Phenacetin nephritis: interstitial nephritis and necrotizing papillitis associated with the chronic ingestion of phenacetin.
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Eating↗
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Results for “NEPHRITIS, INTERSTITIAL”
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Interstitial nephritis.
Interstitial nephritis is an inflammatory process within the renal interstitium, and was one of the first observations made in the description of renal histopathology. Many different conditions are associated with an interstitial nephritis, and as a clinical diagnosis the term has little use unless causation is defined. However, there has been recent interest in the possibility of a common mechanism causing irreversible renal damage and eventually renal failure in many different types of interstitial nephritis. Such damage could take place due to blood-borne inflammatory mediators, or could be due to renal tubular inflammation related to abnormal components of the glomerular filtrate in renal failure, such as proteins or lipids. If such research were to result in effective therapy for interstitial nephritis, the progression of many forms of renal disease to end stage renal failure could be ameliorated.
Acute Disease↗
Suspected ciprofloxacin-induced interstitial nephritis.
Interstitial nephritis is a rare but serious adverse effect of many drugs and usually is diagnosed by clinical signs and symptoms of hematuria, proteinuria, eosinophilia, fever, azotemia, and rash. Ciprofloxacin is one drug that has been reported to cause interstitial nephritis. Renal toxicities have been reported in less than one percent of the patients receiving ciprofloxacin therapy. Limited documentation of this adverse effect exists in the literature. This article describes a patient with suspected ciprofloxacin-induced interstitial nephritis.
Aged↗
The outcome of acute interstitial nephritis: risk factors for the transition from acute to chronic interstitial nephritis.
BACKGROUND: Acute interstitial nephritis has been known as a complication of mainly streptococcal infection for nearly a century. With the advent of infection control, it became a complication caused by antibiotics and later by other drugs, which might have changed the outcome. To determine risk factors for the development of chronic renal insufficiency, and thus, the transition from acute to chronic interstitial nephritis, we performed a retrospective study of all cases of acute interstitial nephritis found by reviewing 1,068 renal biopsies from 1968 to 1997. METHODS: Patients with permanent and reversible renal insufficiency after acute interstitial nephritis were compared with respect to the causative event, the symptoms, and the clinical and histological findings. Differences between the groups were calculated by applying bi- and multivariate analysis. RESULTS: Acute interstitial nephritis was found in 6.5% of all biopsies (64 patients with 68 episodes of acute interstitial nephritis); it was infection-induced in 10%, idiopathic in 4%, and drug-induced in 85% of the cases (antibiotics in 13 cases, analgesics in 17, non-steroidal anti-inflammatory drugs (NSAIDs) in 16, diuretics in 5, and various other drugs in 7). Renal insufficiency was reversible in 69% and permanent in 31% (12% partially reversible, 19% irreversible). The infection-induced and idiopathic types of acute interstitial nephritis were always reversible. Drug-related acute interstitial nephritis caused permanent renal insufficiency in 36% with a maximum of 56% in NSAID-induced cases. In drug-induced cases, intake of the suspected drug for more than a month prior to diagnosis caused permanent renal insufficiency in 88% and interstitial granuloma in 31%. Multivariate analysis disclosed the following significant features separating the permanent from the reversible renal insufficiency group: patients in the first group had more tubular atrophy in their histology, more chronic use of mixed analgesics and/or NSAIDs, less oliguria or anuria as an acute symptom, fewer antibiotics as causative agents, more interstitial granuloma, more pronounced interstitial cell infiltration in their histology, and more imaging of renal shrinkage. Renal histology had the highest predictive value. CONCLUSION: Today, acute interstitial nephritis is mainly drug-induced. NSAIDs are the most frequent cause of permanent renal insufficiency after acute interstitial nephritis. Clinically, subacute symptoms, a prolonged intake of the suspect drug, and chronic analgesic or NSAID use are related to a more chronic course of interstitial nephritis. In histology, tubular atrophy, interstitial granuloma, and pronounced interstitial cell infiltration indicate chronicity.
Acute Disease↗
[Acute recurrent uveitis and idiopathic interstitial nephritis-- a nosologic entity (tubulo-interstitial nephritis and uveitis)].
So far 34 cases of idiopathic acute tubulo-interstitial nephritis and uveitis (TINU syndrome) have been reported by nephrologists. The patients have mainly been girls and only female adults. The authors describe a 53-year-old woman with this nosological entity, presenting with a granulomatous anterior uveitis and chronic course of nephritis. This is the first such case reported. All other cases described in the literature are compared and an attempt is made to locate the immune deficiency.
Acute Disease↗
Diagnosis and management of acute interstitial nephritis.
Acute interstitial nephritis is an important cause of acute renal failure resulting from immune-mediated tubulointerstitial injury, initiated by medications, infection, and other causes. Acute interstitial nephritis may be implicated in up to 15 percent of patients hospitalized for acute renal failure. Clinical features are essentially those of acute renal failure from any cause, and apart from a history of new illness or medication exposure, there are no specific history, physical examination, or laboratory findings that distinguish acute interstitial nephritis from other causes of acute renal failure. Classic findings of fever, rash, and arthralgias may be absent in up to two thirds of patients. Diagnostic studies such as urine eosinophils and renal gallium 67 scanning provide suggestive evidence, but they are unable to reliably confirm or exclude the diagnosis of acute interstitial nephritis. Renal biopsy remains the gold standard for diagnosis, but it may not be required in mild cases or when clinical improvement is rapid after removal of an offending agent or medication. The time until removal of such agents, and renal biopsy findings, provide the best prognostic information for return to baseline renal function. Corticosteroids appear to provide some benefit in terms of clinical improvement and return of renal function, but no controlled clinical trials have been conducted to confirm this.
Acute Disease↗
Epstein-Barr virus infection of renal proximal tubule cells: possible role in chronic interstitial nephritis.
Chronic interstitial nephritis frequently accompanies renal diseases of different etiologies. Far less common is the entity of primary interstitial nephritis wherein the glomerular and vascular structures of the kidney are not the primary focus of the disease process. Using in situ hybridization and the polymerase chain reaction, we detected DNA from the Epstein-Barr Virus (EBV) exclusively in renal tissue of patients with the idiopathic variety of chronic interstitial nephritis. The EBV genome, but not that of cytomegalovirus or adenovirus, was detected primarily in renal proximal tubule cells. Furthermore, the CD21 antigen, which serves as the receptor for EBV in B lymphocytes, was detected by immunocytochemistry primarily on proximal tubule cells and was markedly upregulated in the EBV-infected tissue. Western blot analysis of primary cultures of normal proximal tubule cells identified a 140-kDa protein, confirming the expression of the CD21 antigen. Colocalization experiments using proximal and distal tubule markers confirmed that EBV DNA and the CD21 antigen are found primarily in proximal tubule cells. EBV infection of renal proximal tubular cells may participate in evoking a cellular immune response that results in a damaged renal interstitium.
Adult↗
Rabeprazole-induced acute interstitial nephritis.
Acute interstitial nephritis is an uncommon but important cause of acute renal failure. Proton pump inhibitors are now thought to be the most common class of drugs implicated in drug-induced acute interstitial nephritis. This is the first reported case of rabeprazole-induced acute interstitial nephritis.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Granulomatous interstitial nephritis.
Granulomatous interstitial nephritis is a rare condition whose pathogenesis is poorly understood. Of 203 renal biopsies performed between 1974 to 1994 in which interstitial nephritis was the predominant change, granulomata occurred in 12. The authors reviewed the records of these patients and performed immunopathologic and immunohistochemical studies in their biopsies to characterize the phenotype of infiltrating cells. The authors used markers for T cells, B cells, and macrophages, and determined whether they were activated through assessment of upregulation of HLA-DR molecules. Additionally, the authors attempted to delineate whether or not tubules contributed to giant cell formation through assessment of intermediate filament for keratins and macrophage markers in epithelioid cells. Drug (aspirin, gentamycin, or combination of drugs), infection (Echerichia coli or various organisms), and sarcoidosis accounted for granulomatous inflammation in three patients each, Wegener's granulomatosis and oxalosis resulting from intestinal bypass in one patient each, and in one patient the possible cause could not be determined. Except for biopsies of granulomatous inflammation resulting from infection, in which neutrophils predominated, in all other biopsies, T cells and macrophages made up most of the inflammatory cell infiltrate. HLA-DR was upregulated in mononuclear cells infiltrating the interstitium and was expressed in proximal tubular cells and endothelial cells in all but biopsies of patients with sarcoidosis. In no instance was there evidence that tubules contributed epithelial cells to giant cell formation. These findings are consistent with the notion that granulomatous interstitial nephritis is a cell-mediated form of tissue injury in which T cell-macrophage seem to play a major role.
Adult↗
[Murine autoimmune interstitial nephritis. II. Genetic control of induction of interstitial nephritis].
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Animals↗
Antibiotic-induced recurring interstitial nephritis.
Acute interstitial nephritis (AIN) is often induced by drug therapy and accounts for 1%-3% of adult cases of renal failure. A 13-year-old white female with cystic fibrosis developed two episodes of biopsy proven AIN following antibiotic use over a 5-year period. The first episode resolved with pulse steroid therapy and the second resolved without intervention. Steroid therapy may play a role in aborting subsequent AIN attacks.
Adolescent↗
Drug-induced acute interstitial nephritis.
Acute interstitial nephritis (AIN) is a form of inflammatory renal disease affecting predominantly the tubules and the interstitium. Drugs, particularly beta-lactam antibiotics and non-steroidal anti-inflammatory drugs, are currently the most common causes. The pathogenesis of drug-induced AIN is complex but there is good clinical evidence for an immune-mediated reaction. Clinical findings may be variable depending on the drug involved and the individual response. Most patients recover from the acute renal failure; however, in older patients or in patients with pre-existing renal insufficiency the recovery of renal function may be incomplete.
Acute Disease↗
[Drug-induced acute interstitial nephritis].
Acute interstitial nephritis (AIN) due to the drugs is caused by allergic reaction and it is presented by acute renal failure, rush, eosinophilia and eosinophiluria. AIN due to NSAID in comparison with AIN caused by other drugs is presented with nephrotic syndrome and acute renal failure. Kidney biopsy is necessary for diagnosis of AIN. The most important and first step in the treatment is the discontinuation of the drug. In severe cases, the corticosteroids are indicated (1 mg/kg of body weight), or intravenous bolus of corticosteroids followed by high-oral dose administration for several weeks. Symptomatic therapy (diet, diuretics) is indicated for all patients, and hemodyalisis is indicated in patients with severe acute renal failure.
Humans↗
Severe reversible renal failure due to naproxen-associated acute interstitial nephritis.
UNLABELLED: Acute interstitial nephritis is uncommon in children and has very rarely been described with naproxen treatment. We report the occurrence of severe acute renal failure in a 10-year-old girl with juvenile rheumatoid arthritis after 1 month of naproxen therapy. Renal biopsy showed severe acute interstitial nephritis. The patient recovered completely after discontinuation of naproxen and administration of methylprednisolone. A review of the literature regarding non-steroidal anti-inflammatory drug-associated acute interstitial nephritis is provided. CONCLUSION: In an era of increasing popularity of non-steroidal anti-inflammatory drugs for use in children, paediatricians should be aware of the potential renal complications of this class of drugs.
Acute Disease↗
Murine interstitial nephritis. V. The auto-induction of antigen-specific Lyt-2+ suppressor T cells diminishes the expression of interstitial nephritis in mice with antitubular basement membrane disease.
We observed the emergence of an antigen-specific Lyt-2+ suppressor T cell after the i.v. injection of tubular antigen-derivatized lymphocytes into mice already immunized to produce interstitial nephritis. The auto-induction of these suppressor T cells effectively attenuated both the expression of renal injury and a delayed-type hypersensitivity response to tubular antigen. This suppressive effect was also genetically restricted by gene products in I-J and Igh-1. Although this suppressor system had a marked inhibitory effect on the nephritogenic effector cell repertoire, there was no diminution of titers of antibodies to the tubular basement membrane. Our results demonstrate a protective role for antigen-specific suppressor cells in autoimmune renal injury, and the strategy for their induction may have important therapeutic implications for other immune-mediated disorders.
Animals↗
Acute interstitial nephritis.
Acute allergic interstitial nephritis is manifested clinically by rash, fever, eosinophilia, hematuria, oliguria and azotemia. Histologically a monocytic inflammatory process in the renal interstitium is seen. The clinical course of a patient after excessive sodium cephalothin administration suggested allergic interstitial nephritis and implicates this drug as an etiologic agent.
Acute Disease↗
[Allopurinol-induced chronic granulomatous interstitial nephritis].
Although drug induced interstitial nephritis is a relatively common cause of renal failure,granulomatous forms remain a rare condition. The development of a chronic granulomatous interstitial nephritis due to allopurinol is exceptional, only three cases have been described previously. We report on a patient who presented a granulomatous interstitial nephritis after 10 years of allopurinol administration (300 mg/day). At diagnosis, he had end stage renal disease and dialysis treatment was needed. Two months after drug withdrawal and on corticoid treatment a slow recovery of renal function was observed, allowing the interruption of dialysis. Two years after, the creatinine clearance is 23 ml/min,being dialysis free. We discuss the differential diagnosis of granulomatous interstitial nephritis and its rare association with allopurinol treatment.
Adrenal Cortex Hormones↗
The distal nephron is preferentially infiltrated by inflammatory cells in acute interstitial nephritis.
In acute interstitial nephritis (AIN), mononuclear cells invade the tubules (tubulitis). The segmental localization of tubulitis is not precisely known. To clarify this question, formalin-fixed kidney biopsy specimens from 13 patients with AIN were studied stereologically by identifying cortical tubules with segment-specific markers. The periodic acid-Schiff reaction, peanut lectin, and antibodies against Tamm-Horsfall protein and epidermal cytokeratins all applied to the same section were used to identify the proximal tubules (PTs), distal convoluted tubules, distal straight tubules, and the cortical collecting system (connecting tubules and cortical collecting ducts), respectively. Morphometrically, an estimate of the relative volume of the inflammatory cell infiltrates within each category of tubular segments was obtained. Inflammatory cells were infrequently found in PTs (1.2%) but were frequently localized in distal tubules and the cortical collecting system (7.6%). There was no difference in the amount of the inflammatory cell infiltrate within these segments. Re-examination of an electron microscopic study of AIN carried out in this laboratory revealed that mononuclear cells were rarely seen in convoluted PTs but were frequently observed in straight PTs and all segments distal to them. The observations indicate that it is the distal nephron which is primarily affected by inflammatory cell infiltration in AIN.
Acute Disease↗