Renal tubular collapse

Introduction The glomerulus is collapsed due to mandatory diuretic and severe interstitial edema. Individuals with small lesions of kidney disease, especially those older, may have renal insufficiency, the main reason for which is forced diuresis, and severe interstitial edema leads to tubular collapse. Minimalchangenephrosis (MCN), formerly known as lipoid nephrosis, is also known as hormone-sensitive NS because most patients are sensitive to hormone therapy. The disease is a group of glomeruli under light microscopy is normal, proximal renal tubular epithelial cell steatosis electron microscopy glomerular epithelial podocyte protrusion fusion and disappearance of mesangial cell proliferation, matrix broadening and immune deposition The primary manifestations of primary glomerular disease are minimally pathological nephropathy, which is characterized by nephrotic syndrome, ie, massive proteinuria, hypoproteinemia, edema, and hyperlipidemia. Often after the respiratory infection, complications include thrombosis, acute renal failure pneumonia, peritonitis and other infections. MCN is a very common type of kidney disease in children. MCN is sensitive to steroid hormone therapy and has a tendency to ease and recur. This disease rarely progresses to end-stage renal failure.

Cause

MCN can be divided into primary and secondary types. The primary cause is unknown. The onset may be related to infection and allergic reaction. It is now considered to be an immune system mediated by abnormal T-lymphocyte cloning. Reaction-related diseases. Secondary onset may be associated with antigens and major histocompatibility complexes in humans. Patients often have a significantly higher incidence of specific hypersensitivity such as allergic rhinitis, urticaria and other allergic diseases. Secondary common factors are radiotherapy with allergens such as pollen biotoxin drugs (penicillamine, non-steroidal anti-inflammatory drugs) and lymphoma, which can also trigger MCN.

an examination

Related inspection

Uric acid renal tubular ammonia uric acid maximum excretion test renal tubular glucose maximum reabsorption test HCO3-reabsorption test ammonium chloride load test

The main clinical features of this disease is that the onset age is less acute, and there is a clinical manifestation of typical nephrotic syndrome, that is, a large amount of urinary protein (3.5g/d), high edema, hyperlipidemia, low plasma proteinemia (30g/ L). Generally no high blood pressure, hematuria and renal dysfunction. Proteinuria is highly selective for glucocorticoid therapy, but is prone to recurrent episodes. According to the above characteristics combined with laboratory tests can make a diagnosis of individual cases, the diagnosis conditions are not sufficient, such as excessive hypoproteinemia, the amount of urine protein may not reach the diagnostic criteria of nephrotic syndrome can be confirmed by renal biopsy pathological examination.

Differential diagnosis

Children between the ages of 1 and 6 were given experimental treatment without renal biopsy. Cases that are insensitive to adequate glucocorticoids, especially adults, require renal biopsy to be diagnosed and identified for other nephropathy. Especially in the early stage of focal segmental sclerosis and membranous nephropathy, the early lesions of FSGS are mostly confined to the border of the skin and the bone. The renal biopsy is often difficult to identify due to the inability to identify the renal biopsy. Can increase the diagnostic rate. In addition, the diagnosis of MCN must exclude the secondary cause, and should be differentiated from lupus nephritis, purpura nephritis, diabetic nephropathy, amyloidosis and constrictive pericarditis, and other middle and old patients should be excluded from lymphoma and other solid tumors. In some cases, the earliest signs of MCN and even lymphoma should be identified.

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