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What are the symptoms of membranous proliferative glomerulonephritis?
Membrane proliferative glomerulonephritis (MPGN) is less common in patients with primary glomerulonephritis, nephrotic syndrome is one of the few proliferative glomerulonephritis, the clinical manifestations of various pathological types are similar, regardless of the Alzheimer's disease clinical manifestations of what syndrome, almost all proteinuria and hematuria exist, proteinuria is non-selective, hematuria often microscopic persistent hematuria, 10% to 20% of patients often developed paroxysmal hematuria after respiratory tract infection, which is a severe, perse type of glomerular hematuria with erythrocyte malformation.
Symptoms of membranous proliferative glomerulonephritis:
About one-third of patients with hypertension, hypertension is generally mild, but there are inpidual cases, especially type Ⅱ patients, may occur severe hypertension, high-dose hormone therapy may also induce hypertensive crisis, at least half of patients with acute or chronic renal insufficiency, renal failure often appears in the early onset of poor prognosis, patients often have more serious positive cell positive after onset, showing pale, shortness of breath, Fatigue, and the degree of anemia and renal dysfunction is disproportionate, the mechanism is unclear, may be related to the activation of complement on the surface of red blood cells may also be due to capillaries to shorten the life span of red blood cells.
At onset of MPGN, at least one-half of patients develop nephrotic syndrome, about one-quarter of patients have asymptomatic hematuria and proteinuria, and one-fourth to one-third of patients develop acute nephritic syndrome , with red blood cell and red cell tube urine, high blood pressure and renal insufficiency, about half of patients may have a history of respiratory tract infection, 40% before onset with anti-"O" titer and other evidence of streptococcal infection, Some patients may develop partial lipid malnutrition (Barraquar-Simmons disease), especially type II lesions, even in the absence of clinical manifestations of renal disease.
Some patients with MPGN may exhibit X-linked inheritance. Congenital complement and a1-antitrypsin deficiency also predispose to this type of disease, and in patients with nephrotic syndrome, renal venous thrombosis may occur, although this disease develops to a high degree Of the inpidual differences, but the overall disease was slow progression, MPGN type I and type II histopathological and immune pathological changes are not the same and for the two types of morphology, the current clinical more that they represent different Disease, the clinical type Ⅱ tend to show signs of nephritis, crescentic glomerulonephritis and acute renal failure associated with high rates, and type I have more features of kidney disease, often with precursor infection and anemia, type Ⅱ patients often serum There is persistent hypocomplementemia, and the age of onset is small, with almost all patients under 20 years of age, with the exception that type II is more likely to relapse after kidney transplantation.
Tips: MPGN Ⅲ type is rare, mainly in children and young people at the age of 10 to 20 years old, less than 2 years old, more than 40 years old are rare, the clinical manifestations of this type are rarely described, and are similar to the long-term clinical changes of type I, according to Strife's description, Type III has decreased C3 level, but no C3 nephritis factor. The prognosis of non renal comprehensive proteinuria is better than that of nephrotic syndrome. This type has greater inpidual difference in end-stage renal disease. In the long term course, some patients can be relatively stable or even gradually improve.
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