenous infusion therapy, and integrative approaches to pain treatment. He is the founder of Med4Care, a medical information platform delivering evidence-based, physician-reviewed health content. Every article published under his name reflects his commitment to making complex medical topics accessible to patients without compromising scientific rigor.
