Inflammation after renal tubular cell damage

Introduction The release of virulence factors from renal tubular cells is the release of some cytokines such as IL-1 and tumor necrosis factor (TNFa) after the cells are damaged. These cytokines attract a series of inflammatory cells (such as white blood cells, lymphocytes, platelets, mononuclear-macrophages, etc.) in the blood to infiltrate the mesangial area, vascular area, and renal interstitial area, and release a series of inflammation. Sexual mediators cause an inflammatory response that in turn promotes phenotypic transformation of the kidney's innate cells. At this time, the function of the kidney's intrinsic cells has changed, and a series of nephrotoxic cytokines and growth factors such as TGF-B, PDGF, Bfgf, EGF, etc., which cause fibroblast proliferation in the renal interstitium, begin to be released. With differentiation and transformation to myofibroblasts.

Cause

It is an allergic toxicity to medical treatment. In most cases, only a few drugs (in more than 80 related drugs) are important for the identification of drug-related causes because severe kidney damage can often prevent or reverse sarcoidosis. Leptospirosis streptococci infection may also be associated with certain Chinese herbal medicines. Common antibiotics (such as aminoglycosides, penicillins, cephalosporins, amphotericin, tetracyclines, sulfonamides, doxorubicin, anti-tuberculosis drugs, etc.), non-hormonal anti-inflammatory drugs (indomethacin, Blo Long-term exposure to heavy metal salts (such as lead, mercury, etc.), anti-epileptic drugs, anesthetics, central stimulants, immunosuppressive agents, diuretics, etc.

an examination

Related inspection

Ammonium chloride load test plasma cell dynamic imaging urine dehydroepiandrosterone renal blood flow (RPF)

Renal biopsy is the only indication of a clear diagnosis. Including the diagnosis is not certain or the progression of renal failure, the earliest manifestation of glomeruli is normal is typical of interstitial edema. Subsequently, interstitial lymphocyte plasma eosinophils and a small amount of neutrophil infiltration occurred. In severe cases, inflammatory cells invaded the intercellular space (tubule inflammation) lining the basement membrane of the tubule, and secondary specimens may be seen in other specimens. The granulomatous response of methicillin sulfonamides to mycobacteria and fungi, the presence of non-caseous necrotizing granulomas suggests that nodular immunofluorescence or electron microscopy rarely shows pathological changes.

Differential diagnosis

Renal tubular necrosis: Acute tubular necrosis (ATN) is the most common type of acute renal failure, accounting for 75% to 80%. It is a clinical syndrome that occurs due to renal ischemia and/or nephrotoxicity caused by various causes of renal function and progressive decline. Mainly manifested as progressive azotemia caused by a significant decrease in glomerular filtration rate, as well as imbalance of water, electrolyte and acid-base balance caused by renal tubular reabsorption and excretion.

Tubulotoxic lesions: small tube lesions are caused by nephropathy due to poisoning of immunosuppressive drug and anticancer drug, which refers to glomeruli caused by the application of immunosuppressive agents and anticancer drugs. Renal tubules and interstitial lesions and bladder damage.

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