nephritis Glomerulonephritis, abbreviated as nephritis, is not a single disease, but a group of diseases caused by various etiologies and pathogenetic mechanisms, with diverse pathological types and overlapping clinical manifestations. Patients exhibit damage to the morphology and/or function of the glomeruli, characterized by altered permeability of proteins and cells in the glomeruli, impaired renal regulation of water, electrolytes, acid-base balance, and blood pressure, as well as compromised glomerular filtration function.

Nephritis, also known as glomerulonephritis, is not a single disease but a group of conditions caused by various factors and mechanisms, resulting in diverse pathological types and overlapping clinical manifestations. The characteristic features include:

- Alterations in the permeability of the glomeruli to proteins and cells

- Impaired renal function in water, electrolyte, acid-base balance, and blood pressure regulation

- Impairment of glomerular filtration function

Based on the etiology, primary glomerulonephritis, secondary glomerulonephritis, and hereditary glomerulonephritis are distinguished.

Primary Glomerulonephritis

Acute Glomerulonephritis

Acute glomerulonephritis, also known as acute nephritis, has a relatively sudden onset with a duration of generally within three months, and the severity of the condition varies. It commonly presents with hematuria, proteinuria, hypertension, and edema, often accompanied by transient renal function decline. Some cases are preceded by a history of acute streptococcal or other pathogenic microbial infections, typically occurring 1-4 weeks after the infection. Most cases resolve spontaneously within several months, but microscopic hematuria may persist for six months or longer. It often involves pronounced edema, hematuria, proteinuria, hypertension, rapidly progressing anemia, and may exhibit nephrotic syndrome features. Progressive deterioration of renal function may lead to oliguria or anuria. Without timely and effective control, it can progress to renal failure within weeks to months, requiring renal replacement therapy to prolong life.

Chronic Glomerulonephritis

Chronic glomerulonephritis has a slow onset with variable clinical manifestations and a duration of over three months. Most patients have insidious onset, which often goes unnoticed. Manifestations may include edema, hypertension, proteinuria, hematuria, and may be accompanied by nephrotic syndrome or severe hypertension. As the condition progresses, renal function may decline, leading to anemia, electrolyte and mineral metabolism disorders, among other complications.

Asymptomatic Hematuria and/or Proteinuria

Formerly known as latent glomerulonephritis, it typically presents with only hematuria and/or proteinuria, without edema, hypertension, or renal function impairment. Most cases are detected during routine physical examinations.

Nephrotic Syndrome

Characterized by massive proteinuria (>3.5g/24h), hypoalbuminemia (serum albumin <30g/L), significant edema, and hyperlipidemia, with the first two being essential criteria.

Secondary Glomerulonephritis

Lupus Nephritis

The kidneys are one of the most commonly affected organs in systemic lupus erythematosus, with over 50% of patients clinically experiencing renal involvement. It exhibits diverse clinical and pathological presentations.

Henoch-Schönlein Purpura Nephritis

Renal involvement in patients with Henoch-Schönlein purpura, the most common secondary glomerulonephritis in childhood. Patients often present with microscopic hematuria and proteinuria, with macroscopic hematuria being rare. Nearly half of the patients manifest nephrotic syndrome. The renal histopathology resembles IgA nephropathy, presenting as mesangial proliferative glomerulonephritis.

Hereditary Glomerulonephritis

Alport Syndrome

Also known as the eye-ear-kidney syndrome, it is the most common hereditary kidney disease. It primarily presents with hematuria and gradual decline in kidney function, accompanied by ear and eye lesions. The main mode of inheritance is X-linked dominant, with males typically experiencing more severe symptoms than females.

Hematuria

Visible red urine, often transient; or the presence of red blood cells in the urine detected through laboratory tests. Blood in the urine originates from glomerular hematuria.

Proteinuria

Proteinuria may be detected during medical examinations. When proteinuria is significant, persistent fine foam may be observed in the urine. Based on the amount of urinary protein, it is categorized as nephrotic-level proteinuria (≥3.5g/d, also known as massive proteinuria) or non-nephrotic-level proteinuria.

Edema

Caused by decreased glomerular filtration rate and impaired tubular reabsorption, leading to increased blood volume. Edema typically starts from the eyelids and face, eventually progressing to edema in the eyelids, lower limbs, and even the whole body.

Hypertension

Approximately 90% of patients with chronic kidney disease develop hypertension, primarily due to sodium and water retention and increased renin secretion. Persistent hypertension can accelerate the deterioration of kidney function.

Renal Failure

This is the most common complication of nephritis, characterized by a decrease in the glomerular filtration rate, retention of nitrogenous waste products, and disturbances in water, electrolyte, and acid-base balance. In advanced chronic kidney disease, it progresses to end-stage renal disease, known as uremia.

Renal Anemia

In the late stages of chronic nephritis, anemia is the most common complication. Many patients require erythropoiesis-stimulating agents to alleviate anemia symptoms. Patients with iron-deficiency anemia should receive iron therapy.

Infection

Due to impaired renal function, patients with chronic nephritis are at a 3-4 times higher risk of infection than the general population. It is important to prevent upper respiratory tract infections and urinary tract infections. Considering that many nephritis patients have autoimmune disorders or receive corticosteroids and/or immunosuppressive therapy, vaccination should be approached cautiously.

Rest

Patients with acute nephritis or those experiencing acute exacerbations of chronic nephritis should be on bed rest for 1-2 weeks. They should only resume activity once urine color returns to normal and edema subsides. Patients with chronic nephritis should ensure adequate rest and sleep and avoid excessive fatigue.

Diet

Nephritis patients should adhere to a bland diet.

Dietary Recommendations

The diet should primarily consist of high-quality protein from eggs, milk, and lean meat, while reducing the intake of high-purine foods (such as animal offal). Consuming plenty of fruits and vegetables is essential for maintaining adequate vitamin intake.

Dietary Restrictions

Maintain a bland diet, restrict salt intake (sodium chloride <3g/d), and avoid greasy foods.

Exercise

Patients with acute nephritis should strictly avoid physical activity. Under a doctor's guidance, patients with chronic nephritis can engage in appropriate physical activities, gradually increasing intensity and duration. Walking, swimming, and tai chi are recommended forms of exercise.

Prevent respiratory and skin infections. Prompt and thorough treatment should be sought in case of tonsillitis and impetigo.

Adopt a low-salt, low-fat, high-quality protein diet while ensuring adequate fluid intake.

Engage in appropriate physical exercise to enhance immune resistance.

Maintain regular daily routines, ensure adequate rest, and avoid prolonged periods of fatigue.

Use medications rationally and avoid drugs with nephrotoxic effects.

Maintain hygiene and pay attention to genital hygiene.

Undergo regular medical check-ups.