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At least 865 records · Page 48Linked to original sources
PubMed1986

Idiopathic acute interstitial nephritis and uveitis in the adult. Report of 1 case and review of the literature.

In a 59-year-old female, concurrence of acute interstitial nephritis and uveitis was observed. While the clinical signs resolved after a few weeks, signs of renal tubular dysfunction persisted for 9 months, and creatinine clearance was still impaired (22 ml/min) more than 2 years after beginning of the symptoms. This is the 5th case of idiopathic interstitial nephritis with concomitant uveitis reported in adult patients. In contrast to the benign evolution observed in children, the renal function may remain impaired in adults.

Creatinine↗
PubMed2001

The prevalence of interstitial nephritis and leptospirosis in 283 raccoons (Procyon lotor) from 5 different sites in the United States.

A retrospective histopathological study was carried out on tissues of 283 raccoons from 5 different geographical locations for presence of interstitial nephritis and renal leptospirosis. Results of this study indicate that although interstitial nephritis was common in raccoons from all locations, the presence of renal leptospiral spirochetes was not.

Animals↗
PubMed1999

[Renal failure secondary to granulomatous interstitial nephritis as initial manifestation of sarcoidosis].

Sarcoidosis is a rare cause of renal failure and it has been associated with a wide spectrum of renal manifestations, including granulomatous interstitial nephritis. We present the case of a 48-year old male patient with rapidly progressive renal insufficiency due to sarcoid normocalcemic granulomatous interstitial nephritis who lacked the pulmonary signs of sarcoidosis. Prednisone therapy yielded a favorable outcome with fall in serum creatinine level and resolution of abnormalities of the urinary sediment.

Acute Kidney Injury↗
PubMed1998

Post-transplant neutrophilic interstitial nephritis--an important cause of graft dysfunction.

Post-transplant neutrophilic interstitial nephritis (NIN) is characterized by an interstitial infiltrate consisting of polymorphonuclear cells that leads frequently to acute graft dysfunction. In 220 graft biopsies performed because of renal dysfunction over 2 years in our unit, 11 (5%) diagnoses of NIN were made. Only two patients had chronic pyelonephritis as original disease. Four patients had urological problems before transplantation. After transplantation, five patients had urinary tract infection, one had urethral stenosis, two had vesicourethral reflux and one patient had a perinephritic abscess. Seven patients had fever (63%). Only in six patients did urine culture lead to microorganism isolation. After 6 months, only two patients had a serum creatinine level < 1.4 mg/dl, five patients had abnormal function, three had lost their grafts, and one patient had died with sepsis. We conclude that 5% of the biopsies performed in our center disclosed NIN, an entity that causes graft dysfunction and progresses frequently to chronic renal failure. In some cases, no infectious etiology could be detected.

Female↗
PubMed2002

Interstitial nephritis, acute renal failure in a patient with non-fulminant hepatitis A infection.

This is the first report from Norway of a patient with interstitial nephritis and renal failure due to non-fulminant hepatitis A virus (HAV) infection. HAV infection was confirmed by positive anti-HAV IgM serology. All tests for other virus infections were negative. At admittance serum creatinine (s-Creat) and blood urea nitrogen (BUN) concentration were 539 microlmol/l and 32.6 mmol/l increasing the following days to 890 micromol/l and 39.9 mmol/l, respectively. Nine courses of hemodialysis had to be given. Kidney biopsy specimen showed interstitial edema, lymphocytic cell infiltration and acute tubular injury with normal glomeruli. Examination with immunohistochemistry was negative. In contrast to the findings associated with HBV and HCV infection in which glomerular disease is predominantly found, the HAV infection in our patient was associated with interstitial nephritis and acute tubular necrosis. The prognosis of the renal failure due to HAV infection was good although the recovery was substantially delayed.

Acute Kidney Injury↗
PubMed1980

Acute interstitial nephritis associated with gentamicin and lincomycin therapy.

A case of acute oliguric renal failure following gentamicin and linocomycin therapy is described. Renal biopsy showed an acute interstitial nephritis. This was associated with high serum gentamicin levels and the later development of ototoxicity. Withdrawal of antibiotics and conservative measures was followed by rapid recovery of renal function. Attention is drawn to the association between gentamicin and lincomycin therapy and the development of an acute interstitial nephritis.

Acute Disease↗
PubMed1986

Acute interstitial nephritis and non-oliguric renal failure after cefaclor treatment.

A case of acute interstitial nephritis (AIN) developing after cefaclor treatment is reported. Diagnosis was proofed by kidney biopsy and lymphocyte transformation test. The clinical course of the patient with non-oliguric renal failure was favourable. Four weeks after discontinuation of cefaclor treatment the renal function was completely restored and remained stable over the ten-month follow-up period. It is concluded that cefaclor can cause hyperallergic AIN and acute renal failure.

Acute Kidney Injury↗
PubMed1996

Heterogeneous T cell receptor V beta gene repertoire in murine interstitial nephritis.

Anti-tubular basement membrane disease (alpha TBM) produces T cell-mediated interstitial nephritis in SJL/J mice following immunization with heterologous renal tubular antigen. Initial mononuclear infiltrates appear in vivo after six to eight weeks, with subsequent progression to renal fibrosis and endstage kidney disease. Cultured lymph node derived nephritogenic T cells from these mice react to a small epitopic region of the 3M-1 target antigen and share a common amino acid motif in their V beta CDR3 regions. We now have used RT-PCR to further characterize the renal expression of T cell receptor (TcR) V beta gene repertoires during the course of this disease. Individual kidneys with focal mononuclear infiltrates characteristic of early alpha TBM disease express up to three different TcR V beta genes; however, the same V beta genes are not found in all kidneys at the same early stage of injury. DNA sequencing of the V beta RT-PCR products reveals a heterogeneous population of VDJ recombinations and deduced CDR3 amino acid sequences. Our studies do not support TcR V beta region gene restriction in histologically-detectable alpha TBM disease, but are more consistent with a dynamic, organ-specific autoimmune disease, directed at multiple autoantigenic epitopes.

Amino Acid Sequence↗
PubMed1983

[Acute interstitial nephritis caused by drugs].

Within 30 months the diagnosis of drug-induced acute interstitial nephritis was made in ten patients with acute onset of renal failure of clinically unknown cause. Allergenic substances were discovered to be antibiotics, pyrazol and indol derivatives, piromidic acid and chlorazanil. In contrast to the known course of methicillin nephritis the clinical signs were undramatic. Non-oliguric renal failure predominated, sometimes with leucocyturia, microhaematuria and moderate proteinuria. Intermittent haemodialysis was necessary in half the cases. Renal function developed favourably without further specific treatment, however, plasma creatinine did not return to normal levels in most cases. Percutaneous renal biopsy was the definitive diagnostic step. Indications for biopsy in cases of unclear acute renal failure should thus be handled liberally in order to prevent continued drug exposure with the danger of irreversible renal failure.

Acute Disease↗
PubMed1997

Autoantibodies against a kidney--liver protein associated with quinolone-induced acute interstitial nephritis or hepatitis.

In the present study we report on four cases of acute interstitial nephritis (AIN) and two cases of hepatitis induced by quinolone. We show by immunoblotting analysis that all sera from these patients contained autoantibodies that recognize a 65-kDa protein expressed in normal human kidney and liver microsomes. Only 6% of sera from healthy individuals who did not ingest quinolone recognized the same protein. These findings suggest that the presence of autoantibodies could be used as a sensitive marker and that a modification of microsomal proteins by quinolone itself or by a metabolite could generated an autoimmune response.

Acute Disease↗
PubMed1995

Acute interstitial nephritis and uveitis with bone marrow granulomas and anti-neutrophil cytoplasmic antibodies.

Acute interstitial nephritis (AIN) and uveitis of unknown etiology developed in a 15-year-old girl. Symptoms and urinary abnormalities improved spontaneously but moderate renal dysfunction and anterior uveitis persisted. A repeat biopsy performed 2 years later showed focal tubulointerstitial changes, while bone marrow examination revealed granulomas. Simultaneously, antineutrophil cytoplasmic antibodies (ANCA) were detected, and decreases in T cell population and lymphocyte function were found. These immunological abnormalities normalized in parallel with clinical improvement with corticosteroid therapy, strongly suggesting that in some patients autoimmune disorders contribute to the pathogenesis of the disease.

Acute Disease↗
PubMed1976

Role of sensitized cells in antitubular basement membrane interstitial nephritis.

The pathogenic effect of antitubular basement membrane (TBM) antibodies in anti-TBM interstitial nephritis has been demonstrated. To determine the relative role of sensitized cells in inducing this lesion, lymph node cells (LNC) alone or a combination of LNC and peritoneal exudate cells were transferred from Brown Norway (BN) rats, previously immunized with TBM into unimmunized BN-recipient rats. Cells were transferred directly under the recipients' renal capsules. Although significant tubular lesions were induced by the cells, the lesions were usually mild and always focal. Hence, sensitized cells do not appear to be central to the pathogenesis of anti-TBM nephritis.

Animals↗
PubMed2004

Acute interstitial nephritis due to cefoperazone.

OBJECTIVE: To describe a case of cefoperazone-induced acute interstitial nephritis (AIN) in which the diagnosis was supported by renal biopsy. CASE SUMMARY: A 35-year-old woman presented to our hospital with decreased urine output and no past history of renal problems. Fifteen days prior to presentation, she had started treatment with intramuscular cefoperazone 1 g/day for a scalp infection. On day 12 of therapy, the patient noted decreased urine output, anorexia, and weakness, but she continued taking cefoperazone for 3 more days. Hemodialysis and oral prednisolone 1 mg/kg (30 mg twice daily) were started. Renal function returned to normal after 2 months of prednisolone treatment. DISCUSSION: Although AIN has been linked with other cephalosporins, as of June 18, 2004, to our knowledge, this is the first report of a cefoperazone-induced case. We based our diagnosis on the features of acute-onset renal failure, abnormal urinalysis findings, eosinophilia, inflammatory infiltrate in the interstitium, and recovery from renal failure after initiation of corticosteroid treatment. Application of the Naranjo probability scale indicated a probable relationship between the acute renal failure secondary to the possible AIN and cefoperazone therapy in this patient. CONCLUSIONS: This case indicates that cefoperazone, like other cephalosporins, can cause AIN. We recommend close monitoring of renal function in patients who are prescribed this drug.

Acute Disease↗
PubMed1986

[Acute interstitial nephritis following the use of gentamycin].

The authors describe a patient that developed acute interstitial nephritis after gentamycin administration. The disease progressed with general lassitude, subfebrile temperature, oliguria, and increased nitrogen bodies in blood. After a short oliguric stage, polyuria followed and the renal function was completely normalized one month after the onset of the disease.

Acute Disease↗
PubMedDate not supplied

[Acute interstitial nephritis induced by loratadine].

Loratadine is a second generation histamine H1 receptor antagonist, that has high potency antiallergic properties and is associated with low adverse effects compared with other antihistamines. Acute interstitial nephritis is a cause of acute renal failure that is most often induced by drugs or, less frequently, infection or sarcoidosis. Although the number of drugs associated with acute intersticial nephritis is too large, the antihistaminic loratadine have never been reported before. We report a case of an interstitial nephritis with acute renal failure that suggesting hypersensitivity reaction in a 77 old man who had received loratadine (10 mg/day) during ten days before his assessment to our hospital by disseminated pruritic syndrome. The initial suspect was rapidly progressive glomerulonephitis and renal biopsy was practice and treatment with corticosteroids were initiated (prednisone bolus of 500 mg three days and 1 mg/kg/day/later). The loratadine therapy was cessation. He exhibiting a slow and progressive improvement on renal function and one month later, urea and creatinine levels was normal and hematuria and proteinuria had disappeared. The corticosteroids therapy were progressive decreased until withdrawal. We think that this is an interesting case, basing in its clinical presentation and that it had never been reported before.

Acute Disease↗
PubMed1999

Nephrotic syndrome and acute interstitial nephritis associated with the use of diclofenac.

Commonly reported renal complications of non-steroidal anti-inflammatory drugs (NSAID) include acute renal failure and/or acute interstitial nephritis; in rare cases a nephrotic syndrome was also observed. In most cases this was due to the development of secondary membranous nephropathy. Following withdrawal of the drug the nephrotic syndrome usually resolved rapidly. We report a 65-year-old woman who developed a nephrotic syndrome and acute renal failure during 6 months of treatment with the NSAID diclofenac. Renal biopsy revealed both, membranous nephropathy and interstitial nephritis. After discontinuation of diclofenac and treatment with prednisone 1 mg/kg/day, furosemide 400 mg/day and simvastatin at a dose of 20 mg/day, creatinine clearance gradually increased and after 5 months of treatment complete remission of the nephrotic syndrome was observed.

Acute Disease↗
PubMed1997

The syndrome of autoimmune interstitial nephritis and membranous nephropathy.

A 2-year-old male patient was evaluated for Fanconi syndrome with hypertension and failure to thrive. Renal biopsy revealed autoimmune interstitial nephritis with membranous nephropathy. The patient developed autoimmune hemolytic anemia and intractable diarrhea with villous atrophy of the jejunum. He progressed to end-stage renal disease and was transplanted without recurrent disease. Immune work-up done prior to immunosuppressive therapy showed marked elevation of IgE. Studies of T lymphocyte cytokine production showed normal production of interleukin-4 but depressed levels of interferon-gamma. The simultaneous occurrence of autoimmune interstitial nephritis and membranous nephropathy in a young male represents a unique syndrome. Abnormalities of T lymphocyte subpopulations and their cytokines may be involved in the pathogenesis of this disorder.

Autoimmune Diseases↗