Pathology of acute glomerulonephritis

2021-01-26 12:00 AM

May be severe oedema with systemic oedema such as pleural effusion, peritoneal, acute pulmonary oedema, cerebral oedema. Oedema in acute glomerulonephritis depends on diet.

General and epidemiology


The acute glomerulonephritis syndrome is a clinical manifestation of an acute inflammatory lesion of the glomeruli, characterized by sudden onset of erythrocytes, proteinuria, oedema, and hypertension.

Currently, thanks to scientific advances, especially kidney biopsy technology. It is agreed that: Acute glomerulonephritis (VCTC) is not just a simple disease but a syndrome called acute glomerulonephritis. The reason is that the clinical conditions are often the same, but the histopathological lesions are diverse, the disease arises not only due to streptococcus but possibly after staph infection, pneumococcal, virus. appears secondary to diseases such as systemic lupus erythematosus, rheumatoid erythema, and peri-nodular inflammation.

The present malignant acute glomerulonephritis or subacute glomerulonephritis is known as rapidly progressive glomerulonephritis. This name characterizes the disease is rapid progression, premature death from kidney failure and rarely survived 6 months without treatment.


Incidence: The incidence of acute glomerulonephritis following streptococcal infection is not known precisely because many cases are kept for immediate treatment. The prevalence of the disease decreased in modern industrial countries but is still common in tropical and developing countries. (Africa, Caribbean, Asia, South America ...).

The disease occurs as a flare or can be epidemic, especially in areas with poor sanitation (outbreaks in Trinidad, Maracaibo, Minnesota)

Gender and age relation: The disease is very rare before the age of two, common in children from 3 to 8 years old, boys are more common than women (ratio male/female = 2/1). It is less common in adults than in children.


Acute glomerulonephritis may or may not be caused by infection.

Acute glomerulonephritis due to infection includes

The bacteria that most commonly cause the disease is group A (group A) haemolytic streptococcus, which is considered a pattern of acute glomerulonephritis. The most common strain that causes the disease is strain 12, and other strains (1, 2, 4, 18, 24, 25, 49, 55, 57, 60) can also cause disease, but more rarely, strain 4, 12, 24 if it is a throat infection, strains 14, 19, 50, 55, 57 if it is a skin infection (different from acute rheumatoid arthritis because in acute rheumatoid arthritis can cause disease)

Some other rarer bacteria can also cause acute glomerulonephritis such as staphylococci, pneumococcus, typhoid, meningococcal brain, Klebsiella Pneumoniae, ...

Some viruses cause epidemiological pharyngitis, mumps, measles, chickenpox, Epstein Barr, hepatitis B virus, Cyto megalo Virus (CMV) ...

Causes of fungal infection: Histoplasmoses.

Causes of parasitic infections: Plasmodium falciparum and Malaria, Toxoplasma Gondii, schistosomiasis, ...

Acute glomerulonephritis is not caused by a bacterial infection

Colloid diseases: in particular systemic lupus erythematosus, peri-nodular inflammation, low haemorrhagic malaise.

The diseases manifest hypersensitivity to some drugs such as Penicillin, Sulfamide, Vaccine or some foods such as shrimp, crab.


In acute glomerulonephritis due to bacterial infection

Below is a typical case of acute glomerulonephritis following streptococcal infection.


The disease is common in children and appears after an infection of the throat or skin from 7 to 15 days. Skin infections often incubate longer.

Onset stage:

Usually sudden, but there can be signs of warning with:

Fatigue in the whole body, fever 38 - 39 0 C or less.

Bilateral lumbar pain, digestive disorders, anorexia, abdominal pain, nausea.

It is also possible that the patient is hospitalized for a sore throat and dermatitis.

Full-play stage:

Oedema: Usually appears on the face at first, such as heavy eyelids, oedema can go away quickly, but can also spread to limbs and then body swelling. Oedema in acute glomerulonephritis features:

Soft, white oedema, indentation leaving finger imprints.

Swelling around ankles, front of the tibial plateau, instep.

May be severe oedema with systemic oedema such as pleural effusion, peritoneal, acute pulmonary oedema, cerebral oedema. Oedema in acute glomerulonephritis depends on diet.

Little or anuria: Appears early, urine is only 500 - 600ml / 24 hours. In the presence of oliguria (urine below 500ml / 24 hours) or anuria (urine less than 100ml / 24 hours) is manifesting acute renal failure.

Hypertension: Both maximum and minimum hypertension, usually evident in the first two weeks. Over 60% of acute glomerulonephritis has hypertension. Acute pulmonary oedema in acute glomerulonephritis is a common complication due to increased blood pressure, swelling and left heart failure.

Haematuria: Rarely, gross haematuria, if present, usually appears early with oedema, red or dark urine (then red blood cells over 300,000 / min). More common is microscopic haematuria. Distorted red blood cells fragile. RBC casts are the most valuable sign, indicating red blood cells from the glomerulus down. Major haematuria usually resolves early, but microscopic haematuria is prolonged, erythrocytes may go away after 3-6 months.

Laboratory testing:

Blood: The blood count has mild anaemia; blood sedimentation increases for several weeks and returns to normal when it is stable.


Protein: 0.2 - 3g / 24 hours. Proteinuria is not selective (alb / globulin ratio <1, clearance IgG / transferrin> 10%). Proteinuria in VCTC is always present and is a factor to monitor the progress of the disease.

Addis residue: Red blood cells 100,000 - 500,000 / 1 minute, WBC 20,000 / 1 minute.

Red blood cell cast is a valuable test to diagnose but also has an uncommon rate.

Urea, blood creatinine:

Blood urea may be normal or slightly increased and have little prognostic significance when not exceeding 1 g / l. If increasing blood urea is a bad indicator, blood creatinine is normal, and if it rises in parallel with urea is a bad indicator.

The best way to monitor acute glomerulonephritis is to calculate glomerular clearance with creatinine. If Ccr is below 50ml / min that is a conservative prognosis.

Reduced blood complement:

90% of patients have decreased blood complement, the main reduction in C3 component. It will return to normal until the sixth week of illness.

Other tests:

Mainly to detect streptococci and antibodies such as strep throat to find strep, ALSO increases more than 400dv Todd, ECG has prolonged PR.

Kidney biopsy:

Only needed in the elderly, helping to diagnose the pathology and help prognosis.

In fact, 2 tests of erythrocytes and proteinuria are sufficient to confirm acute glomerulonephritis.


Good: is a common course of acute glomerulonephritis, after 8-15 days the patient has a lot of urination, oedema is gone, blood pressure and urine return to normal. There are cases that after 3 months, sometimes 6 months, the above symptoms return to normal. These cases are called slow healing, and this rate is small. In children, the cure rate is high (85 - 95%) compared to adults (50 - 75%).

Acute glomerulonephritis can progress rapidly or malignancy only lasts a few weeks or months, sometimes more persistent, but usually dies within 6 months, accounting for less than 10%. Clinical onset is classic acute glomerulonephritis but leads to rapid acute renal failure.

Bad progression also leads to death beyond 6 months: persistent oedema and proteinuria, usually nephrotic syndrome, formerly known as subacute glomerulonephritis, progressive, irreversible kidney failure.

The disease progresses for many years with each episode of recovery, but eventually leads to death, coma due to hyperaemia or a stroke caused by high blood pressure called chronic kidney failure.

Other clinical forms of acute bacterial glomerulonephritis:

Simple haematuria:

Common in children, haematuria can be alone, not oedema, not minimal, anuria. Overall progress is good, but it is possible to return.


Common in adults, children with severe onset of hypertension, pulmonary oedema, and cerebral oedema the primary diagnosis is based on urine tests with erythrocytes and proteinuria. Progressive if not fatal in the early stages, later oedema lasts many years.


Expression of an acute kidney failure, sometimes spontaneous onset, today with artificial kidneys, the rate of recovery is higher, when the urine recovers, the disease can be completely cured like other forms.

Mild or transient form:

Discovered by accident by systematic testing, especially in patients with rhinitis, pharyngitis, very rarely turn chronic.

Infants and young children:

Onset can sometimes be as intense as seizures and acute heart failure, but when it passes, the prognosis is usually better in adults.

Acute glomerulonephritis is not caused by a bacterial infection

Systemic lupus erythematosus:

70% of lupus has acute glomerulonephritis, which can manifest itself in two forms:

Mild: but often exacerbated because of renal traumatic cortical hormone therapy.

Severe: accompanied by polyarthritis, poly membrane inflammation.

Low form board:

30% had acute leucocytosis manifested by haematuria and proteinuria.

Acute glomerulonephritis due to hypersensitivity:

As with drugs and vaccines, progress usually goes well after discontinuation.


Implementing the quadrants

Based on 3 clinical signs, oedema, hypertension, minimal or anuria and two subclinical signs: proteinuria and erythrocyte.

Separate diagnosis

The exacerbation of chronic glomerulonephritis is based on history and history. In addition, an ultrasound can measure the size of the kidney. If the kidney is smaller than normal, it is chronic glomerulonephritis.

Acute glomerulonephritis following streptococcal infection with non-streptococcal acute glomerulonephritis: based on history, the culture of bacteria, nasopharyngeal fluid, pus, ALSO antibodies and other anti-streptococcal antibodies.

Tracking and prognosis

Post-streptococcal glomerulonephritis is more common in children and has a better prognosis, less common in adults, but a worse prognosis.

In general, the prognosis is usually good if the disease fully recovers. In acute glomerulonephritis immediately during the exacerbation, can die from acute pulmonary oedema, heart failure, acute renal failure, a bacterial infection.


Patients with minimal and anuria have increased urea, blood creatinine: water intake 500-600ml / day, salt 2g / day, Protide 20g / day.

Minimize and anuria with hypertension, urea, and creatinine in the blood do not increase: salt 0.5 - 1g / day, Protide 40g / day.

Absolutely rest from 3 weeks to 1 month until symptoms disappear. Then return to activity slowly as soon as proteinuria is present and microscopic haematuria usually lasts 6 weeks to 2 months.


Only give antibiotics when signs of streptococcal infection persist.

There are no documents that confirm that antibiotics can prevent the aggravation of the acute streptococcal disease, the antibiotic has no effect on the glomeruli, commonly used as Penicillin 1 million units/adult, 500,000 units/children. If penicillin allergy, then uses Erythromycin 0.2 x 5 tablets/day in adults or Tetracycline. Antibiotics are used for 10-12 days.


Includes prednisolone, methylprednisolone. No effect in common, even harmful forms. This class of drugs can be used in rapid progression forms.

Treatment of complications


Abstain from salt, absolute rest.

Antihypertensive drugs: The groups of commonly used antihypertensive drugs are:

Calcium inhibitors: There are many drugs such as nifedipine, amlodipine, felodipine, and manidipine. This is a group of drugs commonly used to combat hypertension caused by kidney disease today.

ACE inhibitors: such as captopril, enalapril, perindopril. A group of drugs that are considered to have protective effects on the kidneys. Note the side effects of hyperkalaemia.

CNS inhibitors: In this group, the commonly used drug is methyldopa (Aldomet).

Pulmonary oedema:

Treatment as another pulmonary oedema, for high dose Lasix, can be up to 200mg intravenous, Uabain, oxygen, Morphine when needed.

Cerebral oedema:

Hypertonic glucose infusion, Mannitol.


Places, where artificial dialysis is not available, can try high-dose Furosemide (Lasix) or peritoneal dialysis.

The best for both pulmonary oedema, brain, and anuria is the extra-renal dialysis where the artificial kidney plays a leading role.

Other symptoms

Increasing blood urea, blood creatinine, limiting the amount of Protide taken but must ensure enough energy from 1200-1600 calories/day to fight catabolism, Durabolin or Testosterone 25-50 mg/day.

Treatment of hyperkalaemia with glucose 20-30%, 300-500ml + 10-20đv insulin intravenously for 1 hour to 1g30 minutes or alkaline solution, or can use Resonium (Kayexalate) 30g / day.

Delay vaccinations during acute glomerulonephritis and even the first two years after the end of acute glomerulonephritis, especially whooping cough and tetanus vaccine.

In common acute glomerulonephritis treatment sometimes just need rest, bland food is enough. While these are severe, they depend on complications and have different treatments. It is also important to note that when finding the cause of acute glomerulonephritis, it is important to treat the cause


For acute glomerulonephritis following streptococcal infection

Early detection of foci of streptococcal infection: pharyngitis, Amygdales inflammation, dermatitis ...

A thorough treatment of foci of streptococcal infection: antibiotics, amygdales cut.

Improve personal hygiene: quit smoking, keep the neck warm in the cold season for sore throats, personal hygiene for infected scabies.

For non-infectious glomerulonephritis

Early detection of renal manifestations in generalized diseases: systemic lupus erythematosus, rheumatoid purpura.

Good treatment of all diseases prevents glomerulonephritis lesions.