What is Chronic Glomerulonephritis?

Chronic glomerulonephritis is referred to as chronic nephritis, which refers to the basic clinical manifestations of proteinuria, hematuria, hypertension, and edema. The onset methods are different, the disease is prolonged, and the disease progresses slowly. Tendency to worsening function and a group of glomerular diseases that will eventually develop into chronic renal failure. Due to the different pathological types and stages of the disease in this group, the main clinical manifestations can vary. Disease manifestations are diverse.

Basic Information

nickname

Chronic nephritis

English name

chronic glomerulonephritis

Visiting department

Nephrology

Multiple groups

Young middle-aged man

Common causes

High blood pressure, diabetes, and acute nephritis

Common symptoms

Proteinuria, hematuria, hypertension, and edema, with diverse manifestations

Contagious

no

Etiology and pathogenesis of chronic glomerulonephritis

Only a few chronic nephritis are caused by the development of acute nephritis (direct delay or recurrence after several years of clinical recovery), and the pathogenesis of most chronic nephritis is immune-mediated inflammation. In addition, non-immune and non-inflammatory mechanisms play an important role in the development of the disease. For example, the long-term compensation of healthy nephrons is in the "three high" state of high blood flow perfusion, high filtration, and high transmembrane pressure. Glomerular sclerosis.

Clinical manifestations of chronic glomerulonephritis

Chronic nephritis can occur at any age, but it is mainly young and middle-aged, more common in men. Most onsets are slow and insidious. The clinical manifestations are diverse, with proteinuria, hematuria, hypertension, and edema as its basic clinical manifestations, which may have varying degrees of renal dysfunction, mild to severe, prolonged, and progressive development of chronic renal failure. Laboratory tests are usually mild urine abnormalities, urine protein is usually 1 to 3g / d, urine sediment microscopy can increase red blood cells, visible cast. Blood pressure can be normal or slightly elevated. Renal function is normal or slightly impaired (decreased creatinine clearance or mild azotemia). This condition can persist for years, even decades, with renal function gradually deteriorating and corresponding clinical manifestations (such as anemia, blood pressure). Increase, etc.), enter the uremia phase.

Such as poor blood pressure control, renal function deteriorates faster and the prognosis is poor. In addition, some patients have an acute attack due to infection or fatigue, or their condition has deteriorated rapidly after being treated with nephrotoxic drugs. After timely removal of incentives and proper treatment, the condition can be alleviated to some extent, but it may also lead to irreversible chronic renal failure. Most patients with chronic nephritis have chronic progressive impairment of renal function, and the pathological type is an important factor that determines the rapid progress of renal function (such as the rapid progress of mesangial capillary glomerulonephritis and the slow progress of membranous nephropathy), but it is also related to Whether the treatment is reasonable.

Chronic glomerulonephritis pathology

There are various types of pathology. Mesangial proliferative glomerulonephritis (including IgA and non-IgA mesangial proliferative glomerulonephritis), mesangial capillary glomerulonephritis, membranous nephropathy and focal segmental disease are common. Glomerular sclerosis, etc., the disease progresses to the late stage, all the above-mentioned different types of pathological changes can be converted into varying degrees of glomerular sclerosis, with renal tubular atrophy, renal interstitial fibrosis. In the late stage of the disease, the kidneys shrink and the renal cortex becomes thinner, and the pathological types can be converted into sclerosing glomerulonephritis.

Diagnosis of chronic glomerulonephritis

All patients with abnormal urine tests (proteinuria, hematuria, cast urine), edema and hypertension have a history of more than one year. This disease should be considered with or without renal impairment, except for secondary glomerulonephritis and hereditary kidneys. After glomerulonephritis, chronic nephritis can be diagnosed clinically.

Differential diagnosis of chronic glomerulonephritis

1. Secondary glomerular disease

Such as lupus nephritis, allergic purpura nephritis, diabetic nephropathy, etc., according to the corresponding system performance and specific laboratory tests, generally not difficult to identify.

2.AIport syndrome

Often onset in adolescents, patients have abnormalities in the eyes (globular lens, etc.), ears (neurological deafness), kidneys (hematuria, mild and moderate proteinuria, and progressive renal impairment), and have a positive family history (mostly Sex-linked dominant inheritance).

3. Other primary glomerulopathy

(1) Symptomatic hematuria and / or proteinuria (occult glomerulonephritis: urinary protein <1g / d, no edema, hypertension and renal failure.

(2) Acute nephritis: Some chronic nephritis is more acute at the onset, much like acute nephritis, but most of them do not have the characteristics of acute nephritis: the precursor infection is 1 to 3 weeks away from nephritis, the transient complement C3 decreases, and the tendency to heal, Helps identify.

4. Primary hypertension renal damage

Chronic nephritis with significantly increased blood pressure needs to be distinguished from primary hypertension secondary to renal damage (ie, benign arteriolar nephrosis), which has long-term hypertension first, and then kidney damage, and urine changes slightly ( Micro-to-mild proteinuria, microscopic hematuria and casts), and other target organs (heart, brain) complications of hypertension.

5. Chronic pyelonephritis

Patients who have a history of recurrent urinary tract infections, imaging abnormalities, and renal dysfunction often have white blood cells in the urine sediment. Positive urine bacteriological examination can be distinguished.

Chronic glomerulonephritis treatment

The main purpose should be to prevent or delay the deterioration of renal function and prevent severe complications. The following comprehensive treatment measures can be used.

1. Actively control hypertension and reduce urine protein

Hypertension and urine protein are important factors that accelerate glomerular sclerosis and promote the deterioration of renal function. Active control of hypertension and reduction of urine protein are two important links. Chronic nephritis often has sodium-water retention causing volume-dependent hypertension, so patients with hypertension should limit salt (NaCl <6g / d); thiazide diuretics such as hydrochlorothiazide can be used. When Ccr <30ml / min, thiazines have no effect and they can be converted to diarrhea diuretics, but they should not be used too much and last for a long time. In addition to reducing blood pressure, ACEI or ARB also has a renal protective effect to reduce urinary protein and delay the deterioration of renal function. It is the first choice drug for chronic nephritis to treat hypertension and / or reduce urinary protein. To achieve the purpose of reducing urinary protein, the applied dose is often higher than the conventional antihypertensive dose. Patients with renal insufficiency should use ACEI or ARB to prevent hyperkalemia. When serum creatinine is greater than 264 mol / L (3mg / d1), blood creatinine and blood potassium must be closely monitored to prevent side effects. In addition, -blockers, calcium channel blockers, etc. can be combined or selected.

2. Limit the amount of protein and phosphorus in food

Patients with renal insufficiency azotemia should limit the amount of protein and phosphorus, adopt a high-quality low-protein diet or add essential amino acids or -keto acids.

3. Glucocorticoids and cytotoxic drugs

Given that chronic nephritis includes a variety of diseases, whether such drugs are used should be treated differently. However, the patient's renal function is normal or only slightly damaged, the kidney volume is normal, the pathological type is light (such as mild mesangial proliferative nephritis, early membranous nephropathy, etc.), and the urine protein is more. Gradually withdrawn.

4. Anticoagulant, fibrinolytic and antiplatelet depolymerization drugs

Such drugs can inhibit fibrin formation, platelet aggregation, and reduce complement activity, but the effect is uncertain.

5. Factors to Avoid Aggravating Kidney Damage

Avoid infection, fatigue, pregnancy and nephrotoxic drugs (such as aminoglycoside antibiotics, aristolochic acid-containing Chinese medicine, etc.) and other factors that may cause deterioration of renal function.