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PubMed1980

Treatment of acute interstitial nephritis.

Treatment for acute interstitial nephritis (AIN) was examined in a retrospective study of 27 cases of AIN confirmed by kidney biopsy, and the results were statistically evaluated. The clinically determined serum creatinine values were taken as the criterion. The observation period ranged from 9 months to 2 1/2 years. The prognosis for seven patients who had received steroid preparations in addition to antibiotic and diuretic drugs in the early phases of the disease was significantly better than that of the other 20 patients who had been treated with only antibiotics and diuretics (p less than 0.05). Since the grade of severity of AIN in the two groups was almost identical (determined by maximal serum creatinine values) the two groups could be compared statistically.

Anti-Bacterial Agents↗
PubMed2006

Involvement of drug-specific T cells in acute drug-induced interstitial nephritis.

Drug-induced interstitial nephritis can be caused by a plethora of drugs and is characterized by a sudden impairment of renal function, mild proteinuria, and sterile pyuria. For investigation of the possible pathomechanism of this disease, drug-specific T cells were analyzed, their function was characterized, and these in vitro findings were correlated to histopathologic changes that were observed in kidney biopsy specimens. Peripheral blood mononuclear cells from three patients showed a proliferative response to only one of the administered drugs, namely flucloxacillin, penicillin G, and disulfiram, respectively. The in vitro analysis of the flucloxacillin-reactive cells showed an oligoclonal immune response with an outgrowth of T cells bearing the T cell receptor Vbeta9 and Vbeta21.3. Moreover, flucloxacillin-specific T cell clones could be generated from peripheral blood, they expressed CD4 and the alphabeta-T cell receptor, and showed a heterogeneous cytokine secretion pattern with no clear commitment to either a Th1- or Th2-type response. The immunohistochemistry of kidney biopsies of these patients revealed cell infiltrations that consisted mostly of T cells (CD4+ and/or CD8+). An augmented presence of IL-5, eosinophils, neutrophils, CD68+ cells, and IL-12 was observed. In agreement with negative cytotoxicity assays, no cytotoxicity-related molecules such as Fas and perforin were detected by immunohistochemistry. The data indicate that drug-specific T cells are activated locally and orchestrate a local inflammation via secretion of various cytokines, the type of which depends on the cytokine pattern secreted and which probably is responsible for the renal damage.

Aged↗
PubMed1995

[Renal biopsy for diagnosis of interstitial nephritis].

Tubulo-interstitial nephropathy or nephritis is suggested if renal function is deteriorated and urinary findings are slight. In most cases, the daily urinary protein excretion is less than 1 g and macrohematuria is not present. Urinary excretion of N- acetyl-beta-glucosaminidase and beta 2-microglobulin is a good indicator for tubulo-interstitial damage. Acute renal failure is caused either by acute tubulo-interstitial nephritis or acute tubular necrosis. In either case, renal biopsy is essential for diagnosis and to characterize the renal damage. In the interstitium, edema and fibrosis are seen and lymphocytes, plasma cells, polymorpholeukocytes, and/or eosinophils infiltrate. Tubular basement membrane is sometimes disrupted and lymphocytes have infiltrated inside (tubulitis).

Adult↗
PubMed1979

Cephradine-induced interstitial nephritis.

A patient developed acute interstitial nephritis following cephradine administration. The clinical illness preceding the interstitial nephritis and the eosinophilia in peripheral blood suggested an allergic reaction. Immunological studies demonstrated an allergy to cephradine and penicillins which was IgG2-mediated. It is probable, therefore, that allergy to cephradine caused the renal lesion from which there was full clinical and biochemical recovery.

Adult↗
PubMed1989

[The TINU syndrome in children (tubular interstitial nephritis with uveitis)].

Acute tubulo interstitial nephritis accompanied by uveitis is identified as TINU syndrome. The TINU syndrome is isolated from other forms of tubulo interstitial nephritis by the particular symptomatology and course: the nephropathy is almost always reversible, the uveitis tends towards relapses. The histopathologic findings are compatible with disturbance of cellular immunity, but the exact etiology is still unknown. In general, the outcome is favourable, but follow up, at least as long as there are signs of nephropathy, is necessary.

Child↗
PubMed2006

Sarcoidosis presenting with hearing loss and granulomatous interstitial nephritis in an adolescent.

Granulomatous interstitial nephritis is an uncommon finding in a kidney biopsy. The differential diagnosis is broad and includes infections, drug exposure, and sarcoidosis. Sarcoidosis, a systemic disorder of unknown etiology characterized by the presence of noncaseating granulomata in affected organs, is rare in children. We discuss an adolescent boy with the unusual presentation of granulomatous interstitial nephritis and acute deafness. Sarcoidosis should be considered as part of the differential diagnosis for children and adolescents with hearing loss and kidney disease.

Adolescent↗
PubMed1980

Tubular basement membrane antibody-induced interstitial nephritis in systemic lupus erythematosus.

Interstitial nephritis characterized by linear staining for human immunoglobulin G (IgG) along the tubular basement membrane of proximal renal tubules is described in a child with systemic lupus erythematosus (SLE). Autoantibodies reacting with the tubular basement membrane of the proximal renal tubules and Bowman capsule of glomeruli were present in serum. The autoantibodies were specific and could be absorbed with a normal human renal cortical fraction. The findings suggest that in addition to the well-known, immune complex-mediated injury, autoantibody-induced interstitial nephritis can also rarely occur in SLE.

Antibody Specificity↗
PubMed1995

Massive eosinophilic infiltration in a patient with the nephrotic syndrome and drug-induced interstitial nephritis.

The pathologic feature of acute interstitial nephritis is the infiltration of mononuclear cells, predominantly lymphocytes and monocytes, into the interstitium. We present an unusual case of a 49-year-old man with drug-induced acute interstitial nephritis whose renal biopsy specimen showed a massive infiltration of eosinophils into the interstitium and eosinophils infiltrating into the glomerulus through a gap in Bowman's capsule and the juxtaglomerular zone. The patient initially was referred to us with a recurrence of the nephrotic syndrome. Deterioration of renal function and an increase in proteinuria was noted at that time. Triazolam, a sleep inducer, was the suspected cause of the acute interstitial nephritis. Renal biopsy revealed sclerotic glomeruli containing eosinophils among massive infiltrated eosinophils and a loss of endothelial cells and mesangial cells in contrast to a preservation of epithelial cells. Infiltrating eosinophils were directly attached to the glomerular basement membrane, and free granules from the eosinophils were observed in the capillary lumen. In addition to chronic sclerotic change, eosinophils may have further damaged the glomerular capillary wall, leading to an increased severity of proteinuria in this case.

Eosinophilia↗
PubMed2006

Drug-induced granulomatous interstitial nephritis in a pediatric patient.

Acute interstitial nephritis (AIN) is a known cause of acute renal failure in children. In most instances, drug therapy is the offending agent. Although granuloma formation has been observed in drug-induced interstitial nephritis, it is not a commonly associated manifestation. This is a case of a 15-year-old white female with Tetralogy of Fallot and pulmonary atresia who developed acute renal failure secondary to drug-induced interstitial nephritis and renal granulomas. In addition to interstitial edema with eosinophils and lymphocytes, her renal biopsy showed interstitial granulomas, immune complexes within tubular basement membranes, and the unusual feature of multinucleated giant cells engulfing tubules. Her acute renal failure resolved after the withdrawal of antibiotics and the initiation of intravenous steroid therapy.

Acute Kidney Injury↗
PubMed1997

Omeprazole-induced interstitial nephritis.

Acute renal impairment secondary to interstitial nephritis is a rare complication of omeprazole. We describe a 50-year-old woman who took 20 mg omeprazole twice daily for endoscopically proved ulcerative esophagitis. At the same time, Duke's C colonic cancer was diagnosed and completely resected. Five fluorouracil/folinic acid adjuvant chemotherapy was tolerated without diarrhea or mouth ulceration. Renal function was normal before her first monthly cycle but markedly deteriorated immediately before the second cycle was due. The patient was symptomatic with lethargy, nausea, and mild vomiting, but she was clinically normotensive and only mildly dehydrated. Her serum creatinine concentration increased despite prolonged intravenous hydration, peaking at 4.4 mg/dl 1 week later. Results of a renal ultrasound were normal, and urinary microscopic findings were unremarkable. Renal biopsy showed interstitial nephritis, and renal function improved on cessation of omeprazole, eventually returning to normal. We describe the 12 cases of omeprazole-induced interstitial nephritis reported previously.

Anti-Ulcer Agents↗
PubMed1978

[Radiology of bacterial and abacterial interstitial nephritis (author's transl)].

The x-ray findings of 727 patients with chronic interstitial nephritis are evaluated; these patients have been controlled over a period of several years: 594 suffer from chronic bacterial interstitial nephritis (pyelonephritis) and 133 patients from chronic abacterial interstitial nephritis of different etiology. The causes for the abacterial type of nephritis are phenacetin and primary gout. The radiological signs of the two forms of chronic interstitial nephritis in different degrees of involvement are pointed out. Whereas with the chronic abacterial interstitial nephritis symmetrical affection is typical, the chronic bacterial interstitial nephritis shows asymmetrical findings, especially in ascending pyelonephritis. Differentiation between the chronic bacterial nephritis and the chronic abacterial nephritis can be achieved in most cases by radiological signs, (morphological findings). The microscopic evaluation does not always allow a differentiation; because there are mixed forms and secondary bacterial infections are associated with primary chronic abacterial interstitial nephritis in the late stages. The multiple causes for chronic abacterial interstitial nephritis is radiologically reflected mostly by uniform signs during the different degrees of involvement.

Chronic Disease↗