Post-infectious glomerulonephritis

Glomerulonephritis are inflammations of the glomerulus, the part of the renal nephron where blood filtering occurs, secondary to an immune process. Glomerulonephritis can be primary, caused by immune reactions that affect the kidney, or secondary to other diseases, as in the case of systemic lupus erythematosus or Henoch-Schönlein purpura.

A type of primary glomerulonephritis is the one that occurs after an infection that generates an immune mechanism that affects the kidney. The main infections that can trigger these processes are bacterial infections, especially those caused by Streptococcus pyogenes, a bacterium that usually causes pharyngotonsillar and skin infections. It produces a picture of nephritic syndrome, that is, a kidney injury that causes the appearance of blood and protein in the urine as well as a decrease in the ability of urine to filter.

Other infections that much less frequently can generate immune reactions that trigger postinfectious glomerulonephritis are endocarditis, atrioventricular shunt infections, or sepsis. Likewise, viral infections, parasites or some fungi could cause it, but they are very isolated cases.

How is it produced?

S. pyogenes is a bacterium of the streptococcus family that can cause various infections. Some subspecies of S. pyogenes, known as serotypes, have been shown to be more closely related to kidney involvement after acute infection. These serotypes are 12 in the case of infections of the pharynx and tonsils and 49 in the case of skin infections. In general, kidney involvement occurs 6-10 days after pharyngoamidalar infection and 2 to 3 weeks after skin infection.

After the infection occurs, antibodies are generated against antigens of the bacterium, which bind to them and form larger units called immune complexes. These immune complexes are deposited in the areas of the capillaries and the tissue that surrounds them in the glomeruli and generate inflammation, which is what alters the structure and causes the symptoms.

When deposited in the glomerulus, an inflammatory reaction occurs, which is why white blood cells accumulate in the tissue, mainly neutrophils and lymphocytes, as well as IgG antibodies and complement factor C3, a factor that intervenes in an immune response system . These deposits are characteristic of post-streptococcal glomerulonephritis when observed with the electron microscope, producing humps that are deposited in the glomerulus in a non-linear manner.

Symptoms

Most of the time, postinfectious glomerulonephritis occurs in children, with the stage between 3 and 7 years being the one with the highest incidence. It is the main cause of nephritic syndrome in children, that is, of the appearance of hematuria, proteinuria and a decrease in the filtering capacity of the glomerulus. Clinically we observe that, after a pharynx, tonsil or skin infection has occurred in the last month, a picture of edema appears, especially at the level of the eyelids and predominantly in the morning, which later can also occur in the lower extremities.

Along with this clinic there is the appearance of hematuria and a decrease in daily diuresis (oliguria). In 75% of cases, elevated blood pressure figures can be recorded with or without associated symptoms (headache, blurred vision, dizziness).

Diagnosis

The diagnosis is based on both clinical and laboratory data. It will be suspected in a child who presents edema, hematuria and a decrease in daily urine production and who has recently suffered from a bacterial infection at the pharyngo-tonsillar or cutaneous level. Hematuria is not always appreciated with the naked eye, sometimes it is only microscopic and is observed when performing a urine test.

In the 24-hour urine test, red blood cells will be seen, as well as the presence of protein in the urine in an amount less than 2 grams. Proteinuria and hematuria, together with a decrease in urine output, give us the diagnosis of nephritic syndrome, the main cause of which in children is post-streptococcal glomerulonephritis. Hematic casts will also be seen, indicating that the origin of the condition is glomerular, a decrease in sodium excretion, and an increase in urinary urea levels.

When carrying out a blood test, it will be appreciated if there is an alteration in renal function by assessing the levels of urea and creatinine, although this is not frequent. It can also be seen that there is a transitory decrease, that is, that with time the complement factor C3 is recovered.

In the blood test we will also see antistreptolysin antibodies (ASLO), typical of streptococcal infection. These will appear in 75% of cases secondary to pharyngotonsillitis, while in cases derived from skin infections they are not as frequent.

Cultures can be performed to detect S. pyogenes, which, if positive, and in the presence of ASLO antibodies or a decrease in complement factor C3 that recovers in about 8 weeks, will confirm the diagnosis.

The diagnosis of certainty would be given by the renal biopsy, but this should only be performed in cases of poor evolution, such as a decrease in complement factor C3 greater than 8 weeks, an oliguria greater than 3 weeks or a microscopic hematuria of more than 6 months duration. In these cases, a biopsy should be performed due to the possibility that there is another underlying glomerular alteration that explains the symptoms.

Treatment

Treatment is symptomatic, since the condition appears once the infection has passed. Early antibiotic treatment of pharyngotonsillar or skin infection, within the first 36 hours, can prevent the appearance of kidney involvement.

A restriction of the intake of water and salts should be carried out to favor the disappearance of edema. If these are important or arterial hypertension appears, diuretics will be used, mainly furosemide, and hypotensive drugs could be combined if necessary. In the event of failure of conservative treatment, it may be necessary to put the patient on dialysis.

The prognosis is usually good, with a complete cure and without sequelae in the vast majority of cases, especially when there is an epidemic that has caused the triggering infection. In the case of adults, a third of them evolve unfavorably towards a progressive deterioration of renal function.

The condition usually resolves in about 2 or 3 weeks. Microscopic hematuria can take up to months to disappear, as well as the decrease in complement factor C3, which can take up to two months to normalize.

Precautionary measures

There are no preventive measures except hygiene measures to avoid skin infections and pharyngitis and tonsillitis in the coldest months.