Glomeruli with pathological changes

Introduction Morphological changes in glomerular cases, one of the manifestations of IGA nephropathy. IgA nephropathy, also known as Berger's disease, is a special type of glomerulonephritis, which occurs mostly in children and young people. It usually has upper respiratory tract infection before onset. The lesion is characterized by mesangial mesangial hyperplasia. The mesangial membrane is detected by immunofluorescence. The area has IgA deposits.

Cause

Pathological changes: The degree of lesions is very different, early lesions are mild, focal, only a small number of glomeruli have mild mesangial widening and stage hyperplasia, focal hyperplastic changes can develop into focal sclerosis. Some lesions are more obvious, there may be diffuse mesangial hyperplasia, and occasionally there may be crescent formation. The most prominent feature is that immunofluorescence shows that there is lgA deposition in the mesangial area, and there are also C3, lgG and IgM at the same time. Electron microscopy confirmed that there is electron dense deposit in the mesangial area.

Clinical pathology: The main symptoms are microscopic or gross recurrent hematuria, which may be associated with mild proteinuria. A small number of patients have nephrotic syndrome.

IgA nephropathy is mostly a chronic progressive process, and about half of the patients develop progressive lesions, which may lead to chronic renal insufficiency.

IgA nephropathy is a group of chronic glomerular diseases with the same immunopathological features caused by multiple causes. Clinically, about 40% to 45% of patients present with gross or microscopic hematuria, and 35% to 40% of patients present with microscopic hematuria with proteinuria, and the rest are nephrotic syndrome and renal failure. IgA nephropathy is a common glomerular disease worldwide. The prevalence of IgA nephropathy varies greatly from continent to continent, from country to country, and from country to region, such as Japan, Singapore, and IgA nephropathy. It accounts for 50% of primary glomerular diseases, while the low-incidence areas of Indians in the western United States account for only 2%. In general, whites and yellows are significantly higher than blacks. The incidence of IgA nephropathy in China accounts for 26% to 34% of primary glomerular diseases. The ratio of men to women is about 2:1. There is currently no specific treatment for hematuria-based IgA nephropathy. The pathological type of IgA nephropathy and the degree of glomerular damage are quite different. Therefore, the frequency of hematuria seizures, the degree of proteinuria, the presence or absence of hypertension and the degree of impaired renal function should be closely observed, and corresponding prevention measures should be taken.

It can be seen from the above that IgA nephropathy is not malignant.

Factors associated with the prognosis of IGA nephropathy:

(1) Male patients, those with a higher onset age have a poor prognosis.

(2) persistent microscopic hematuria with proteinuria, poor prognosis.

(3) Moderate and severe proteinuria often suggest a final progression to renal insufficiency with a poor prognosis. However, IgA nephropathy is a patient with nephrotic syndrome. If the renal tissue pathology changes slightly, the response to glucocorticoid therapy is good and the prognosis is good.

(4) Patients with IgA nephropathy have high blood pressure, especially severe hypertension that is difficult to control, and the prognosis is poor.

(5) The effect of pregnancy on patients with IgA nephropathy, IgA nephropathy patients without hypertension and renal dysfunction, pregnancy is generally safe.

an examination

Related inspection

Cerebral glomerular function test of lysozyme urinary dehydroepiandrosterone cyclic guanosine monophosphate

1. Repeated episodes of gross hematuria or persistent microscopic hematuria; without edema, hypertension or other abnormal renal function.

2. The level of IgA in the blood increased; renal tissue immunofluorescence detected significant IgA deposition in the mesangial area.

3. Except for other diseases such as allergic purpura that can cause mesangial IgA deposition:

a. Paroxysmal gross hematuria: more common in children. The gross hematuria occurs after the upper respiratory tract infection (tonitis, etc.), and some of them occur after acute gastroenteritis or urinary tract infection, and the interval is more than 24-72 hours. Gross hematuria can last from several hours to several days, and then it can be converted to continuous microscopic hematuria. Some patients with hematuria can disappear, but often attack, recurring gross hematuria at the time of onset, may be accompanied by mild systemic symptoms such as muscle soreness, dysuria, Lumbar pain, or transient blood pressure and elevated urea nitrogen.

b. Microscopic hematuria and asymptomatic proteinuria: This is the main clinical manifestation of IgA nephropathy in children and adolescents. It is often found in physical examination, which can be characterized by simple microscopic hematuria or microscopic hematuria with a small amount of proteinuria.

c. Proteinuria: mild proteinuria, urine protein is generally <1g/24h, a small number of patients may have a large number of proteinuria or even nephrotic syndrome.

d. Others: Some patients with IgA nephropathy may have nephrotic syndrome, acute nephritic syndrome, renal failure, and a small number of lumbar and/or abdominal pain with hematuria.

Differential diagnosis

Increased glomerular volume: An increase in glomerular volume refers to a physiologic and pathological characteristic morphological change in the glomerular volume of the glomerulus due to lipoprotein glomerulopathy. Lipoprotein glomerulopathy (lipoprotein glomerulopathy) is a kidney disease characterized by the presence of lipoprotein emboli in the glomerular capillaries and extrarenal lipoprotein embolism. Lipoprotein glomerulopathy is more common in men, with a male to female ratio of 15:8; the average age of onset is 32 years (4 to 49 years). Most cases are sporadic and a few are familial. Lipoprotein glomerulopathy (lipoprotein glomerulopathy) is a kidney disease characterized by the presence of lipoprotein emboli in the glomerular capillaries and extrarenal lipoprotein embolism. The clinical manifestations were similar to type III hyperlipidemia with elevated plasma apolipoprotein E (apoE). The disease was first reported by Saito T et al. at the 17th Annual Meeting of the Society of Nephrology in 1987. In 1989, Sakaguchi et al. proposed the disease as an independent glomerular disease based on the patient's clinical manifestations and pathological features. In the same year, the disease was named lipoprotein glomerulopathy. However, lipoprotein glomerulopathy does not improve glomerular lesions by lowering blood lipids. It is currently believed that this disease is a rare disease in which the glomerular type III is limited to the lipidation of the kidney.

Glomerular basement membrane moth phagocytosis: glomerular basement membrane moth phagocytosis is one of the diagnostic criteria for nail-sacral syndrome. Judging the renal biopsy specimens can not only use the glomerular basement membrane moth phagocytosis, it must be identified by phosphotungstic acid staining because of its higher sensitivity, it is more valuable for diagnosis. Nail-sacral syndrome is a hereditary disease that is autosomal dominant. The incidence rate is 4.5/1 million to 22/1 million, and there is no gender difference. The patient's chance of delivery to his offspring is 50%, and the locus is linked to the adenylate cyclase and ABO blood group sites on chromosome 9. Looij et al., based on their own data and data, concluded that if a patient with this syndrome family had significant clinical kidney performance, the risk of developing kidney disease was 1/4, and the probability of developing renal failure was 1/ 10.

Glomerular hyperplasia: Glomerular hyperplasia syndrome, alias: Bart syndrome. Bartle's syndrome; Bartter syndrome; congenital hyperaldosteronism; chronic idiopathic hypokalemia; Barttersyndrome. This syndrome is an autosomal recessive disorder, first reported by Bartter (1962) and called Bartter syndrome. Renal small ball hyperplasia syndrome with severe hypokalemia, alkalosis mainly blood sodium, chlorine are low, normal blood pressure with polydipsia, constipation, dehydration. Plasma renin-angiotensin and aldosterone were elevated. This syndrome is an autosomal recessive disorder, first reported by Bartter (1962) and called Bartter syndrome. Its clinical features are severe hypokalemia and metabolic alkalosis, accompanied by hyperrenin hyperaldosteronism, mesangial hyperplasia and hypertrophy, renal tubular maintenance and dysfunction, but no hypertension and edema And no response to exogenous angiotensin II. This syndrome is considered to be a clinical syndrome caused by mutations in ion channel genes. The disease is also known as congenital aldosteronism. Chronic idiopathic hypokalemia. Adrenal hyperplasia syndrome. Recent molecular diagnostic studies have revealed that Bartter syndrome has three different clinical and genetic types, namely congenital Bartter. The syndrome is typical of Bartter syndrome and Gitelman syndrome. The so-called Bartter syndrome refers to the typical Bartter syndrome. Congenital Bartter syndrome patients have two genotypes, type I is due to N+-K+-2CL-degeneration gene mutation type II is due to ROMK gene mutation caused by typical Bartter syndrome due to CLC-kb channel Caused by mutations in genes.

Glomerulosclerosis: focal glomerulosclerosis (focal glomeruloscerosis) refers to a type of glomerular capillaries in which glomerular capillary vasospasm has focal segmental sclerosis or hyaline degeneration without obvious cell proliferation. Can be used as mesangial hyperplasia, mesangial IgM deposition and focal glomerular sclerosis, but minimally pathological nephropathy is resistant to steroids and the consequences of repeated episodes of chronic progression. Early renal biopsy of primary nephrotic syndrome, which is ineffective against hormones, is focal glomerular sclerosis. Therefore, there is still debate about whether the disease is an independent glomerular disease. However, from a clinical pathological type that is different from other kidney diseases, it can also be regarded as an independent disease, which is more common and has a tendency to increase gradually.

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