SEARCH · PubMed Health

Results for “NEPHRITIS, INTERSTITIAL”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources

PubMed1997

Role of leucocyte adhesion molecules in aminonucleoside of puromycin (PAN)-associated interstitial nephritis.

Rats receiving a single dose (10 mg/l00 g body wt) of PAN develop severe proteinuria and acute interstitial nephritis. To investigate the mechanisms involved in interstitial leucocyte accumulation, we examined the expression of adhesion molecules on kidney tissue sections as well as on endothelial cell cultures. We also performed in vivo treatments with antibodies against adhesion molecules. Enhanced expression of intercellular adhesion molecule-1 (ICAM-1) was found on day 7 of the disease, when interstitial nephritis was first detected. Also, rat endothelial cells in culture showed maximal expression of ICAM-1 in the presence of 10(-9) - 10(-11) M PAN. Adhesion of peripheral blood mononuclear cells (PBMC) on kidney sections from PAN-treated rats was highest on day 7 (3.05 +/- 0.7 (mean +/- s.e.m.); controls 0.75 +/- 0.5). Such increased adhesion was notably blocked after PAN-treated rat kidney sections were incubated with anti-ICAM-1 MoAb (0.9 +/- 0.4). In addition, adhesiveness of PBMC to PAN-stimulated endothelial cells in culture was enhanced (25 +/- 2.5%; non-stimulated cells 13 +/- 3.1%). The addition of specific MoAbs against ICAM-1 and lymphocyte function-associated antigen-1 (LFA-1) produced a high blockage of adhesiveness induced by exposure to PAN (inhibition 58 +/- 3%; non-stimulated cells 40 +/- 7%). Simultaneous administration to PAN-treated rats of anti-LFA-1 and anti-ICAM-1 MoAbs reduced the number of interstitial cells by 70% compared with the 30% of reduction obtained when anti-very late antigen-4 (VLA-4) MoAb and anti-vascular cell adhesion molecule-1 (VCAM-1) antibodies were used. Our results suggest that the LFA-1/ICAM-1 pathway plays a principal role in the interstitial nephritis occurring in rats with PAN-nephrosis.

Animals↗

PubMed1992

[A case of idiopathic chronic interstitial nephritis progressed to renal failure without proteinuria nor hematuria].

A case of idiopathic interstitial nephritis who underwent to chronic renal failure without history of hematuria nor proteinuria is discussed. A 46 years old woman who showed gradually elevation of serum creatinine (1.3-2.5 mg/dl) admitted on our hospital. On occasions of pregnancy, health examination or hospital visit, she has never been pointed out hematuria nor proteinuria. Immunological disorders such as SLE, metabolic diseases, urinary tract obstruction and chronic urinary tract infection were excluded by the examinations after admission. Because of the severe enzymuria (beta 2-microglobulin, N-acetyl glucosaminidase), chronic interstitial nephritis was considered, and renal biopsy was performed. Severe tubulointerstitial changes were observed histologically, however, glomerular damage was comparatively mild. From these results, she was diagnosed idiopathic chronic tubulointerstitial nephritis. In this case, hematuria and proteinuria were absent until severe renal dysfunction. This may be caused by that inflammation was located to the tubulointerstitial area. The observation of enzymuria seemed to be important to diagnosis and follow-up of the interstitial nephritis.

Chronic Disease↗

PubMed2003

Membranous glomerulopathy and acute interstitial nephritis following treatment with celecoxib.

Both membranous glomerulopathy and acute interstitial nephritis have been reported to occur following treatment with non-steroidal anti-inflammatory drugs. We report the first cases of membranous glomerulopathy and acute interstitial nephritis following treatment with celecoxib (Celebrex), a selective COX-2 inhibitor. The rapid and complete resolution of both conditions following discontinuation of Celebrex strongly implicates this agent in disease pathogenesis. These cases enlarge the spectrum of potential renal toxicities of the COX-2-specific non-steroidal anti-inflammatory drugs.

Acute Disease↗

PubMed1987

Chronic predominant interstitial nephritis in a patient with systemic lupus erythematosus: a follow up of three years and review of the literature.

Predominant interstitial nephritis is a rare manifestation of systemic lupus erythematosus. Only seven cases have been reported in the literature. Owing to the rarity of this entity, the natural history of predominant interstitial nephritis in lupus has not been adequately recorded and an appropriate therapeutic approach has yet to be defined. In this report we present the case of a 25 year old woman with active systemic lupus erythematosus complicated by kidney failure and renal tubular acidosis due to predominant interstitial nephritis. We describe the course of her disease over a three year period. Seven additional patients with systemic lupus erythematosus and predominant interstitial nephritis are reviewed.

Adult↗

PubMed2002

[Interstitial nephritis induced by mesalazine].

This report concerns the first case in Japan of interstitial nephritis induced by mesalazine, a new therapeutic agent for inflammatory bowel disease, such as ulcerative colitis. Twenty-two cases have already been reported in other countries. The patient, a 27-year-old woman, was treated with mesalazine for her ulcerative colitis at another hospital. At the beginning of her treatment, her serum creatinine level was within the normal range. After 12 months, this level increased up to 5.7 mg/dl. She was then referred to our hospital for renal investigation and therapy. A renal biopsy revealed that severe tubulo-interstitial nephritis had occurred. Her mesalazine treatment was withdrawn and prednisolone was administered. Her serum creatinine level decreased gradually. However, this level remained at about 2.8 mg/dl and stabilized at that level. She was then discharged from the hospital. Glomeruli appeared to have minor glomerular abnormalities except for one globally sclerosed glomerulus as observed by light microscopy. However, IgM and C3 deposition on glomeruli were also observed. Glomerular lesions were suspected from these histological findings. A similar case that showed IgM. C3 depositions in glomeruli has previously been reported. The possibility of glomerular lesions being induced by mesalazine should be further researched. From the summary of reported cases, a delay of diagnosis of interstitial nephritis induced by mesalazine has resulted in permanent irreversible renal failure. Intensive monitoring of renal function is required when a patient is treated with mesalazine.

Adult↗

PubMed1985

Acute interstitial nephritis with bone marrow granulomas and uveitis.

A case of interstitial nephritis with bone marrow granulomas and uveitis was presented. A 53-year-old woman was found to be uremic in the course of rheumatoid arthritis. The renal biopsy revealed acute interstitial nephritis with eosinophilic infiltration. She also had bone marrow granulomas and uveitis. These findings were compatible with those of the syndrome described by Dobrin et al. The etiology and the pathogenesis of this syndrome remain unknown. However, the elevation of the erythrocyte sedimentation rate, raised levels of serum immunoglobulins, presence of circulating immune complexes and decreased T-cell population observed in this patient suggest the involvement of immunological disorders.

Acute Disease↗

PubMed1985

[Mefenamic acid (Ponstan)-induced acute interstitial nephritis with reversible, severe, non-oliguric renal failure].

Acute interstitial nephritis is a rare complication of treatment with non-steroidal antiinflammatory drugs. A case is reported with severe, reversible, non-oliguric renal failure caused by biopsy-proven acute interstitial nephritis after therapy with mefenamic acid (Ponstan). Prednisone treatment resulted in normalization of renal function within 4 weeks.

Acute Kidney Injury↗

PubMed1995

Tumefactive megalocytic interstitial nephritis in a patient with Escherichia coli bacteremia.

Megalocytic interstitial nephritis is rare and primarily affects the cortex in an otherwise normal kidney. We recently encountered a patient with Escherichia coli bacteremia and oliguric acute renal failure who died of gram-negative septicemia. At autopsy, this patient's kidneys displayed typical features of megalocytic interstitial nephritis. We were able to perform special stains suggesting that the histiocytic interstitial cells originated from infiltrating macrophages. Our patient illustrates that macrophage proliferation can result in interstitial inflammation sufficiently severe to cause anuric acute renal failure.

Acute Kidney Injury↗

PubMed1995

Karyomegalic interstitial nephritis: further support for a distinct entity and evidence for a genetic defect.

Karyomegalic interstitial nephritis was first described in 1979 by Mihatsch, who was reporting three such cases. We report here four additional cases as well as two family investigations. Our findings support the association of karyomegaly and interstitial nephritis as a distinct entity. Typical clinical features are asymptomatic progressive renal failure in the third decade of life and recurrent infections, mostly of the upper respiratory tract. Histologic alterations consist of markedly enlarged and hyperchromic nuclei in many tubular epithelial cells throughout the nephron accompanied by interstitial fibrosis in the surrounding atrophic tubules. Karyomegaly is not limited to the kidneys. In one case, autopsy revealed karyomegaly in epithelial and mesenchymal cells of many other organs. However, no association of karyomegaly with further histologic damage is evident except in the kidneys. Because of the familial clustering, karyomegalic interstitial nephritis seems to be an inherited disease. Examination of the nuclear proliferation-associated structures proliferating cell nuclear antigen/cyclin, Ki 67, and p53 suggests an inhibition of mitosis in karyomegalic cells. The finding of the same HLA haplotype, A9/B35, in four of six HLA-typed cases suggests the possibility of a genetic defect on chromosome 6, which is inherited and linked to the HLA locus.

Adult↗

PubMed1992

[A case of acute interstitial nephritis and nonoliguria acute renal failure induced by cimetidine].

Cimetidine is a histamine H2-receptor antagonist. Widely it is prescribed, and then various side effects have been increasingly recognized. Acute renal failure as a result of acute interstitial nephritis is one of the most important adverse effect. We report a case of biopsy-proven acute interstitial nephritis following cimetidine therapy. Farther more, we review other reported cases of cimetidine-induced acute interstitial nephritis, and discuss the clinical features and a role of immunological mechanisms of these cimetidine-induced disorders. A 52-year-old woman was admitted because of fever and protenuria. A month before admission, she developed gastric ulcer and was given cimetidine 600mg orally a day by a near physician. Laboratory data on admission included the following: white blood cell count, 14700/microliters; eosinophils, 6%; BUN, 50.7mg/dl; Cr, 7.6mg/dl; CRP, 34.0mg/dl. All drugs were discontinued because we suspected drug-induced acute renal failure, especially by cimetidine. Renal biopsy performed on day 3 showed interstitial nephritis with lymphocyte infiltration which was composed mainly of T cell. T4/T8 ratio was determined to be 1. There was neither predominance of helper nor cytotoxic cells in T cell subpopulation. We reviewed 22 cases reported and discussed the features of cimetidine-induced interstitial nephritis. The most important thing is to monitor renal function periodically with the suspicion of this disorder. On the detection of abnormality of laboratory data, cimetidine should be discontinued.

Acute Kidney Injury↗

PubMed1983

Drug-induced acute interstitial nephritis with granulomas.

To shed more light on the immunopathogenesis of drug-induced acute interstitial nephritis, a combined histologic, immunopathologic, and ultrastructural study of renal biopsy specimens from nine patients with drug-induced renal disease was performed. None of the patients had pre-existing renal disease or evidence of sarcoidosis or tuberculosis. The principal drugs included a hydrochlorothiazide-triamterene combination (Dyazide), hydrochlorothiazide, fenoprofen, and furosemide and triamterene. Renal insufficiency developed approximately four to ten weeks after initiation of drug therapy. In all cases, withdrawal of the drug(s) with or without steroid therapy resulted in restoration of normal or near-normal renal function. Histologically, all biopsy specimens showed acute interstitial nephritis characterized by an intense but patchy mononuclear cell interstitial infiltrate consisting of lymphocytes, monocytes, and plasma cells, modest numbers of eosinophils, patchy tubular atrophy, interstitial edema, and normal glomeruli. All biopsy specimens contained interstitial (and, in two cases, perivascular) non-caseating granulomas, which were numerous in one case, moderate in four cases, and rare in the remainder. Direct immunofluorescence was negative for IgG, IgM, IgA, C1q, C4, and C3 along glomerular and tubular basement membranes. Immunoperoxidase staining for lysozyme (performed in three cases) demonstrated many positive cells in the infiltrate. In two cases in which granulomas were present in prepared sections, the epithelioid and multinucleated giant cells did not stain for lysozyme. Electron microscopy of the granulomas in two cases revealed that the epithelioid and giant cells had "secretory" features characteristic of hypersensitivity granulomas. These findings provide further evidence for the participation of cell-mediated immunity in the pathogenesis of at least some cases of drug-induced acute interstitial nephritis.

Adult↗

PubMed1981

Megalocytic interstitial nephritis, xanthogranulomatous pyelonephritis, and malakoplakia. An ultrastructural comparison.

Light-microscopic and ultrastructural examinations of megalocytic interstitial nephritis, xanthogranulomatous pyelonephritis, and malakoplakia of the kidney were compared. The cases of megalocytic interstitial nephritis and xanthogranulomatous pyelonephritis represent the first reported electron-microscopic studies on human kidney of these diseases. The study confirmed the presence of a polymorphous cellular infiltrate with predominate histiocytes containing crystalloid material in the case of megalocytic interstitial nephritis; a polymorphous cellular infiltrate with histiocytes predominating in the case of xanthogranulomatous pyelonephritis; and macrophages containing Michaelis-Gutmann bodies in the case of malakoplakia. The characteristic sites of involvement within the kidney by each of the three lesions are discussed. It is believed that the lesions are distinct entities, but related to one another, and represent varied and unusual host responses to inflammation.

Female↗

PubMed2004

[Acute interstitial nephritis associated to lamotrigine use. Report of one case].

Acute interstitial nephritis is a mononuclear and sterile inflammation of the renal interstice caused by drugs, infections or immune phenomena. The clinical presentation is characterized by the triad of rash, fever and eosinophilia. We report a 32 years old man, in treatment with lamotrigine for depression, admitted to the hospital due to fever, abdominal pain, jaundice, cutaneus rash and malaise. Due to an oliguric renal failure of acute onset, a renal biopsy was done. The pathological study showed a granulomatous acute interstitial nephritis. He was started on hemodialysis and treated with cessation of the drug and corticosteroids, with complete recovery of the renal function.

Acute Disease↗

PubMed1954