Acute glomerulonephritis

Etiology and pathogenesis

In the vast majority of cases, the disease has an infectious nature. The main trigger is a prior streptococcal infection, such as tonsillitis, erysipelas, scarlet fever, or pneumonia. The primary culprit is $\beta$-hemolytic Streptococcus group A. At the same time, its 12th strain poses a particular danger—it has a high tropism for the basement membrane of the renal glomeruli, which is why it is called «nephritogenic».

In addition to infections, non-infectious antigenic loads can act as a triggering factor: vaccination, administration of therapeutic sera, or the use of certain medications. Environmental factors play an important role in the development of pathology—severe hypothermia of the body, especially in high humidity conditions, is considered a potent nephritogenic factor.

The pathogenesis of the disease is based on immune mechanisms. In response to antigenic stimulation, immune complexes (antigen-antibody) are formed in the patient's blood. These macromolecular structures circulate in the bloodstream and eventually deposit on the basement membrane of the renal glomeruli. The deposition of immune complexes provokes membrane damage and triggers a complex cascade of autoimmune inflammation. As a result, vascular permeability increases sharply, which determines the development of all subsequent clinical symptoms.

Clinical picture and dynamics

The classical (cyclic) course is characterized by an extremely rapid onset with the formation of a typical triad of syndromes:

• Urinary syndrome. Manifests as pronounced proteinuria and oliguria (a sharp decrease in daily diuresis). The most striking sign is gross hematuria, in which the urine acquires a characteristic dirty-brown color visually resembling «meat swill».
• Edematous syndrome. Patients note a rapid and noticeable increase in body weight due to massive fluid retention in the body, and pronounced visible edema appears.
• Hypertensive syndrome. Characterized by a persistent increase in blood pressure.

In a favorable scenario, the recovery dynamics have a strict sequence: first, diuresis is restored and increases, then edema gradually subsides, and last of all, blood pressure values normalize.

Course variants and outcomes

Depending on the severity of symptoms and the duration of the process, several variants of the disease course are distinguished.

1. Cyclic variant. Differs by an acute, rapid onset with the deployment of all classical symptoms. As a rule, it ends with the complete clinical recovery of the patient.
2. Protracted course. Signs of nephrotic syndrome begin to predominate in the clinical picture. This variant is prognostically less favorable, as it often transforms into chronic glomerulonephritis.
3. Latent (mild) form. The disease begins insidiously, without prominent manifestations. Patients may notice only slight puffiness of the face, and only moderate changes are detected in urine tests. Due to meager symptoms, the diagnosis is often made late, and the disease in many cases imperceptibly passes into a chronic form.

Severe complications at the peak of the disease

In the active phase of the disease, massive sodium and water retention leads to hypervolemia, which can provoke a number of life-threatening conditions.

• Cardiovascular catastrophes. Volume overload causes acute left ventricular failure, which manifests as shortness of breath and attacks of cardiac asthma. In severe cases, cardiogenic pulmonary edema develops.
• Neurological disorders. Cerebral hemorrhages, transient blindness, and eclampsia (severe renal encephalopathy with pronounced convulsive syndrome) are possible.
• Kidney damage. The glomerular filtration rate (GFR) drops sharply, and azotemia increases. The extreme degree is acute renal failure (ARF), for which the formidable triad is typical: anuria, azotemia, and hyperkalemia. In terminal situations, uremic pulmonary edema may develop.

Diagnostics and principles of therapy

In international practice, the gold standard for verifying glomerulonephritis is morphological confirmation of the diagnosis using vital kidney biopsy—abroad this is a routine procedure. In domestic medicine, the traditional clinical approach is still often used, when the diagnosis is established based on comparing the clinic with the most likely morphological variant without a biopsy. With progression to the terminal stage, sclerosis of the majority of glomeruli and interstitial fibrosis are morphologically observed.

With a rapid course of the disease, therapy must be as strict as possible:

• Regimen: Exclusively strict bed rest in a hospital setting.
• Dietary therapy: A plant-milk diet is prescribed with maximum restriction of table salt and animal protein. The volume of fluid consumed is strictly limited and calculated individually, based on daily diuresis.
• Pharmacotherapy: Diuretics are used to combat fluid retention, and antihypertensive drugs are used to control pressure. If nephrotic syndrome joins the process, the appointment of glucocorticosteroids (GCS) is indicated.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Morphological variants of glomerulonephritis and indications for kidney biopsy.
• Pathogenesis of nephrotic syndrome formation in a protracted course.
• Mechanisms of development of renal encephalopathy (eclampsia).
• Chronic renal failure (CRF) as an outcome of the terminal stage.

Other topics in the "Urinary System" section

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