Tubulointerstitial nephritis is a primary renal tubular injury and interstitial space, which leads to a decrease of renal function. The acute form usually based on an allergic drug reaction or an infection. The chronic form occurs with a wide range of causes, including genetic or metabolic disorders, obstructive uropathy and chronic exposure to environmental toxins and certain medicines and herbs. The diagnosis is suspected based on history and the urine finding, and often confirmed by biopsy. Treatment and prognosis differ depending on the etiology and the possible reversibility of the damage at the time of diagnosis.

Tubulointerstitial nephritis is a primary renal tubular injury and interstitial space, which leads to a decrease of renal function. The acute form usually based on an allergic drug reaction or an infection. The chronic form occurs with a wide range of causes, including genetic or metabolic disorders, obstructive uropathy and chronic exposure to environmental toxins and certain medicines and herbs. The diagnosis is suspected based on history and the urine finding, and often confirmed by biopsy. Treatment and prognosis differ depending on the etiology and the possible reversibility of the damage at the time of diagnosis. Etiology The tubulointerstitial nephritis may be primary, but a similar process can also occur as a result of glomerular damage or renovascular disease. A primary tubulointerstitial nephritis can occur in two forms acute (see Table: causes of acute tubulointerstitial nephritis) Chronic (see Table: Causes of chronic tubulointerstitial nephritis) Acute tubulointerstitial nephritis Acute tubulointerstitial nephritis (ATIN) shows up with inflammatory infiltrate and edema ds renal interstitium concern and often develops over days or months. More than 95% of cases result from infections or allergic reactions to drugs. The ATIN leads to acute Niereninschädigung. Severe cases, delayed therapy or the continued ingestion of a harmful drug can lead to permanent damage of chronic kidney failure. Renal eyepiece syndrome, ATIN plus. Uveitis also occurs and is idiopathisch.Chronische tubulointerstitial nephritis Chronic tubolointerstitiale nephritis occurs when a chronic tubular damage usually over years to a gradual interstitial infiltration and fibrosis, tubular atrophy and dysfunction as well as a gradual deterioration renal function leads. A simultaneous glomerular involvement (glomerulosclerosis) is at CTIN much more frequently than in ATIN. The causes of CTIN are manifold. These include immune-mediated diseases, followed by infections, Reflux or obstructive nephropathy, medicines and other disorders. A caused by toxins, metabolic disorders, hypertension, and inherited disorders CTIN results in a symmetrical and bilateral disease. If the CITN has other causes that Nierenvernarbung can be uneven and even affect a kidney. Some well-characterized forms of CTIN include Analgesic nephropathy Metabolic Schwermetallnephropathie reflux nephropathy myeloma kidney Hereditary cystic kidney disease are discussed elsewhere. Causes of acute tubulointerstitial nephritis cause Examples Drug therapy antibiotic beta-lactam antibiotics (the most common cause) Ciprofloxacin ethambutol isoniazid indinavir macrolides minocycline rifampin tetracycline trimethoprim / sulfamethoxazole Vancomycin anticonvulsants carbamazepine, phenobarbital, phenytoin valproate diuretics Bumetanide, furosemide, thiazides triamterene NSAID diclofenac fenoprofen Ibuprofen Indomethacin Naproxen Other: allopurinol aristolochic † captopril cimetidine interferon alpha lansoprazole omeprazole ranitidine mesalamine metabolic disorders Hyperoxalaturie ethylene glycol poisoning hyperuricosuria tumor lysis syndrome Parenchyminfektion renal Bacterially Brucella sp Corynebacterium diphtheriae Legionella sp Leptospira sp Mycobacterium sp Mycoplasma sp Rickettsia sp Salmonella sp staphylococci streptococci Treponema pallidum Yersinia sp Fungal Candida sp parasitic Toxoplasma gondii Viral Cytomegalovirus Epstein-Barr virus Hantavirus Hepatitis C virus HIV mumps Polyomavirus Other conditions Idiopathic with and without uveitis – Immunological cryoglobulinemia granulomatosis with polyangiitis idiopathic hypocomplementaemic interstitial nephritis IgA nephropathy IgG4-related tubulointerstitial nephritis rejection of the kidney transplant sarcoidosis Sjogren’s syndrome SLE (rare) Neoplastic lymphoma myeloma * The most common causative drugs are listed; among which are> 120 drugs. † Included in some medicinal plants used in traditional Chinese medicine. Causes of chronic tubulointerstitial nephritis cause examples Balkan nephropathy – Cystic disease Acquired cystic disease Medullary cystic kidney disease (MCKD) Medullary sponge kidney Nephronophthisis Polycystic Kidney Disease * Drug therapy analgesics cytostatics (cisplatin and nitro urea) Chinese herbs ((due to aristolochic †) immunosuppressive cyclosporine * and tacrolimus *) Lithium * granulomatous granulomatous Aplastic with polyangiitis Inflammatory bowel disease sarcoidosis TB Hematologic anemia leukemia lymphoma Multiple myeloma Sickle Cell Disease Hereditary nephropathy with hyperuricemia and gout – Idiopathic – Immunological amyloidosis cryoglobulinemia Goodpasture’s Syn syndrome IgA nephropathy rejection of the kidney transplant sarcoidosis Sjogren’s syndrome SLE infection Parenchymin kidney: pyelonephritis Hantavirus “Puumula Type Infection” (epidemic nephropathy) Systemic Mechanical Obstructive uropathy reflux nephropathy Metabolic Chronic hypokalemia Cystinosis Fabry’s disease hypercalcemia, hypercalciuria hyperoxaluria hyperuricemia * Hyperuricosuria Bestrahlungsnephritis- toxins aristolochic † heavy metals (eg. As arsenic, bismuth, cadmium, chromium, copper, gold, iron, lead, mercury, uranium) Vascular Atheroembolie hypertension renal vein thrombosis * Common causes. † Included in some medicinal plants used in traditional Chinese medicine. Symptoms and signs Acute tubulointerstitial nephritis symptoms and ailments of ATIN may be non-specific and often appear not to, unless it develop symptoms and complaints of kidney failure. Many patients develop polyuria and nocturia as a result of a defect in urine concentration and sodium reabsorption. The symptoms of ATIN can only use short-term within 3-5 days after further exposure for several weeks after the first contact with the toxin or. In extreme cases, the latency period ranging from a day at rifampicin to 18 months with NSAIDs. Fever and urticarial rash are characteristic early manifestations of drug-induced ATIN, but the triad classically described from fever, rash and eosinophilia seen in <10% of patients with drug-induced ATIN. Abdominal pain, weight loss, bilateral enlargement of the kidneys (caused by interstitial edema) can also occur in ATIN and suggest along with fever incorrectly a Nierenmalignom or polycystic kidney disease. If it does not come to kidney failure, peripheral edema and hypertension are rare Befunde.Chronische tubulointerstitial nephritis CTIN missing unless developing kidney failure in general symptoms and findings. Usually there is no edema. Blood pressure is increased normal or only slightly in early stages. Polyuria and nocturia develop. Diagnosis Risk Factors In ATIN, active urine sediment with sterile pyuria kidney biopsy Sometimes Usually imaging to rule out other causes few clinical and routine laboratory findings are specific to tubulointerstitial nephritis. Thus, there is a strong suspicion if the following occurs: Typical symptoms or complaints risk factors, in particular a temporal relationship between the start and the use of a potentially causative drug Characteristic findings of urinalysis, especially sterile pyuria Moderate proteinuria, usually (<1 g / day except for the use of NSAIDs, the tubular to proteinuria in the nephrotic range, can lead 3.5 g / day) detection of a tubular dysfunction (z. B. acidosis, Fanconi syndrome) concentrating the effect in proportion to the degree of renal failure Eosinophilurie can not be used to make the diagnosis or rule out, but the lack of eosinophils makes the diagnosis less likely (high negative predictive value). Other methods (for. Example, imaging) are usually necessary to distinguish or ATIN CTIN of other disorders. A clinical diagnosis of ATIN is often asked on the basis of the above, specific findings, but a renal biopsy is necessary to make a definitive diagnosis. Acute tubulointerstitial nephritis A urinalysis, the signs of active nephritis (active urine sediment) shows, including erythrocytes, leukocytes and Leukozytenzylinder and the absence of bacteria in cultures (sterile pyuria) is typical. A pronounced hematuria and dysmorphic erythrocytes are rare. In Eosinophilurie it is traditionally assumed that this indicates a ATIN; However, the presence or absence of urinary eosinophils is not particularly useful diagnostically. Proteinuria is usually only slightly, but can accept alfa and ranitidine nephrotic proportions in combination with a ATIN and glomerular disease by NSAIDs, ampicillin, rifampicin, interferon. To the blood findings of tubular dysfunction hyperkalemia include (caused by a defect in the Kaliumreabsorption) and metabolic acidosis non-anion (caused by a defect in the proximal tubular reabsorption of bicarbonate or in the distal tubular acid excretion). Ultrasonography, radionuclide scanning, or both may be necessary to ATIN from other causes of acute kidney injury such. As to distinguish acute tubular necrosis. In a ATIN ultrasonography can show due to interstitial inflammatory cells and edema greatly enlarged and echogenic kidneys. Kidney can save plenty of radioactive gallium-67 or radionuclide-labeled leukocytes in Radionukliduntersuchungen. Positive scans point strongly to a ATIN out (and show that acute tubular necrosis is less likely), but a negative scan does not rule ATIN from a kidney biopsy is usually done in patients with: One uncertain diagnosis Progressive kidney damage without improvement after discontinuation of possible causative medications findings suggestive of disease in early stage drug-induced ATIN for which a corticosteroid treatment is contemplated When ATIN the glomeruli are usually normal. The earliest finding is interstitial edema, typically followed by an interstitial leukocyte infiltration (with lymphocytes, plasma cells, eosinophils, and some polymorphonuclear leukocytes). In severe cases, it can be seen inflammatory cells that invade the space between the cells of the tubular basement membrane (tubulitis). In other samples, a granulomatous reaction due to the exposure to beta-lactam antibiotics, sulfonamides, mycobacteria and fungi may be immediately apparent. The presence of granulomas nichtverkäsender speaks for sarcoidosis. The immunofluorescence or electron microscopy rarely reveals any pathognomonic changes. Acute tubulointerstitial nephritis figure provided by Agnes Fogo, M.D., and the American Journal of Kidney Disease, Atlas of Renal Pathology (see www.ajkd.org). var model = {thumbnailUrl: '/-/media/manual/professional/images/tubulointerstitial_nephritis_high_de.jpg?la=de&thn=0&mw=350' imageUrl: '/-/media/manual/professional/images/tubulointerstitial_nephritis_high_de.jpg?la = en & thn = 0 ', title:' Acute tubulointerstitial nephritis 'description:' u003Ca id = "v38397010 " class = ""anchor "" u003e u003c / a u003e u003cdiv class = ""para "" u003e u003cp u003eDie biopsy acute tubulointerstitialer nephritis shows interstitial edema with infiltration of eosinophils

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