Chronic glomerulonephritis (chronic nephritis) is a group of primary glomerular diseases with multiple etiologies and pathological types, characterized clinically by a long course, which can have a period of asymptomatic disease with a slowly progressive course, with basic manifestations of edema, hypertension, proteinuria, hematuria and varying degrees of renal function impairment.
I. Etiology and pathogenesis
The etiology of chronic nephritis is mostly unknown. Most of them are not related to acute nephritis, but are caused by other pathological types that determine the delayed development of the disease, which starts as chronic nephritis.
Pathogenesis: Most of the immune complexes activate the complement, causing tissue damage that can also activate the complement through the “bypass system”; this causes a series of inflammatory reactions leading to glomerulonephritis. Non-immune-mediated renal damage also plays an important role in the development of chronic nephritis, including: intrarenal arteriosclerosis, compensatory changes in renal hemodynamics, the effects of hypertension on glomerular structure and function, and the proliferation and sclerosis of the thylakoid zone due to glomerular tethering overload.
II. Pathology
Chronic lesions are consistent glomerular lesions in both kidneys, with secondary lesions in the tubules and interstitium, and a thinning of the renal cortex over time, resulting in a progressively smaller kidney. Chronic nephritis can be divided into the following types according to the major lesions of most glomeruli.
1, thylakoid proliferative nephritis (including IgA nephropathy and non-IgA nephropathy).
2, thylakoid capillary nephritis.
3, Membranous nephropathy.
4, focal segmental glomerulosclerosis.
5, proliferative sclerosing glomerulonephritis.
[Clinical manifestations]
1, edema Mostly eyelid edema and/or sunken edema of the lower extremities, usually without body cavity effusion.
2. Hypertension Mostly sustained moderate increase in blood pressure, especially diastolic increase is obvious, often accompanied by retinal artery thinning, tortuous and arterial and venous cross-compression phenomenon in the fundus, a few can be seen flocculent exudate and/or hemorrhage.
3, proteinuria urine protein quantification is often 1-3g/24ho.
4.Hematuria is renal unit hematuria and may also appear as sarcoid hematuria. Mostly seen in those with proliferative or focal sclerosis as the main pathological change.
5. Renal impairment Chronic progressive impairment, the rate of progression is related to the type of pathology. It is also related to the treatment and the presence or absence of many factors that accelerate the progression of the disease (such as infection, exertion, elevated blood pressure).
III. Laboratory tests
1.Blood routine The changes are not obvious, and orthochromic orthocytic anemia is seen in renal insufficiency.
2, urine abnormalities are particularly prominent, urine volume is mostly below 1000ml / d, urine specific gravity is lower than 1, 020. urine protein increase can reach 1-2g per day, for selective or non-selective. Urine sediment can be seen as granular tubular with clear tubular type. Hematuria is generally mild.
3, renal function The urea nitrogen and creatinine can be within the normal range in the early stage of the disease, but may increase to varying degrees as the disease progresses, Ccr decreases, concentration and dilution function is reduced, and urine osmolality is below 400-600mOsm/kg.
4. Serum complement C3 is always normal, or continues to decrease for more than 8 weeks without recovery.
Ultrasound In the early stage, the volume of both kidneys is normal, but in the late stage, the renal cortex is thin or the intrarenal structure is disturbed.
5. Renal biopsy can clarify its pathological typing.
IV. Diagnosis and differential diagnosis
Diagnostic criteria: Generally, it is common in young males, with slow onset and prolonged disease.
1. There is proteinuria, edema, intermittent hematuria, hypertension and renal function impairment.
2. The duration of the disease lasts for more than one year.
3.Excluding secondary and hereditary nephritis.
Differential diagnosis
1.Primary hypertensive renal damage.
(1) Damage occurs later, mostly in middle-aged and elderly.
(2) Long-term persistent hypertension first, and then renal damage.
(3) Clinically, renal tubular function damage (urinary concentration hypofunction) is earlier than glomerular function damage.
(4) The urinary changes are mild, with at least trace amounts of urinary protein and a small number of red blood cells and tubular patterns visible.
(5) Often accompanied by cardiac and cerebral complications of hypertension.
2. Chronic pyelonephritis.
(1) Prevalent in women.
(2) Often have a history of recurrent urinary tract infections.
(3) Renal function damage is dominated by tubular damage, and azotemia progresses slowly.
(4) Imaging examination can be seen asymmetric damage in both kidneys, showing interstitial renal damage imaging signs.
3, hereditary nephritis (A1port syndrome).
(1) There are renal (hematuria, mild to moderate proteinuria and progressive renal impairment), ocular (spherical crystals, etc.) and ear (neurological deafness) abnormalities.
(2) Family history of heredity.
4. Lupus nephritis
(1)Prevalent in females.
(2) Systemic disease may be accompanied by fever, skin rash, arthritis and other manifestations of multi-system damage.
(3) Blood cells are decreased, immunoglobulins are increased, lupus cells can be detected, antinuclear antibodies are positive, and serum complement levels are decreased.
(4) Kidney biopsy shows that immune complexes are widely deposited in all parts of the glomerulus, and immunofluorescence examination shows “full brightness”.
5, other Allergic purulent nephritis, diabetic glomerulosclerosis, gout kidney, multiple myeloma kidney damage, renal amyloidosis, etc., each have their own characteristics, in the diagnosis of chronic nephritis, should be excluded.
V. Treatment
The treatment of chronic nephritis should be aimed at preventing and delaying the progressive deterioration of renal function; improving and relieving clinical symptoms and preventing serious comorbidities, and striving to remove the factors that reversibly damage the kidney.
1, dietary protein rhyme restriction Restriction of protein intake can slow down the process of impaired renal function. For people without renal hypoplasia, protein intake of 0,8g/(kg?d) is appropriate. For people with renal insufficiency, the daily protein intake should be limited to 0.5~0.8e/(kg?d), of which animal protein with high bioefficiency should account for 1/3 or more, such as eggs, milk, lean meat, etc. In the low-protein diet, carbohydrate content can be increased appropriately, while appropriately supplemented with essential amino acids,? to supplement the shortage of essential amino acids in the body, to meet the basic energy needs of the body and prevent negative nitrogen balance.
2, actively control hypertension In chronic nephritis, the remaining and lesioned renal units are in a compensatory high hemodynamic condition, systemic hypertension will undoubtedly aggravate this lesionj and lead to progressive glomerular damage, so hypertension should be actively controlled.
(1) Angiotensin-converting enzyme inhibitors (ACEl) can reduce systemic hypertension while lowering intra-glomerular pressure, reduce proteinuria, and inhibit thylakoid fine demon proliferation and extracellular matrix accumulation to reduce glomerulosclerosis and delay renal failure.
Commonly used oral preparations of ACEI are: Kaipotong Enalaprilodin New Asta Application should be noted to prevent hyperkalemia, with renal insufficiency such as Scr>178-356umol / L (2-4mg / d1) should be used with caution or do not use such drugs.
(2) Calcium antagonists: have a very similar effect to ACEI in delaying renal failure, but no significant reduction in proteinuria. In addition, calcium antagonists can reduce oxygen consumption, anti-platelet aggregation, reduce calcium ion deposition in the interstitium and excessive oxidation of the cell membrane through the cell membrane effect, in order to reduce renal damage and stabilize renal function.
Long-acting calcium ion antagonists are often used: loxoprogesterone, pelteparin, nifedipine.
(3)-receptor blockers: have better efficacy in renin-dependent hypertension. Certain ? -receptor blockers, such as aminoglutethimide and norethindrone, have low lipid solubility and are excreted from the kidneys, so the dose should be adjusted and the duration of medication should be prolonged in cases of renal insufficiency. Commonly used betalactam: 12,5-25mg, 2-3 times / d.
(4) α-blocker: It has dilating effect on both small arteries and small veins. Prazosin 0,5~2,0mg, 2-3 times/d, because its main adverse effects are upright hypotension and allergy, so it should be started in small doses and gradually increased to therapeutic doses.
(5) Diuretics: Diuretics can be added to those with significant water and sodium retention or using ACEI to enhance the antihypertensive effect. However, attention should be paid to the appearance of electrolyte disturbance, hypercoagulable state and aggravation of hyperlipidemia.
Depending on the patient’s specific situation, the above-mentioned types of antihypertensive drugs can be used alone or in combination with 2 or more. The traditional view calls for lowering blood pressure to 18,7/12,0kPa (140/90mmHg). It is now believed that: for patients with renal disease with urine protein exceeding 1g/24h, blood pressure must be strictly controlled to a mean arterial pressure (MAP) of 92mmHg to effectively delay the progression of renal damage. The amount of urine protein is also a factor that affects the prognosis of kidney disease. ACEI therapy should be preferred for those with substantial renal hypertension and acceptable renal function.
3, anticoagulation and platelet depolymerization drugs anticoagulation and platelet depolymerization drugs for certain types of nephritis (such as IgA nephropathy) have a good role in stabilizing renal function and reducing renal pathological damage. They can be used for a long time in pathological types with clear hypercoagulable state and prone to hypercoagulable state such as membrane nephropathy and thylakoid capillary proliferative nephritis.
4.Other
(1) Avoid aggravating factors such as infection and exertion.
(2) Caution or avoid the use of nephrotoxic and induced renal donor drugs, such as aminoglycoside antibiotics, sulfonamides and non-steroidal anti-inflammatory drugs.
(3) For the accompanying hyperlipidemia, hyperglycemia, hyperuricemia, etc. should be treated accordingly.
(4) The application of hormones and cytotoxic drugs is generally not recommended.
VI. Prognosis
Chronic nephritis is prolonged, the clinical manifestations are sometimes mild and sometimes severe, the pathological changes progress slowly, and eventually will develop into chronic renal failure. The rate of progression of the lesion depends mainly on the type of pathology, but also related to health care and treatment effects.