[CHRONIC INTERSTITIAL NEPHRITIS].
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Drug-induced interstitial nephritis is being recognized with increasing frequency. Pharmacologic agents responsible for inducing this entity include antibiotics, diuretics, and nonsteroidal anti-inflammatory drugs. We recently examined five patients with glomerular disease and drug-induced interstitial nephritis. In three patients prior biopsy specimens documented their glomerular disease (membranous nephropathy, crescentic glomerulonephritis, and presumptive lipoid nephrosis). A second biopsy specimen showed acute interstitial nephritis and the glomerular lesion. Two additional patients had single biopsy specimens demonstrating acute interstitial nephritis and either membranous nephropathy or crescentic glomerulonephritis. Our cases emphasize the need for recognizing this complex pattern of renal disease and the difficulties encountered in rendering a proper diagnosis.
Acute interstitial nephritis in children is rare. We present a case of acute interstitial nephritis in a 10-year-old boy, which was probably drug-induced. Initial symptoms included fever, loss of appetite, weight loss, alterations in urine analysis and mild renal failure. Treatment with steroids produced a good clinical response and renal function returned to normal within a few months.
The combination of interstitial nephritis and minimal-change nephrotic syndrome has been well described in adults receiving nonsteroidal anti-inflammatory agents. The association of interstitial nephritis and minimal-change nephrotic syndrome has recently been described in 1 adult patient receiving ampicillin and in 1 patient receiving rifampin. We describe an 8-month-old child who developed reversible interstitial nephritis and minimal-change nephrotic syndrome while taking antibiotics.
Interstitial renal lesions containing T cells and macrophages develop after 14 days in guinea pigs immunized to produce anti-tubular basement membrane-induced interstitial nephritis. We serially examined the renal venous and systemic arterial sera from such animals to determine if chemotactic factors were released across their kidneys. Our findings demonstrated the presence of a macrophage-specific renal chemoattractant with peak detectability on Days 10-14, just subsequent to the deposition of alpha TBM-Ab, but prior to the development of significant renal injury. We propose that such factors may provide important communication signals in the immunopathogenesis of this form of interstitial injury.
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Although acute interstitial nephritis has been well described with the histamine H2-receptor antagonist cimetidine, we found only one previous case report of ranitidine-induced interstitial nephritis in the literature. We describe an additional patient who developed acute interstitial nephritis after taking ranitidine. Electron microscopy showed focal fusion of the epithelial cell foot processes that was not described in the previous report of ranitidine-induced interstitial nephritis.
Hereditary interstitial nephritides are a heterogeneous group of disorders comprising medullary cystic disease, several varieties of Alport's syndrome and also one familial disorder with a distinct clinical syndrome and without characteristic ultrastructural glomerular basement membrane changes. Our family consisted of 11 members, 5 of which presented with renal dysfunction of varying degrees. Clinically, the affected siblings presented with long-standing hypertension, minimal proteinuria and no hematuria. All known causes of a secondary diffuse interstitial nephritis, Alport's syndrome and medullary cystic disease have been excluded. An HLA association is suggested between the affected and unaffected members of the family. Renal biopsy subsequently showed the typical features of a chronic interstitial nephritis without basement membrane changes.
Chronic interstitial nephritis with diffuse zonal fibrosis (CINF) occurs in Japanese Black cattle (Wagyu) as an autosomal recessive disorder leading to death prior to puberty, first six months or a year of life. We performed a genome-wide scan using microsatellite markers in a Wagyu pedigree segregating for CINF and mapped the CINF locus to bovine chromosome 1. CINF was closest to microsatellites BM9019 and INRA49 (Z score = 12.0; P < 3.4 x 10(-10)).
Drug-induced acute interstitial nephritis (AIN) is a rare, potentially correctable cause of acute renal failure. Early recognition and appropriate therapy are essential to its management. Several drugs have been associated with the development of AIN, including antibiotics and nonsteroidal antiinflammatory, agents, all with characteristic mechanisms of toxicity.
UNLABELLED: Interstitial nephritis (IN) can occur as a result of different injury factors, among them: infections, drugs, toxins. The aim of the study was the presentation of rare causes of IN in 2 patients who were hospitalized in the Department of Pediatrics and Nephrology of Medical University of Warsaw. Case 1. A 15-years-old girl, with biopsy proven IN, who presented with a slight impairment of kidney function (creatinine level 1.1 mg/dl) and symptoms of tubulopathy at the beginning of the illness. Hypergammaglobulinemia, anemia, increase of CRP level and high ESR were noticed. Among others causes CMV infection was suspected. After CMV detection seroconversion in titres of anti- CMV IgM and IgG antibodies was observed. Kidney biopsy revealed IN and positive reaction to CMV antigen in tubular epithelial cells. Case 2. A 12,5-years-old boy with acute renal failure (ARF) (creatinine and urea concentration respectively: 11.3 mg/dl, 131.4 mg/dl) was admitted to the hospital. In kidney biopsy acute IN with tubulopathy and intense involvement of renal tissue was found. In further investigation inhaled stimulating factor was suspected as the possible cause of renal changes development - IN and ARF. CONCLUSION: Considering the etiology of IN in children, CMV infection, the application of drugs and other chemical substances should be mentioned among the rare causes of the illness.
Granulomatous interstitial nephritis occurred in a patient five years after jejunoileal bypass surgery was performed. Calcium oxalate crystals were present in the kidney. This finding was associated with renal failure and to our knowledge has not been previously reported. Hepatic granulomas were also present.
Acute interstitial nephritis associated with hepatitis, exfoliative dermatitis, fever and eosinophilia is uncommon. The syndrome has been described previously in association with phenindione administration, leptospirosis and heavy metal poisoning. Four cases are described, two of which were due to phenindione sensitivity. The other two patients had been exposed to a number of toxins including allopurinol, frusemide, chlorothiazide and methyldopa so that the exact aetiological agent is unclear. Interstitial nephritis should be considered as a cause of acute renal failure in patients with other features of drug hypersensitivity.
BACKGROUND: Interstitial nephritis caused by BK polyomavirus is a recognized complication of renal transplantation. A study of renal transplant recipients at Duke University Medical Center was undertaken to evaluate diagnostic modalities and assess clinical outcomes in transplant polyomavirus infections. METHODS: Polyomavirus nephritis was identified in 6 of 240 patients who received renal transplants between January 1996 and June 1998 and an additional patient who underwent transplantation in 1995. The clinical records of these seven patients were reviewed, as were all renal biopsy and nephrectomy specimens. Electron microscopy (EM) was performed on negatively stained urine samples from 6 patients with polyomavirus infection and 23 patients with other diagnoses. RESULTS: Patients with polyomavirus infection shared several clinical features, including ureteral obstruction (5/7 patients), lymphocele (3/7), bacterial urinary tract infection (3/7), hematuria (3/7), cytomegalovirus infection (3/7), and immunosuppression with mycophenolate mofetil (6/7). All patients experienced elevations in serum creatinine, which stabilized or decreased in four patients with altered or decreased immunosuppression. The diagnosis of polyomavirus infection was established by renal biopsy and EM of urine in five patients, by biopsy alone in one, and by EM alone in one. Sequential examinations of urine by EM were used to monitor the course of infection in six patients. CONCLUSIONS: Interstitial nephritis due to BK polyomavirus occurred in 2.5% of patients receiving renal transplants at our center since 1996. Polyomavirus infection can cause transplant dysfunction and graft loss, but progression of the infection can frequently be abrogated with alterations in immunosuppressive therapy. Both renal biopsy and EM of urine samples are useful in the diagnosis and monitoring of polyomavirus infections.
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