What causes interstitial nephritis?

The reasons for the development of tubulointerstitial nephritis are diverse. Acute tubulointerstitial nephritis can develop with various infections, as a result of the use of certain drugs, poisoning, burns, trauma, acute hemolysis, acute circulatory disorders (shock, collapse), as a complication of vaccination, etc.

Chronic tubulointerstitial nephritis also represents a heterogeneous polyethological group of diseases in which, in addition to the above factors, hereditary predisposition and renal dysembryogenesis, metabolic disorders, chronic infection and intoxication, immunologic diseases, adverse environmental factors (heavy metal salts, radionuclides ), etc. Chronic tubulointerstitial nephritis can develop as a continuation of acute.

For the first time, tubulointerstitial nephritis was described by WTCouncilman in 1898 after examining 42 cases of acute nephritis after suffering from scarlet fever and diphtheria. Later, other bacterial, viral and parasitic agents were identified, leading to the development of tubulointerstitial nephritis. Among bacteria, in addition to streptococcus and diphtheria bacillus, they may be pneumococcus, meningococcus, chlamydia, syphilis, typhoid, etc. These bacterial agents cause damage to the renal interstitium by toxic effects, while leptospira and mycobacterium tuberculosis can directly invade the kidney tissue. Among the viruses, the causative agent of mononucleosis, hepatitis viruses, measles virus, etc., as well as herpes viruses persistent in the renal tissue, Coxsackie, Epstein-Barra, AIDS, cytomegalovirus, etc., may have a toxic effect on tubulointerstitium. The possibility of forming tubulointerstitial nephritis as a result of prolonged persistence respiratory viruses - influenza viruses, parainfluenza, adenoviruses, which lead to activation of the persistent urinary system of endogenous coxsackievirus infection. According to various authors, postviral tubulointerstitial nephritis is up to 50% in the structure of all interstitial nephritis.

Among parasites to the emergence of tubulointerstitial nephritis can lead to toxoplasma, mycoplasma, the causative agent of leishmaniasis.

Particular importance in the development of tubulointerstitial nephritis is given to medicinal preparations, especially (beta-lactam antibiotics, sulfonamides, nonsteroidal anti-inflammatory drugs, diuretics, not so much the dose as the duration of the drug intake and individual sensitivity to it.The high risk of tubulointerstitial nephritis originates after 10 days of taking the drug.

Toxic effects on tubulointerstitutions can be provided by various chemical agents, especially heavy metal salts (cadmium, lead chromium, mercury, gold, silver, arsenic, strontium).

Among endogenous factors, a special role in the development of tubulointerstitial nephritis is played by dysmetabolic nephropathies and instability of cytopoietes; vesicoureteral reflux, polycystosis and other developmental anomalies, accompanied by a violation of tubular differentiation and tubular dysfunction. The development of tubulointerstitial nephritis is possible against the background of congenital disorders of hemodynamics and urodynamics, accompanied by circulatory hypoxia, impaired lymph flow.

Medications that can cause tubulointerstitial nephria

Beta-lactam antibiotics	Other antibiotics and antiviral drugs	Anti-inflammatory drugs	Diuretic drugs	Other medicines
Methicillin Penicillin Ampicillin Oxacillin Nafcillin Carbenicillin Amoxicillin Cephalothin Cephalexin Cefradine Cefotaxime Cefoxytin Cefotetan	Sulfonamides Co-trimoxazole Rifampicin Polymyxin Ethambutol Tetracycline Vancomycin Erythromycin Kanamycin Gentamicin Colistin Interferon Acyclovir Ciprofloxacin	Indomethacin Phenylbutazone Fenoprofen Naproxen Ibuprofen Fenazone Metafenamic acid Tolmetin Diflunizal Aspirin Fenacetin Paracetamol	Thiazides Furosemide Chlorthalidone Triamterene	Fenindion Glafenin Diphenyl-hydantoin Cimetidine Sulfinpyrazone Allopurinol Carbamazepine Clofibrate Azathioprine Phenyl-propanolamine Aldomet Phenobarbital Diazepam D-Penicillamine Antipyrine Carbimazole Cyclosporin Captopril Lithium

Some of the most common nephrotoxic agents

Heavy metals	Inorganic mercury (chloride), organomercury compounds (methyl-, ethyl-, phenylmercury, ethyl mercuricothiosalicylate sodium, mercury diuretics), inorganic lead, organic lead (tetraethyl lead), cadmium, uranium, gold (especially sodium arothiomalate), copper, arsenic, arsine arsenious hydrogen), iron, chromium (especially trioxide), thallium, selenium, vanadium, bismuth
Solvents	Methanol, amyl alcohol, ethylene glycol, diethylene glycol, cellosol, carbon tetrachloride, trichlorethylene, various hydrocarbons
Substances that cause oxalosis	Oxalic acid, methoxyflurane, ethylene glycol, ascorbic acid, anticorrosive substances
Antineoplastic agents	Cyclosporine, cisplatin, cyclophosphamide, streptozocin, methotrexate, nitrosoureas derivatives (CCNU, BCNU, methyl-CCNU), doxorubicin, daunorubicin
Diagnostic Agents	Sodium iodide, all organic iodide contrast agents
Herbicides and pesticides	Paraquat, cyanides, dioxin, cyphenyl, cyclohexamides and organochlorine insecticides: endrin, aldrin, endosulfan, dieldrin, lindane, hexachlorobenzene, dichlorodiphenyltrichloroethane (DDT), heptachlor, chlordecone, polychlorine derivatives of terpene, chlordane, dicofol (keltan), chlorobenzylate, mirex, methoxychloro
Biological factors	Mushrooms (for example, Amanito phalloides causes severe muscarinic poisoning), poisons of snakes and spiders, insect bites, aflatoxins
Inductors of immune complexes	Penicillamine, captopril, levamisole, gold salts

An important role in the development of tubulointerstitial nephritis is also played by allergic reactions and immunodeficiency states.