Chronic glomerulonephritis (CGN) is a group of immune diseases caused by a variety of causes originating in the glomerulus, with a variety of pathologies and different prognoses. The clinical features are insidious onset and a period of asymptomatic disease with varying degrees of proteinuria, erythrocytes and tubular urine on routine urinalysis. Most patients have varying degrees of fatigue, edema, hypertension and renal function impairment. With the further development of the disease, as little as 2~3 years and as much as 20~30 years, the surviving kidney units become less and less, the fibrous tissues continue to proliferate and the kidneys shrink. The disease is stubborn, recurrent, and persistent, eventually leading to renal failure, and the prognosis is very poor.
Chronic nephritis is one of the most common diseases in internal medicine and can develop at any age, but it is more common in adolescents. 188,697 people in 13 provinces and autonomous regions were screened for urinary tract disease in 1982, and the detection rate of urinary tract disease was 2.25%, of which glomerulonephritis accounted for 21.63%, with the highest rate in the 14-20 age group. Analysis of the causes of death due to chronic kidney disease in 1398 cases revealed that chronic nephritis accounted for the first place, 64.10%, and in terms of kidney disease, the incidence of chronic nephritis was second only to renal meningo-nephritis.
Although the name chronic nephritis does not exist in the Chinese medical literature, some pathologies similar to the clinical manifestations of chronic nephritis can be found. Edema is the main clinical symptom of the disease, so most of the components of chronic nephritis can be classified as “edema”. When edema is not obvious, but fatigue and weakness, lumbago, dizziness, proteinuria and hematuria are the main manifestations, it can be classified as “deficiency labor”, “lumbago”, “dizziness”, “blood in urine”, etc. “Blood in urine”.
Clinical manifestations
I. Symptoms
1. Edema
Most patients have different degrees of edema. In mild cases, it only manifests in the face, eyes and loose tissue, but in severe cases, it spreads over the whole body, and there may be thoracic fluid and ascites.
2.Lumbar pain
In mild cases, the lumbar region is sore and tender, while in severe cases, the lumbar pain is aggravated after exertion, and the location is mainly the spinal rib angle.
3. Abnormal urine changes
It is a necessary symptom for patients with chronic nephritis. The change in urine volume is related to the degree of edema and the state of kidney function. Oedema can occur clinically due to water and sodium retention caused by oliguria or anuria. Urine protein content varies, usually between 1 and 3 g/d, but can also be a large amount of proteinuria (>3.5 g/d). The urine sediment often has granular and clear tubular patterns, and is accompanied by mild to moderate hematuria, and occasionally carnivorous hematuria.
4. Hypertension
Most patients will develop hypertension sooner or later, with a sustainable increase or intermittently, manifested as head swelling, dizziness, headache, insomnia, and memory loss. Persistent high blood pressure not only accelerates the deterioration of kidney function, but also causes damage to the heart muscle.
5, renal insufficiency
The renal impairment of chronic nephritis mainly shows a decrease in glomerular filtration rate and a decrease in creatinine clearance, but since most patients do not drop below 50% of normal value when they visit the clinic, serum creatinine and urea nitrogen can be within the normal range, and symptoms of renal insufficiency such as azotemia do not appear clinically. Subsequently, glomerular insufficiency, such as hypoconcentration of urine, occurs. In the later stages of chronic nephritis, the number of destroyed kidney units increases and the glomerular filtration rate drops to less than 50% of the normal value. In emergency situations (such as trauma, bleeding, infection, surgery or drug damage), the burden on the kidneys increases and symptoms of uremia can occur.
6.Anemia
Chronic nephritis can have mild to moderate anemia, mostly related to reduced intrarenal erythropoietin, to end-stage nephritis, then severe anemia. In addition, patients with chronic nephritis are prone to acute exacerbations, where the disease deteriorates rapidly within a short period of time (3-5 days or even within 1-2 days) due to respiratory infections or other sudden malignant stimuli, whenever the disease is relatively stable. This is when the patient presents with massive proteinuria, even carnitic hematuria, increased tubularity, marked edema and hypertension, and deterioration of renal function. With adaptation, the disease can be remitted and basically restored to its original level, but it may also lead to disease progression and enter the uremic phase.
Physical signs
Patients may have an anemic appearance, pale lips and nails, swollen eyelids and face and even both lower limbs, and in severe cases, pleural fluid and ascites.
Diagnosis
I. Laboratory tests
1.Urine
(1) Urine volume: The urine volume can be normal without edema, and the urine volume decreases during edema and is below 1000ml/d. With the development of the disease, the urine volume can be changed from polyuria, nocturia to oliguria, and even urine shutdown, when the kidney function is often in extreme failure.
(2) Urine specific gravity: low, mostly below 1.020, often fixed at about 1.010 in the late stage of the disease.
(3) urine protein: the most important finding in the urine is urine protein, it can be said that all chronic nephritis have proteinuria. The amount of urine protein varies, generally 1 to 3g/d, but can also be a large amount of proteinuria (>3.5g/d). The amount of protein in the urine is not significant for the prognosis, but it decreases in the presence of renal failure. The proteinuria caused by chronic nephritis is caused by the increased permeability of the glomerulus to protein and the reduced reabsorption of protein by the renal tubules.
(4) Urinary red blood cells: Increased red blood cells are common in the urine sediment, usually 3 to 5/high, sometimes not, but in the acute phase of the attack there can be obvious hematuria, or even carnal hematuria. The increase in red blood cells in urine reflects the active stage of the disease. Leukocytes, most granules and clear tubular patterns are also common in the urine sediment. The urine red blood cell phase is predominantly aberrant, generally accounting for more than 80%, with a total of >8000 cells/ml.
(5) Urine C3 measurement: the highest positive rate of membrane proliferative nephritis and crescentic nephritis, which can reach more than 90%, followed by focal segmental glomerulosclerosis, membranous nephropathy, and thylakoid proliferative nephritis (including lgA nephropathy). The lowest positive rate was found in microscopic lesions and focal segmental nephritis.
(6) Urine disc electrophoresis: polymeric proteinuria is more common in membranoproliferative nephritis, tegumentoproliferative nephritis and focal segmental glomerulosclerosis.
(7) Urine protein selectivity index: the clinical significance is similar to that of urine disc electrophoresis, and most cases of membrane proliferative nephritis, focal segmental glomerulosclerosis and lgA nephropathy are non-selective proteinuria with selectivity index (SPI) > 0.2. More than half of the cases of microscopic lesions, IgM nephropathy, membrane proliferative nephropathy and membranous nephropathy have SPI ≤ 0.2.
(8) Other: urinary fibrin degradation products may be increased or positive; urinary β2 microglobulin may be normal or increased.
2.Blood
(1) Routine blood test: may show mild to moderate anemia.
(2) Fibrin degradation product measurement: normal or elevated.
(3) β2-microglobulin content measurement: may be normal or elevated.
(4) Immune function tests: some patients may have elevated IgA or IgM, decreased IgG, decreased C3 and CH50.
(5) Renal function tests: some patients are normal, some patients have elevated urea nitrogen and creatinine, and decreased carbon diazide binding capacity.
(6) Liver function tests: in patients with severe proteinuria lasting longer, a decrease in albumin and an inversion of the albumin/globulin ratio can be seen.
3.Both kidneys B
Ultrasound examination is normal or slightly reduced
4.Glomerular filtration rate (BCT) of both kidneys
Part of it is normal, part of it can be reduced.
5.Kidney biopsy
It can determine the type of pathological changes of chronic glomerulonephritis, which has positive significance for diagnosis, guiding treatment and estimating prognosis.
Diagnostic points
1, slow onset, prolonged, sometimes mild, sometimes severe, progressive decline in renal function, late may appear anemia, electrolyte disorders, blood urea nitrogen, blood creatinine elevation and other conditions.
2. There are different degrees of proteinuria, hematuria, tubular urine, edema and hypertension, etc.
3. Acute attacks may be induced by respiratory infections and other causes during the course of the disease, with manifestations similar to those of acute nephritis.
Differential diagnosis
I. Primary hypertension secondary to renal damage
Nephritis mostly occurs in young adults; while hypertension secondary kidney damage occurs later. The medical history is very important for differentiation. Whether hypertension or proteinuria comes first plays a major role in the differential diagnosis. Therefore, in patients with hypertension, urinalysis and, if necessary, renal function tests should be routinely performed. In patients with hypertension secondary to renal damage, the amount of urine protein is low, usually <1-1.5g/d. Rarely, there is persistent hematuria and erythrocyte tubular pattern, and the tubular function is usually impaired earlier than the glomerulus. Renal puncture is often useful for identification. It has been found that 20% of patients clinically diagnosed with primary hypertension are diagnosed with primary glomerular disease by renal puncture.
II. Chronic pyelonephritis
In the late stage of chronic pyelonephritis, there can be a large amount of proteinuria and hypertension, which is sometimes difficult to distinguish from chronic nephritis. Chronic pyelonephritis is mostly seen in female patients. Detailed questioning often includes a history of urinary tract infection. Multiple urine sediment microscopy and urine bacterial cultures are necessary for the diagnosis of chronic pyelonephritis with active infection. In patients with chronic pyelonephritis, the impairment of renal function is mostly tubular damage, and there may be hyperchloremic acidosis, hypophosphorous renal bone disease, while azotemia and uremia are mild and progress very slowly. Intravenous pyelogram and nuclear examination (renogram and renal scan, etc.) are more helpful in the diagnosis of chronic pyelonephritis if asymmetrical damage to the two sides of the kidney is found.
Lupus nephritis
The clinical manifestations and renal histological changes of lupus nephritis can be similar to those of chronic nephritis. However, lupus erythematosus is more prevalent in women and is a systemic disease that can be associated with fever, rash, arthritis and other manifestations of multisystem damage. Blood cells are decreased, immunoglobulins are increased, lupus cells can be detected, antinuclear antibodies are positive, and serum complement levels are decreased. Histological examination of the kidney reveals extensive deposition of immune complexes in various parts of the glomerulus. Immunofluorescence examination often shows “full brightness”.
Acute nephritis
Acute attacks of chronic nephritis should be differentiated from acute nephritis. The most common cause of an acute attack of chronic nephritis is in adults, with clinical symptoms appearing within 2 to 3 days of infection, and a history of nephritis or a history of more pronounced hematuria, edema, hypertension, etc. The condition is delayed and often accompanied by varying degrees of anemia and renal insufficiency. Acute nephritis often has a prodromal infection, and symptoms such as hematuria, proteinuria, edema, and hypertension appear only after 1 to 3 weeks, and complement C3 in the blood is reduced (recovered within 8 weeks).