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PubMed2001

Molecular genotyping of BK and JC viruses in human polyomavirus-associated interstitial nephritis after renal transplantation.

The human polyomaviruses BK virus (BKV) and JC virus (JCV) have been linked to ureteric stenosis and allograft interstitial nephritis, but molecular characterization of the species involved has not been performed. We studied paraffin-embedded renal tissue from 19 cases of allograft viral interstitial nephritis. Histological sections were subjected to polymerase chain reaction amplification using consensus, BKV-, and JCV-specific primers, with subsequent DNA sequencing for strain determination. BKV was present in all (100%) interstitial nephritis kidneys and placed in genotypes corresponding to serological groups I (n = 11), II (n = 1), and IV (n = 5). Fourteen of 17 isolates (82%) showed sequence variations in the viral capsid protein-1 (VP1) capsid region, with predicted changes in the encoded amino acids and sometimes with potential implications for the secondary and tertiary structure of the corresponding protein molecules. An additional case showed a previously reported glutamine-->leucine T-antigen region mutation. JCV was seen in seven interstitial nephritis kidneys (37%), with types 4 (n = 3), 3A (n = 2), and 2A (n = 1) identified. Most white individuals with asymptomatic infection are reported to shed type 1 JCV in the urine. Simian 40 polyomavirus was not identified in any case. These observations may have pathogenic relevance to the development of an extremely refractory form of polyomavirus interstitial nephritis seen after kidney transplantation.

Amino Acid Sequence↗

PubMed1993

Acute interstitial nephritis. Why do the kidneys suddenly fail?

Acute interstitial nephritis is a clinical and pathologic entity with diverse causes. The most common cause at present is reaction to drug use, but infection, a concomitant uveitis syndrome, and other rare causes have been reported. Acute interstitial nephritis should always be considered in a patient with acute renal failure, because it is a treatable cause that may result in interstitial fibrosis and irreversible disease if not arrested.

Acute Disease↗

PubMed2006

[A severe case of interstitial nephritis caused by sodium valproate].

A case of acute interstitial nephritis caused by sodium valproate is reported. The sodium valproate treatment was continued after initial diagnosis and the patient developed end-stage renal failure. After transplantation, interstitial nephritis was demonstrated in the renal graft.

Adult↗

PubMed1977

Spontaneous glomerulonephritis in dogs. II. Correlation of glomerulonephritis with age, chronic interstitial nephritis and extrarenal lesions.

A morphologic study of 103 dogs, including two with renal amyloidosis, showed that different types of diffuse glomerulonephritis are correlated with different age groups. Membranous and membranoproliferative glomerulonephritis were more common in middle-aged and older animals, whereas mesangial lesions were found predominantly in younger dogs and considered to be early glomerular changes. Glomerulonephritis largely occurred independently of interstitial nephritis. The incidence of interstitial lesions was 71%. Chronic interstitial nephritis was rare in dogs under 1 year old. Glomerulonephritis did not seem to induce interstitial nephritis. Glomerulonephritis occurred not only in kidneys with severe interstitial damage, but also in those with slight damage. The indicated that glomerulonephritis occurred independently of interstitial nephritis. In end-stage kidneys with severe fibrosis, mesangial changes seemed to predominate.

Age Factors↗

PubMed2004

Drug-induced tubulo-interstitial nephritis secondary to proton pump inhibitors: experience from a single UK renal unit.

BACKGROUND: Acute tubulo-interstitial nephritis (TIN) is an important cause of acute renal failure, and is often caused by hypersensitivity to drugs. The aim of this study was to determine the aetiology of interstitial nephritis among an unselected cohort of patients, and to identify those drugs commonly implicated. METHODS: A single-centre retrospective analysis was carried out of renal biopsy results from 296 consecutive patients between 1995 and 1999. RESULTS: Acute TIN was identified in 24 (8.1%) biopsies. Eight out of 14 cases with presumed drug-related TIN could be attributed to the proton pump inhibitors omeprazole and lansoprazole. The two cases of lansoprazole-associated TIN are the first to be reported with this drug. The presentation and favourable response to treatment of these patients are described. CONCLUSION: Drugs are the most common cause of interstitial nephritis in the population studied. Those drugs most commonly associated with interstitial nephritis were the proton pump inhibitors omeprazole and lansoprazole.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed1983

Chronic interstitial nephritis associated with gold therapy.

A patient suffered chronic interstitial nephritis after receiving large quantities of gold salts for rheumatoid arthritis. Gold deposits were seen with transmission electron microscopy and confirmed by microprobe x-ray analysis both within renal tubular epithelial cells and interstitial macrophages and free within the renal interstitium. Clinical resolution of renal failure followed discontinuation of therapy with gold salts. Probable mechanisms of injury to renal tubular epithelial cells include uptake of gold by tubular epithelial cells and incorporation of gold into mitochondria, with subsequent cellular injury; interstitial deposits probably occur after necrosis of tubular epithelial cells, with release of gold into the interstitium and resultant inflammation. Thus, chronic interstitial nephritis can be added to the patterns of renal injury seen after gold therapy for rheumatoid arthritis.

Arthritis, Rheumatoid↗

PubMed1994

Albipunctatus retinopathy in inherited interstitial nephritis.

We describe here a patient with familial interstitial nephritis and albipunctatus retinopathy. Albipunctatus is often seen in patients with Alport syndrome, which is an X-linked disorder characterised in affected males by renal failure by the age of 25, high-tone sensorineural deafness, anterior lenticonus and albipunctatus. The diagnosis of Alport syndrome depends on the electron microscopic appearance of a trabeculated glomerular basement membrane (GBM); and mutations have been demonstrated in the gene for the alpha 5 chain of type IV collagen. In the familial interstitial nephritis described here, the inheritance was autosomal dominant, renal failure developed in middle age, and there was no associated hearing loss or anterior lenticonus. The finding of albipunctatus retinopathy in this patient suggests that the genetic mutation responsible involves a protein common to both retinal and interstitial basement membranes. In addition, we conclude that the demonstration of albipunctatus in an individual with familial nephritis does not necessarily indicate that the underlying disease is Alport syndrome.

Basement Membrane↗

PubMed1999

Clozapine-induced acute interstitial nephritis.

Drug hypersensitivity reactions commonly cause acute interstitial nephritis (AIN). Clozapine, a new antipsychotic, can cause fatal bone-marrow toxicity. We report clozapine-induced AIN as another serious adverse drug reaction.

Acute Disease↗

PubMed1999

New insights into the pathogenesis of interstitial nephritis.

Emerging data on the role of interstitial inflammation in progressive renal disease are redefining our understanding of the pathogenic mechanisms of chronic kidney damage. Recent experimental evidence emphasizes the role for both immune and non-immune mechanisms in interstitial nephritis. New observations regarding maneuvers that downregulate such injurious renal responses may direct further studies that develop new therapeutic modalities.

Angiotensin II↗

PubMed2005

Adjuvant low-dose cidofovir therapy for BK polyomavirus interstitial nephritis in renal transplant recipients.

BK virus interstitial nephritis (BKVIN) is a serious complication after kidney grafting, necessitating drastic reduction of immunosuppressive therapy in order to enable viral clearance. Despite these measures, progressive graft dysfunction and graft loss occur in the majority of recipients. We diagnosed BKVIN in 21 recipients grafted between 1998 and 2004. Eight of 21 patients were treated with weekly, adjuvant low-dose cidofovir in addition to reduction of immunosuppressive therapy. BKVIN caused irreversible deterioration of graft function in all patients but renal function stabilized after antiviral treatment (creatinine clearance: 51.8-32 mL/min; p=0.001) and no graft loss occurred in cidofovir-treated recipients during 24.8 (8-41) months follow-up. Peak serum cidofovir concentrations were dose-dependent and attained approximately one-tenth of thein vitroEC50 for cidofovir against BK-virus, while pre-treatment with probenecid did not alter peak serum concentrations nor affected the incidence of nephrotoxicity. In fact, no cidofovir-related renal toxicity occurred; few patients had minor transient side effects (nausea, skin rash). In contrast, 9 of 13 patient who received no adjuvant cidofovir therapy lost their graft after median 8 (4-40) months. In this selected group of recipients with BKVIN, the use of adjuvant low-dose cidofovir therapy resulted in prolonged graft survival and stabilized graft function.

Adult↗

PubMed1986

Anterior uveitis, a presenting symptom in acute interstitial nephritis.

Two adult women with idiopathic acute interstitial nephritis (AIN) whose presenting symptom was anterior uveitis are described. On histologic examination of the renal biopsy, eosinophilic infiltrates and mononuclear cells were found. Immunofluorescence was negative. Immunological evaluation showed a slight decrease in the number of T cells with a normal subpopulation ratio. AIN responded to steroid treatment.

Acute Disease↗

PubMed1971

Immunologic observations in canine interstitial nephritis.

Immunofluorescence studies in cases of chronic interstitial nephritis (CIN) in the dog demonstrated deposition of canine IgC and C'3 in the thickened capillary walls of the glomeruli and in the mesangium. Eluates obtained from the nephritic kidneys contained antibodies of IgG type and reacted with autologous or homologous nephritic kidneys but not with normal kidneys or with any normal canine tissue. The staining pattern of fluorescein-conjugated eluates was similar to that obtained with anti-canine IgG or anti-canine C'3. The eluates did not contain leptospiral antibodies. The findings indicate that complement-fixing immune complexes are deposited in the damaged glomeruli in CIN. The nature of the antigen involved in these complexes is unknown, but it does not seem to be a component of normal canine tissue and could thus be viral or bacterial.

Animals↗

PubMed1984

Murine interstitial nephritis. II. The adoptive transfer of disease with immune T lymphocytes produces a phenotypically complex interstitial lesion.

The present studies demonstrate that immune Thy-1.2+, Lyt-1.2+ T lymphocytes harvested from SJL mice with anti-tubular basement membrane disease can adoptively transfer interstitial nephritis into naive recipients. The lesions produced after cell transfer do not occur immediately but rather take 4 to 6 wk to fully develop. Interstitial lesions can also be transferred to a lesser degree and over a longer period of time with immune serum containing anti-tubular basement membrane antibodies. The fully formed lesions that developed after the transfer of immune cells or serum were phenotypically characterized by cell-surface antibodies using immunofluorescence. T lymphocytes, natural killer cells, macrophages, and Ig+ cells were all well represented in both lesions. Natural killer cells, however, were slightly more prevalent in the lesions of mice receiving immune serum. These experiments demonstrate a potential role for both immune T lymphocytes and anti-tubular basement membrane antibodies in the development of interstitial nephritis in mice. Unlike guinea pigs and rats, it is only in mice that interstitial lesions can be adoptively transferred with immune T lymphocytes, and as such, this model should prove very useful in the additional dissection of cellular interactions and immunoregulatory events that formulate the final effector mechanisms of disease expression.

Animals↗

PubMed2000

[Tubulo-interstitial nephritis and uveitis syndrome--TINU syndrome].

Acute tubulo-interstitial nephritis and uveitis (TINU syndrome) in a 53-year-old woman is reported. This rare syndrome was described 27 years ago by Dobrin et al. Since then about 50 cases have been described. The syndrome can appear at any age but most patients are under 20 years; about 75% are females. Clinical characteristics include fatigue, general malaise, weight loss, fever, night sweats, anorexia, nausea and vomiting, pallor, nocturia, polyuria, arthralgia and skin rash. Ocular involvement usually includes anterior uveitis but is sometimes posterior; in most cases the uveitis is bilateral. The characteristic laboratory findings are anemia, rapid sedimentation rate, decreased glomerular filtration rate with increased serum creatinine and urea. Total protein is increased because of polyclonal gammopathy and elevated beta 2-microglobulin. Urinalysis characteristically reveals proteinuria and beta 2-microglobulinuria. The histopathologic features on renal biopsy are characteristic of tubulo-interstitial nephritis. Uveitis can precede, accompany or follow onset of the nephropathy. The pathogenesis and etiology of the syndrome are as yet unknown. Treatment consists of large doses of corticosteroids, but the necessity for treatment is unclear, since there is evidence of spontaneous improvement. Although the prognosis of the nephropathy is favorable and most cases are reversible, the uveitis tends to recur.

Female↗

PubMed1984

[Acute interstitial nephritis and Meckel's diverticulum].

A case of acute haematogenous interstitial nephritis secondary to bacterial infection of a Meckel's diverticulum is reported. The incidence of acute infectious interstitial nephritis with a gastro-intestinal portal of entry is discussed.

Acute Disease↗

PubMed1988

Granulomatous interstitial nephritis after nonsteroidal anti-inflammatory drugs.

Electrolyte and renal hemodynamic imbalance, acute interstitial nephritis with nephrotic-range proteinuria, papillary necrosis, tubular necrosis, and vasculitis are complications after intake of nonsteroidal anti-inflammatory drugs (NSAID). We report on 2 cases of biopsy-proven granulomatous interstitial nephritis with rapidly progressing renal insufficiency. Patient 1 was on ketoprofen for 7 months and indomethacin for 10 weeks before admission to hospital. The medication was not discontinued and renal insufficiency progressed to end-stage renal failure. Renal function did not respond to steroid and tuberculostatic treatment. Patient 2 was on diclofenac for 6 months and indomethacin for 7 weeks before admission to hospital. These drugs were withdrawn at diagnosis and renal function rapidly improved. We conclude that granulomatous interstitial nephritis may be a complication of NSAID medication indicating a cell-mediated immunologic disorder. False diagnosis (sarcoidosis, tuberculosis) may lead to end-stage renal disease (case 1). Discontinuation of medication obviates further therapy (case 2).

Adult↗

PubMed2003

Ciprofloxacin-induced acute interstitial nephritis and autoimmune hemolytic anemia.

Ciprofloxacin has been associated with several side effects including interstitial nephritis and hemolytic anemia. The combination of both side effects is extremely rare. In this report, we describe a case of ciprofloxacin-induced interstitial nephritis and autoimmune hemolytic anemia. Hemolytic anemia improved after stopping the drug and initiation of steroid therapy. Unfortunately, acute interstitial nephritis was irreversible and the patient developed end-stage renal disease.

Acute Disease↗

PubMed1980

Interstitial nephritis in a patient with atypical Sjögren's syndrome.

A patient was observed with interstitial nephritis which resulted in renal tubular acidosis (distal type), tubular proteinuria and defective urinary concentrating ability in the absence of edema, elevated arterial blood pressure, glomerular proteinuria or abnormal urinary sediment. The presence of interstitial nephritis was established by renal biopsy which showed dense infiltrates in the interstitium, interstitial fibrosis and thickening and splitting of the pericapillary basal membranes. Immunofluorescence was non contributory. Extrarenal symptoms were discrete (arthralgia of both hands, Raynaud's syndrome upon cold exposure). Mixed connective tissue disease (MCTD) was suspected because of a positive ANF test (speckled pattern), which was completely abolished by ribonuclease pretreatment. However, in hemagglutination tests, no antibodies against ribonuclear protein (ENA) could be demonstrated. The diagnosis of Sjögren's syndrome was established by demonstration of antibodies against SSA and SSB antigens. The observation suggests that in patients with interstitial nephritis the diagnosis of Sjörgren's syndrome must be considered even if extrarenal symptoms of Sjögren's disease are minimal or lacking. The diagnosis can be established with recent serological techniques.

Adult↗