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At least 253 records · Page 14Linked to original sources
PubMed1994

Interstitial nephritis associated with 5-aminosalicylic acid.

A patient with severe Crohn's disease was treated with 5-aminosalicylic acid (5-ASA). Following initiation of treatment, serum creatinine increased slowly from 105 to 530 mumol/l (creatinine clearance 16 ml/min). The diagnosis of an interstitial nephritis was made based on normal urinary findings and the renal biopsy histology of interstitial mononuclear infiltrates and normal glomeruli, 5-ASA was discontinued and serum creatinine decreased to 245 mumol/l (creatinine clearance 40 ml/min) during the following 3 months. Partial reversibility of renal failure following discontinuation of 5-ASA and the absence of other drugs possibly causing interstitial nephritis suggest a causal relationship between 5-ASA and interstitial nephritis.

Adult↗
PubMed1978

[Acute interstitial nephritis with oliguric renal failure following phenylbutazone medication].

Acute oliguric renal failure due to acute interstitial nephritis developed in a patient after treatment with phenylbutazone. The histological, immuno-histological and serological features in this case are compatible with the involvement of a delayed hypersensitivity reaction in the pathogenesis of this drug-induced interstitial nephritis. Other side effects of phenylbutazone on the kidney and the water and electrolyte metabolism are discussed.

Acute Kidney Injury↗
PubMed1998

The evolving contribution of renal pathology to understanding interstitial nephritis.

One hundred years of progress in the study of interstitial nephritis has expanded our diagnostic entities, resulted in identification of numerous pathogenic events, and defined the nature of the inflammatory infiltrate in ways that are useful both for general understanding and for diagnostic classification. We stand poised to enter the next hundred years with new techniques applicable to renal biopsies that detect specific biologic activities in situ in tissue sections. In the future, the information gained from these techniques is likely to result in refined and more accurate assessments of prognosis in patients with kidney disease, and to guide therapeutic interventions designed to interrupt specific sequences of active renal injury.

Biopsy↗
PubMed1987

Suppressor system in murine interstitial nephritis. Analysis of tubular basement membrane (TBM)-specific suppressor T cells and their soluble factor in C57BL/6 mice using a syngeneic system.

We induced typical interstitial nephritis with high titers of anti-tubular basement membrane (TBM) autoantibody in genetically resistant C57BL/6 mice by treating them with sodium aurothiomalate (gold) and immunizing them with syngeneic TBM antigen. When gold was not used, the T-cell fraction of nylon wool adherent splenic cells showed prominent suppressive activity against the proliferative response of nonadherent cells to TBM antigen. However, this suppressive activity was remarkably decreased by the gold treatment. TBM antigen sensitized thymocytes, a thymocyte extract, and a spleen cell extract were transferred to C57BL/6 mice which had been immunized with TBM antigen and treated with gold. This transfer clearly depressed the induction of autoimmune interstitial nephritis in an antigen-specific manner. These results indicate that TBM antigen-specific suppressor T cells and their soluble factor may play an important role in the negative regulation of interstitial nephritis in C57BL/6 mice.

Animals↗
PubMed1984

[Acute interstitial nephritis and kidney failure requiring dialysis after sulfinpyrazone therapy].

We report a case of acute interstitial nephritis (AIN) after a six weeks' therapy with sulphinpyrazone (Anturane, Ciba-Geigy, Wien). The patient presented with acute renal failure requiring hemodialysis. He died from acute cardiac failure three days after admission. According to our available information, it seems to be the first case of histologically proven acute interstitial nephritis with renal failure requiring hemodialysis after sulphinpyrazone therapy. Our observation underlines the suggestions made by Butler (7) and Mayrhofer et al. (19): During sulphinpyrazone therapy, serum creatinine and urea concentrations should be controlled regularly; the drug must be discontinued immediately when renal function is worsening; and the drug should not be administered in patients with even slightly impaired renal function.

Acute Kidney Injury↗
PubMed2001

Interstitial nephritis in patients with inflammatory bowel disease treated with mesalamine.

Mesalamines are slow-release formulations of 5-aminosalicylic acid (5-ASA) and are effective as primary treatment and maintenance therapy in inflammatory bowel disease. Interstitial nephritis is a recognized side effect. We report two cases of biopsy-confirmed interstitial nephritis in patients being treated with 5-ASA. Both had a trial of steroid therapy. One patient had partial recovery of renal function but the other patient was in chronic renal failure and likely was approaching the need for dialysis. Interstitial nephritis is an under-recognized complication of 5-ASA therapy. Early identification and withdrawal of this drug can lead to a partial or complete reversal of renal dysfunction.

Adult↗
PubMed1992

[A case of Bufferin induced acute interstitial nephritis--analysis of immune cells and cytokine].

This paper describes a case report of acute interstitial nephritis associated with Bufferin. A 15-year-old girl were referred to our hospital due to fever and renal dysfunction. Laboratory findings showed elevation of serum BUN and creatinine, and increased urinary beta 2-MG excreation. Light microscopic findings of her renal biopsy specimen revealed edema and numerous inflammatory cells in the interstitium, and minor alterations in glomeruli. The interstitial infiltrates consisted mainly of T cells and also monocytes/macrophages. Interstitial cells were labelled with antibodies to interleukin (IL)-1 and tumor necrose factor (TNF). Bufferin was positive by lymphocyte stimulation test. Thus, we considered that this drug was causative in this case. This observation suggests the participation of cell-mediated immune injury in drug induced acute interstitial nephritis.

Acute Disease↗
PubMed1994

[Systemic karyomegaly with chronic interstitial nephritis. Discussion of the disease picture based on an autopsy case].

Systemic karyomegaly associated with interstitial nephritis was first described in 1978 by Mihatsch. Seven cases have been reported to date. We give an account of an autopsy case of systemic karyomegaly in a 30-year-old Italian man. Bizarre enlargement of nuclei was found in renal tubular epithelial cells, Schwann cells and in smooth muscle cells of vessels and bowel and, less obviously, in endothelial and adventitial cells of vessels, in alveolar epithelial cells and in astrocytes of the brain. These findings were associated with chronic interstitial nephritis, nonspecific hepatopathy, adenocarcinoma of the rectum and multiple sclerosis. The clinical course was marked by chronic renal failure, chronic haemodialysis and renal transplantation. The patient died 8 years after diagnosis in septic-toxic shock. The aetiology and pathogenesis of the disease are discussed.

Adenocarcinoma↗
PubMed1980

Acute interstitial nephritis due to drugs: Review of the literature with a report of nine cases.

Acute interstitial nephritis due to drugs commonly presents as acute renal failure and may be commoner than is presently realized. Drugs implicated include not only methicillin and other penicillins but also diuretics and nonsteroidal anti-inflammatory agents. The mechanism of injury likely involves an immunologic disturbance, possibly a delayed hypersensitivity reaction. Differential diagnosis from other causes of acute renal failure may be difficult, but coincident evidence of an acute allergic reaction may help, as may the detection of eosinophils in the urine or avid uptake of 67Ga by the kidneys. Definitive diagnosis may require renal biopsy, which will reveal normal glomeruli and a patchy but usually heavy interstitial infiltrate with lymphocytes, plasma cells, and eosinophils. Diagnosis of acute interstitial nephritis is important, because withdrawal of the offending agent will usually result in rapid improvement in renal function, and steroid therapy may reduce residual chronic renal damage.

Acute Disease↗
PubMed2001

[Phenotypic characteristics of infiltrated inflammatory cells, renal tubular epithelial cells and interstitial cells and their possible roles in the outcome of human drug-associated interstitial nephritis].

OBJECTIVE: To observe the phenotypic characteristics of infiltrated inflammatory cells, renal tubular epithelial cells (TEC) and interstitial cells in human drug-associated interstitial nephritis (IN) and evaluate their roles in the interstitial inflammation and fibrosis. METHODS: Immuno-histochemical method was employed to observe the renal biopsy specimens collected from 31 patients with acute or chronic drug -associated IN. Infiltration of T lymphocyte and monocyte/macrophage was observed by the marker CD3(+) and CD68(+). Expressions of PCNA, MCP-1 and alpha-smooth muscle actin (alpha-SMA) were also detected in TEC and interstitial cells. Semi-quantitative data and pathological features together with clinical outcome from these patients were further analyzed. RESULTS: A great were large amount of CD3(+) and CD68(+) cells was found in the renal interstitium in all patients, with a CD68(+) cells took a higher proportion of in chronic drug-associated IN (CIN), and the ratio of CD3(+)/CD68(+) cells was closely negatively correlated with the level of serum creatinine. PCNA and MCP-1 expression were both increased in TEC in acute drug-associated (AIN), MCP-1 expression in TEC was positively correlated with the number of CD68(+) cells in the renal interstitium. 54.8% of CD68(+) cells in renal interstitium were PCNA positive. There was a high expression of alpha-SMA in the TEC and interstitial cells in AIN and CIN, positively was correlated with the degree of interstitial fibrosis. In AIN, expression of alpha-SMA and positively PCNA in TEC were that of correlated with each other. Much more expression of alpha-SMA was seen in renal interstitial cells in CIN, with its distribution coincided with that of the expression of collagen IV. The degree of interstitial fibrosis was closely correlated with the recovery of renal function. CONCLUSION: During the early stage of human drug-associated interstitial nephritis, TEC is activated and highly expresses chemoattractants, inducing the infiltration of monocyte/macrophage into the interstitium. Monocyte/macrophage may be used as marker for the chronicity of interstitial inflammation and poor outcome of renal function.

Actins↗
PubMed1995

Granulomatous interstitial nephritis associated with hydrochlorothiazide/amiloride.

A 74-year-old woman developed acute renal failure and granulomatous interstitial nephritis associated with hydrochlorothiazide/amiloride. On stopping the drug the renal function improved, but not significantly. Around 20 months after prednisone administration, the renal function had stabilized, with a moderate degree of renal insufficiency. The case is discussed, and some aspects of acute interstitial nephritis induced by diuretics are briefly reviewed.

Acute Kidney Injury↗
PubMed1999

Acute post streptococcal interstitial nephritis in an adult and review of the literature.

While glomerular lesions are a recognized sequel to infection with group A beta haemolytic streptococci, literature on primary tubular lesions, as remote effects of streptococcal infection, is scanty. A case of interstitial nephritis in a 29-year-old woman following streptococcal sore throat is described. This adult admitted with tonsillitis developed acute renal failure from acute interstitial nephritis and subsequently had full recovery of renal function. Acute interstitial nephritis should be included in the differential diagnosis of patients with streptococcal infections who develop acute renal failure.

Adult↗
PubMed2003

The role of mast cells in acute tubulo-interstitial nephritis with uveitis.

UNLABELLED: We describe the clinicopathological characteristics of two patients with acute tubulo-interstitial nephritis with uveitis (TINU) with mast cells infiltrating the interstitium. The pathogenesis of TINU remains unknown, but a T-cell-mediated immune response was suggested to be involved. Recent studies have shown that infiltrating mast cells are closely associated with the development of renal interstitial fibrosis in glomerulonephritis. To address the role of mast cells in the renal interstitial injury in TINU, immunohistochemical studies were performed in renal biopsy sections using anti-human mast cell tryptase antibody specific for mast cells. In addition, we tried to detect CD68-positive macrophages to compare with the localisation of mast cells within the renal interstitium. Mast cells and macrophages could be detected in renal interstitial lesions of both patients. Massive infiltration of macrophages into interstitial lesions was observed, whereas mast cells were detected in a sporadic rather than a clustered manner, and associated with fibrotic lesions. Repeat renal biopsy findings suggested the involvement of these cells in the renal interstitial injury because the number of infiltrating mast cells and macrophages in the interstitium decreased with the improvements in clinical symptoms and pathological lesions. CONCLUSION: The present study showed that mast cells might play an important role in the development of renal interstitial injury in tubulo-interstitial nephritis with uveitis.

Acute Disease↗
PubMed2002

Epstein-Barr virus-associated acute interstitial nephritis: infection or immunologic phenomenon?

Epstein-Barr virus (EBV) DNA in renal tissue in acute interstitial nephritis (IN) has not been previously reported. An 18-year-old male presented with a sore throat, fever, cervical lymphadenopathy, and oliguric renal failure. The rapid slide test for heterophile antibodies associated with infectious mononucleosis was positive, and a renal biopsy showed an acute interstitial nephritis. A polymerase chain reaction (PCR) assay identified EBV DNA in the renal biopsy. In situ hybridization (ISH) for EBV RNA and immunohistochemistry for latent membrane protein 1 of EBV were negative. Hemodialysis and prednisone 60 mg PO OD were administered and the s-creatinine dropped from 1,224 to 75 micromol/l over 9 days. The identification of EBV DNA in the kidney raises the possibility that direct infection plays a role in acute IN associated with EBV.

Acute Disease↗