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Results for “NEPHRITIS, INTERSTITIAL”

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PubMed1988

Characterization of a renal tubular epithelial cell line which secretes the autologous target antigen of autoimmune experimental interstitial nephritis.

Proximal tubular epithelial cells from mice which develop autoimmune interstitial nephritis were found to express the nephritogenic target antigen, 3M-1. Anti-3M-1 mAbs (alpha 3M-1-Ab) were used to positively select for 3M-1-secreting tubular epithelium and, after stabilization in culture, this new cell line (MCT) was examined for the production of several moieties important to either immune interactions or to the development of extracellular matrix. Alkaline phosphatase-staining MCT cells also express epithelial growth factor receptors with a Kd of 0.87 nM and an epithelial growth factor receptor constant (Ro) of 2.1 X 10(4) receptors/cell. MCT culture supernatants contain greater amounts of laminin, and types IV and V procollagens compared to types I and III procollagens, and growing MCT cells on type I collagen matrix causes them to preferentially secrete even more type IV and V procollagen. The 30,000-Mr 3M-1 antigen could be immunoprecipitated from biosynthetically labeled MCT cell supernatants with alpha 3M-1-Ab. An identical-sized moiety was isolated by immunoaffinity chromatography from collagenase-solubilized mouse kidney tubular basement membranes. The 3M-1 antigen can be found on the MCT cell surface by radioimmunoassay, or deposited in a linear array in the extracellular matrix surrounding the MCT cells in culture by immunofluorescence. Mature messenger RNA species for both class I and class II major histocompatibility complex (MHC) molecules were detected by Northern hybridization, and their corresponding cell surface gene products were detected by cytofluorography of MCT cells stained with haplotype-specific antibodies. Both the cell surface 3M-1 and the small amounts of detected class II MHC molecules appear to be biologically functional, as MCT cells can support the proliferation of 3M-1-specific, class II MHC-restricted helper T cells in culture. These findings suggest that MCT cells provide all the necessary biological parameters for interfacing both as the target of a nephritogenic immune response, and as a potential source for new extracellular matrix which develops as a fibrogenic response to interstitial nephritis.

Animals↗

PubMed1978

Acute interstitial nephritis due to methicillin.

Fourteen patients are described with a syndrome of methicillin-induced interstitial nephritis. In all patients severe renal dysfunction developed with an average peak serum creatinine of 8 mg/100 ml. An increased total peripheral eosinophil count was found in all patients. All patients had sterile pyuria and each of nine patients studied by Wright's stain of urine sediment had marked eosinophiluria. These findings are suggestive of methicillin-induced interstitial nephritis, although proteinura was a variable finding in our patients. Eight of 14 patients in our study received prednisone therapy for their interstitial nephritis, and the time lapse between maximal and final base line serum creatinine levels was statistically less in the prednisone-treated compared to the nontreated groups. Clinical manifestations of this syndrome are discussed, and the light and electron microscopic and immunofluorescent findings on renal biospy are described.

Adult↗

PubMedDate not supplied

BK polyomavirus interstitial nephritis in a renal allograft recipient.

Human polyomavirus (PV) interstitial nephritis has recently been recognized as a cause of severe renal allograft dysfunction. It occurs in immunosuppressed patients after reactivation of the latent virus PV type BK (BK virus) in the renal epithelium. BK disease is defined as a morphologically manifest renal infection with cytopathic signs accompanied by varying degrees of interstitial inflammatory cell infiltrates and functional impairment. It is also identified by the presence of cells containing viral inclusion bodies (decoy cells) in the urine. The authors report a case of BK PV interstitial nephritis in a 36-year-old renal allograft recipient. Under light microscopy the chief diagnostic indicator was detection of intranuclear viral inclusions, which were found exclusively in tubular epithelial cells. Cells with viral changes were often enlarged with nuclear atypia and chromatin basophilia. Widespread interstitial plasma cell infiltrates associated with tubulitis were present. Intranuclear paracrystalline arrays of virus particles 35-38 nm in diameter were present as characteristic ultrastructural indicators. Urine samples revealed decoy cells with ground-glass-type intranuclear inclusions positive for BK virus by electron microscopy.

Adult↗

PubMed1994

T cells reactive to an inducible heat shock protein induce disease in toxin-induced interstitial nephritis.

T cells reactive against immunodominant regions of inducible heat shock proteins (HSPs) have been identified in the chronic inflammatory lesions of several experimental autoimmune diseases. Since HSPs are known to be induced by a number of renal tubular epithelial cell toxins associated with chronic interstitial nephritis, we investigated the relevance of HSP expression and T cell reactivity to HSP70 in a model of progressive inflammatory interstitial nephritis. Chronic administration of cadmium chloride (CdCl2) to SJL/J mice induces HSP70 expression in renal tubular cells 4-5 wk before the development of interstitial mononuclear cell infiltrates. CdCl2 also induces HSP70 expression in cultured tubular epithelial cells from SJL/J mice. CD4+, TCR-alpha/beta+ T cell lines specific for an immunodominant HSP peptide are cytotoxic to heat stressed or CdCl2-treated renal tubular cells. Such HSP-reactive T cells mediate an inflammatory interstitial nephritis after adoptive transfer to CdCl2-treated mice at a time when immunoreactive HSP70 is detectable in the kidneys, but before the development of interstitial mononuclear cell infiltrates. T cells isolated from the nephritic kidneys of mice treated with CdCl2 for 13 wk are also cytotoxic to heat shocked or cadmium-treated tubular cells. These kidney-derived T cells additionally induced interstitial nephritis after passive transfer, indicating their pathogenic significance. Our studies strongly support a role for HSP-reactive T cells in CdCl2-induced interstitial nephritis and suggest that the induction of HSPs in the kidney by a multitude of "non-immune" events may initiate or facilitate inflammatory damage by HSP-reactive lymphocytes.

Amino Acid Sequence↗

PubMed1990

[Chronic interstitial nephritis in cattle with cardiomyopathy].

We tried to characterize the chronic interstitial nephritis as it occurs in bovine cardiomyopathy (CMP). For that reason conventional analysis methods were applied to urine of healthy and CMP-diseased cattle. With all the sick animals used for this study a nephritis of the mentioned type was diagnosed pathologically. By discriminant analysis of our data we were able to show, that the chronic interstitial nephritis due to CMP was best described by the variables protein (precipitation by heat), renal epithelial cells and leukocytes. In 73% of all the affected cattle one or more variables were changed pathologically to a minor to moderate degree. In the remaining 27% they were within the normal range. A possible microhematuria was secondary. Using identification analysis all the healthy animals and 69% of the diseased ones were made out correctly. As a consequence of this study we conclude, that further methods are necessary in order to recognize the different forms of nephritis more reliably.

Animals↗

PubMed2000

Familial interstitial nephritis with progressive renal failure.

We describe a 53-year-old woman with chronic interstitial nephritis and asymptomatic impairment of renal function. Seven members of her family were suffering from renal failure and underwent hemodialysis. At the time of their hospital admissions, they had shown evidence of end-stage renal failure at 40 to 50 years of age. Lack of proteinuria, hematuria, hypertension, hyperuricemia, hearing loss, and visual impairment were present before the deterioration of the renal function. Renal biopsy of the presented case indicated chronic interstitial nephritis without glomerular basement membrane abnormalities. Progressive decline of renal function and the inheritance pattern of autosomal dominance in this family suggested the diagnosis of familial interstitial nephritis.

Female↗

PubMed1996

Mesalazine-associated interstitial nephritis.

BACKGROUND: When used for oral treatment of inflammatory bowel disease, Asacol (a coated form of mesalazine = 5-aminosalicylic acid) can cause interstitial nephritis. The spectrum of severity, frequency of occurrence and the best renal function test to detect this complication are not known. The value of immunosuppression in addition to drug withdrawal is similarly undetermined. METHODS: Four cases of interstitial nephritis which occurred in association with oral Asacol treatment are presented and a further 12 cases who received similar treatment are reviewed. Clinical trials published previously were scrutinized to assess the frequency of impaired renal function. RESULTS: The available evidence suggests that renal impairment of any severity may occur in up to 1 in 100 patients, but that clinically significant interstitial nephritis occurs in less than 1 in 500 patients. This is most reliably detected by an elevated serum creatinine concentration. If the diagnosis of nephrotoxicity is delayed until 18 months after commencement of medication, restoration of renal function, which is seen on withdrawal of medication alone up to 10 months, does not occur and there is no evidence to date to indicate that addition of immunosuppression confers any significant advantage at this later stage. CONCLUSIONS: It is suggested that serum creatinine concentration should be measured each month for the first 3 months of treatment, 3-monthly for the remainder of the first year and annually thereafter. The use of concurrent immunosuppressive therapy may necessitate extension to the period of intensive monitoring. Any elevation of serum creatinine which cannot be related to a relapse of inflammatory bowel disease should prompt immediate withdrawal of Asacol and related medications and substitution of alternative therapy. Neither the lack of urinary abnormalities on routine testing nor the absence of clinical or laboratory features of drug allergy can be relied upon to rule out interstitial nephritis during oral therapy with these drugs.

Administration, Oral↗

PubMed2002

Indinavir-associated interstitial nephritis and urothelial inflammation: clinical and cytologic findings.

The objective of the present study was to characterize the genitourinary syndromes that accompany indinavir-associated pyuria. Of 23 indinavir-treated patients with persistent pyuria, 4 had isolated interstitial nephritis, 10 had both interstitial nephritis and urothelial inflammation, 7 had isolated urothelial inflammation, and 2 had pyuria with nonspecific urinary tract inflammation. A total of 21 patients had multinucleated histiocytes identified by cytologic testing of urine specimens. Urine abnormalities resolved in all 20 patients who stopped receiving indinavir therapy. Pyuria continued in the 3 patients who continued receiving indinavir. Six patients had elevated serum creatinine levels, which returned to baseline levels when indinavir was discontinued. In conclusion, indinavir-associated pyuria was frequently associated with evidence of interstitial nephritis and/or urothelial inflammation, multinucleated histiocytes were commonly present in urine specimens, and cessation of indinavir therapy was associated with prompt resolution of urine abnormalities.

Adult↗

PubMed1989

Granulomatous interstitial nephritis after a jejunoileal bypass: an ultrastructural and histochemical study.

We present a case of granulomatous interstitial nephritis and renal failure after a jejunoileal bypass for obesity. Improvement of the renal function occurred after reversal of the intestinal bypass. The renal biopsy showed an interstitial nephritis, oxalate crystal deposition and several aggregates of multinucleated giant cells related to the crystal material (granulomatous reaction). By ultrastructural and histochemical studies we demonstrated mitochondrial alterations in the tubular epithelial cells, and we suggested the proximal tubule origin of the giant cells. The association of the oxalate crystals with damaged tubules and giant cells suggests that the oxalate crystals are responsible for these alterations. The possibility of an associated immunological process as the cause of the interstitial nephritis cannot be excluded.

Acute Kidney Injury↗

PubMed1995

[Recent advances of studies on interstitial nephritis--definition and pathogenesis].

An abbreviated history describing our understanding of the interstitial nephritis was outlined in the present report. Interstitial nephritis has been recognized with increasing frequency. This nephritis is a diverse group of renal disorders in which the predominant morphologic changes occur in the interstitium included tubules. Recent explosive advances in immunological studies and molecular biological techniques have greatly expanded a study on the mechanisms of interstitial fibrosis.

Collagen↗

PubMed1993

A syndrome of acute interstitial nephritis and anterior uveitis.

A syndrome of acute interstitial nephritis (AIN) and anterior uveitis is described in two children and the literature is reviewed. These disorders appear to improve, in uncontrolled studies, with systemic and topical ophthalmic corticosteroid treatment. Although the renal and ocular prognoses appear good, it is important to recognize that patients with AIN are at risk for uveitis and if present, consultation with an ophthalmologist is recommended.

Acute Disease↗

PubMed1985

Tubular antigen-derivatized cells induce a disease-protective, antigen-specific, and idiotype-specific suppressor T cell network restricted by I-J and Igh-V in mice with experimental interstitial nephritis.

The nephritogenic effector T cell response producing interstitial nephritis in mice can be largely inhibited by the adoptive transfer of suppressor T cells before or after the induction of disease. These suppressor T cells are harvested from donor mice primed with tubular antigen-derivatized syngeneic lymphocytes, and two subsets of suppressor cells can be characterized within this donor cell population. The first suppressor cell in this network is an L3T4+, I-J+, RE-Id+ cell (Ts-1). Ts-1 cells are antigen-binding suppressor cells that inhibit afferent phase immune responses and, in the presence of tubular antigen, specifically induce Lyt-2+, I-J+ cells (Ts-2) that are antiidiotypic (RE-Id-binding) suppressors. The Ts-2 cell is functionally restricted in its suppressive effect by I-J and Igh-V gene products, and acts on the effector limb of the cell-mediated anti-tubular basement membrane immune response. These studies provide an experimental basis for further efforts to use immunoregulatory modulation in the control of autoimmune renal disease.

Animals↗

PubMed1998

Probable diltiazem-induced acute interstitial nephritis.

OBJECTIVE: To describe a case of acute interstitial nephritis (AIN) probably related to administration of diltiazem. CASE SUMMARY: A 53-year-old white man presented to the hospital experiencing abdominal pain radiating to both renal fossae, as well as dysuria. Diltiazem and atenolol had been prescribed to treat an episode of precordial pain associated with effort. An erythematous maculopapular rash developed approximately 2 hours after administration of a single dose of diltiazem, and acute renal failure, associated with elevated liver function test results, developed 6 days later. DISCUSSION: To the best of our knowledge, this is the third reported case of acute renal failure believed to be induced by diltiazem. In all cases, there was an obvious temporal relationship between administration of diltiazem and the onset of acute renal failure. Previous reports failed to discuss a probable pathogenic mechanism. AIN is the most likely etiology of acute renal failure in our patient. Favorable resolution with no relapse, the presence of the skin rash, and the liver sequelae suggest a common immunoallergic mechanism. CONCLUSIONS: Healthcare professionals should consider diltiazem-induced AIN in the differential diagnosis of a patient taking diltiazem who develops acute renal failure.

Acute Disease↗

PubMed1998

Vancomycin-induced acute interstitial nephritis.

OBJECTIVE: To report a case of acute interstitial nephritis (AIN) related to administration of vancomycin for the treatment of Staphylococcus aureus sternal wound infection, osteomyelitis, and infective endocarditis. CASE SUMMARY: Reports in the literature regarding vancomycin-induced AIN are scarce. We describe the fifth known case of AIN, in a 64-year-old white man who developed fever, maculopapular rash, acute renal failure, eosinophilia, and eosinophiluria after approximately 1 month of vancomycin treatment. The results of the renal biopsy were consistent with an allergic drug reaction. Four months after his initial episode of AIN, the patient was rechallenged with vancomycin for the treatment of S. aureus septic arthritis. One day after initiation of vancomycin, serum eosinophils started to rise, his urine tested positive for eosinophils, but his serum creatinine remained stable. CONCLUSIONS: Our case report and others from the literature suggest vancomycin causes allergic AIN. Clinicians should be aware of this adverse effect in an era of increasing use of vancomycin for treatment of resistant gram-positive organisms.

Acute Disease↗

PubMed1986

Urinary indices in acute interstitial nephritis.

Nine patients with biopsy-proven acute interstitial nephritis (AIN) were analyzed for their urinary indices, determined on the basis of the first urinary sample upon admission, before any therapeutic intervention. Isosthenuria was present in all patients with a mean urinary osmolality of 283 +/- 48 mOsm/l and a urine/plasma osmolality ratio of 0.9 +/- 0.1. Urinary sodium was more than 40 mEq/l in 8 out of the 9 patients studied. The other urinary indices studied were indicative for both prerenal and intrinsic renal disease.

Acute Disease↗

PubMed2000

Acute interstitial nephritis and fatal Stevens-Johnson syndrome after propylthiouracil therapy.

We report a case of acute interstitial nephritis and fatal Stevens-Johnson syndrome in a 90-year-old woman with amiodarone-induced hyperthyroidism, who had been treated for 5 weeks with propylthiouracil (PTU). On admission, the patient exhibited acute renal failure and generalized macular purpuric eruption. Acute interstitial nephritis and Stevens-Johnson syndrome were diagnosed and PTU withdrawn. Although renal function recovered after PTU withdrawal and corticosteroid therapy, the patient's condition worsened, and she died after developing multiple organ failure. Acute interstitial nephritis seems to be rarely associated with PTU therapy. Moreover, a literature review suggested that this could represent the first published report of a Stevens-Johnson syndrome developing during PTU therapy.

Acute Disease↗

PubMed2006

Granulomatous interstitial nephritis: a clinicopathologic study of 46 cases from a single institution.

Acute interstitial nephritis is commonly seen in kidney biopsies of patients with acute renal failure; however, granulomatous interstitial nephritis (GIN) is rare. We identified 46 cases of GIN in a 17-year period in this institution and we investigated their most probable etiologies. Complete clinical information was available in 38 patients. Seventeen of 38 patients (44.7%) were classified as drug-induced. Renal sarcoidosis was responsible for 28.9% of cases, and the remaining 15.9% of cases included Wegeners granulomatosis, foreign body giant cell reaction, GIN secondary to intravesical bacillus Calmette-Guérin therapy for bladder cancer, and xanthogranulomatous pyelonephritis. Clinical investigation failed to reveal possible etiology in 4 patients (10.5%), classified as idiopathic. We concluded that three quarters of our cases were either drug-induced or due to sarcoidosis; only a small proportion of our cases occurred secondary to any other cause or to unknown factors.

Acute Disease↗

PubMed2006

Light-chain-mediated acute tubular interstitial nephritis: a poorly recognized pattern of renal disease in patients with plasma cell dyscrasia.

CONTEXT: Acute renal failure may be the first clinical presentation in patients with plasma cell dyscrasia. Recognition of the unusual interstitial inflammatory lesion associated with monoclonal light chains and renal failure described herein is important to guide clinicians in requesting appropriate tests to confirm plasma cell dyscrasia and providing adequate treatment. OBJECTIVE: To describe an unusual pattern of tubular interstitial nephritis in patients with underlying plasma cell dyscrasia characterized by an interstitial inflammatory reaction associated with deposition of light chains along tubular basement membranes. DESIGN: Eight cases of light-chain-mediated acute tubular interstitial nephritis were identified from the archives of 4296 kidney biopsy specimens. In all cases, routine light microscopic examination, direct immunofluorescence, and electron microscopic examination were performed. Ultrastructural immunogold labeling was performed in specimens with inconclusive findings and in specimens from patients with no clinical history of plasma cell dyscrasia. RESULTS: All patients presented with acute renal failure. Light microscopy revealed acute tubular interstitial nephritis. In some of the cases, direct immunofluorescence and electron microscopy failed to show definitive evidence of light-chain deposition along tubular basement membranes. Ultrastructural immunogold labeling aided the demonstration of monotypical light chains along some tubular basement membranes. No light chains were present in other renal compartments. CONCLUSIONS: Accumulation of light chains along tubular basement membranes may induce an interstitial process that mimics acute tubular interstitial nephritis. Recognition of this unusual pattern of renal disease in patients with plasma cell dyscrasia requires ancillary diagnostic techniques.

Acute Kidney Injury↗