Chronic glomerulonephritis is a group of glomerulopathies with proteinuria, hematuria, hypertension and edema as the basic clinical manifestations, with different modes of initiation, prolonged disease, slow progression of lesions, varying degrees of renal hypoplasia, and a tendency to deteriorate renal function and eventually develop into chronic renal failure. Due to the different pathological types and stages of this group of diseases, the main clinical manifestations can be different. The disease manifestations are diversified.
1. Etiology and pathogenesis
Only a minority of chronic nephritis is due to the development of acute nephritis (direct migration or recurrence after several years of clinical healing), and the pathogenesis of most chronic nephritis is immune-mediated inflammation. In addition, non-immune, non-inflammatory mechanisms play an important role in the development of the disease, such as the long-term compensatory state of the surviving renal units in the “three highs” of high perfusion, high filtration and high transmembrane pressure, which leads to sclerosis of the surviving glomeruli over time.
2. Clinical manifestations
Chronic nephritis can occur at any age, but predominantly in young and middle-aged people, and is more common in men. Most of the disease is slow and insidious. The clinical manifestations are diverse, proteinuria, hematuria, hypertension, edema as its basic clinical manifestations, there may be varying degrees of renal hypofunction, the condition is sometimes mild and severe, prolonged, progressive development of chronic renal failure. Laboratory tests are mostly mild urinary abnormalities, urine protein is often in the range of 1 to 3 g/d, urine sediment microscopy may increase red blood cells, visible tube type. Blood pressure may be normal or mildly elevated. Renal function is normal or mildly impaired (decreased creatinine clearance or mild azotemia), which can last for several years or even decades, with gradual deterioration of renal function and corresponding clinical manifestations (such as anemia, increased blood pressure, etc.) and entry into uremia.
If the blood pressure is not well controlled, the kidney function deteriorates faster and the prognosis is poor. In addition, some patients have an acute attack due to infection or exertion, or their condition deteriorates rapidly after the use of nephrotoxic drugs, which can be remitted to some extent after timely removal of the causative factors and appropriate treatment, but may also enter irreversible chronic renal failure. Most patients with chronic nephritis have chronic progressive impairment of kidney function, and the type of pathology is an important factor in determining how fast kidney function progresses (e.g., thylakoid capillary glomerulonephritis progresses more rapidly, while membranous nephropathy often progresses more slowly), but it is also related to whether or not the treatment is reasonable.
3.Pathology
There are various types of pathology, including thylakoid proliferative glomerulonephritis (including IgA and non-IgA thylakoid proliferative glomerulonephritis), thylakoid capillary glomerulonephritis, membranous nephropathy and focal segmental glomerulosclerosis, etc. When the disease progresses to the late stage, all the above-mentioned different types of pathological changes can be transformed into glomerulosclerosis of varying degrees, accompanied by tubular atrophy and interstitial fibrosis. In the late stage of the disease, the kidney volume shrinks and the renal cortex becomes thin, and all pathological types can be transformed into sclerosing glomerulonephritis.
4.Diagnosis
Any history of abnormal urinalysis (proteinuria, hematuria, tubuluria), edema and hypertension for more than one year should be considered, regardless of the presence of renal impairment. After excluding secondary glomerulonephritis and hereditary glomerulonephritis, the clinical diagnosis of chronic nephritis can be made.
5.Differential diagnosis
1.Secondary glomerular diseases
Such as lupus nephritis, allergic purpura nephritis, diabetic nephropathy, etc., according to the corresponding systemic manifestations and specific laboratory tests, it is generally not difficult to differentiate.
2.AIport syndrome
It often starts in adolescents, and patients have abnormalities in the eyes (spherical lens, etc.), ears (neurological deafness), and kidneys (hematuria, mild to moderate proteinuria and progressive renal impairment), and have a positive family history (mostly sex-linked dominant inheritance).
3.Other primary glomerulopathies
(1) Symptomatic hematuria and/or proteinuria (occult glomerulonephritis: urine protein <1g/d without edema, hypertension and hyperalgesia.
(2) Acute nephritis: some chronic nephritis starts more rapidly, much like acute nephritis, but most do not have the characteristic manifestations of acute nephritis: prodromal infection 1 to 3 weeks from nephritis, transient complement C3 decline, and tendency to self-heal, which helps to differentiate.
4, primary hypertensive kidney damage
Chronic nephritis presenting with markedly elevated blood pressure needs to be differentiated from primary hypertension secondary to renal damage (i.e. benign small arterial nephrosclerosis), which starts with longer-term hypertension followed by renal damage with mild urinary changes (micro to mild proteinuria, may have microscopic hematuria and tubular pattern), often with complications in other target organs (heart, brain) of hypertension.
5. Chronic pyelonephritis
Most people with a history of recurrent urinary tract infections and abnormal imaging and renal function, often with leukocytes in the urine sediment, can be distinguished by positive urine bacteriological examination.
6.Treatment
The main objective should be to prevent or delay the deterioration of renal function and to prevent and treat serious comorbidities. The following comprehensive treatment measures can be used.
1.Actively control hypertension and reduce urine protein
Hypertension and urinary protein are important factors that accelerate glomerulosclerosis and promote the deterioration of renal function. Active control of hypertension and reduction of urinary protein are two important links. In chronic nephritis, sodium and water retention often cause volume-dependent hypertension, so hypertensive patients should limit salt (NaCl<6g/d); thiazide diuretics, such as hydrochlorothiazide, can be used. when Ccr<30ml/min, thiazide is ineffective to use collateral diuretics, but generally should not be used too much and for a long time.
ACEI or ARB has the nephroprotective effect of reducing urinary protein and delaying the deterioration of renal function in addition to lowering blood pressure, and is the drug of choice for the treatment of hypertension and/or reduction of urinary protein in chronic nephritis. Usually, to achieve urinary protein reduction, the applied dose often needs to be higher than the conventional antihypertensive dose. In patients with renal insufficiency, ACEI or ARB should be applied to prevent hyperkalemia, and it is important to closely monitor blood creatinine and potassium when blood creatinine is greater than 264 μmol/L (3 mg/d1) to prevent side effects. In addition, beta-blockers and calcium channel blockers can also be combined or used.
2. Limit the amount of protein and phosphorus in food
Patients with renal insufficiency azotemia should limit protein and phosphorus intake, adopt high quality low protein diet or add essential amino acids or alpha-keto acids.
3. Glucocorticoids and cytotoxic drugs
In view of the fact that chronic nephritis includes a variety of diseases, the application of such drugs should be treated differently. However, patients with normal or only mildly impaired renal function, normal kidney volume, mild pathological types (such as mild thylakoid proliferative nephritis, early membranous nephropathy, etc.) and high urinary protein can be tried if there are no contraindications, and gradually withdrawn if ineffective.
4, anticoagulation, fibrinolysis and anti-platelet depolymerization drugs
These drugs can inhibit fibrin formation, platelet aggregation and reduce complement activity, but the efficacy is not certain.
5.Avoid factors that aggravate kidney damage
Avoid factors that may worsen renal function such as infection, exertion, pregnancy and nephrotoxic drugs (e.g. aminoglycoside antibiotics, Chinese medicine containing aristolochic acid, etc.).