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At least 91 records · Page 5Linked to original sources
PubMed1995

Limited TCR repertoire of infiltrating T cells in the kidneys of Sjögren's syndrome patients with interstitial nephritis.

To analyze the mechanism of interstitial nephritis in patients with Sjörgren's syndrome (SS), we examined the TCR repertoire of infiltration T cells in kidney, labial salivary glands, and PBLs using a PCR. The repertoire of the TCR V beta gene on infiltrating T cells from the kidneys of SS patients was more restricted than those on infiltrating T cells in labial salivary glands and PBL. The TCR V beta 2 gene was expressed predominantly in six of seven (86%) SS patients. Junctional sequences of cDNAs encoding the V beta 2 gene on infiltrating T cells in the kidneys of five SS patients showed that some of the cells expanded clonally, indicating Ag-driven stimulation rather than superantigen-induced proliferation. The same V beta 2 clones in the kidney were not detected in labial salivary glands of the same SS patients; the conserved amino acid (arginine at position 96) in the CDR3 region of the V beta 2 gene was found at a frequency of 48.0% in the kidney, whereas it was detected in only 15.4% of the clones in lips. In conclusion, these findings suggest the possibility that T cells that infiltrate the kidneys of SS patients with interstitial nephritis might recognize different autoantigens than those that infiltrate labial salivary glands.

Amino Acid Sequence↗
PubMed2003

Seven cases of granulomatous interstitial nephritis in the absence of extrarenal sarcoid.

BACKGROUND: Renal disease in sarcoidosis may occur due to granulomatous interstitial nephritis. However, granulomatous interstitial nephritis in the absence of features of extrarenal sarcoid, or other causes, has been reported very rarely. In this report we describe seven such patients. METHODS: Since 1995, we have identified a number of patients with biopsy-proven granulomatous interstitial nephritis. Patients were excluded if they had (i) evidence of extrarenal sarcoid, (ii) infections that may have contributed to pathogenesis or (iii) an obvious drug-related aetiology. RESULTS: Seven patients were identified, of whom five were male and two female, with a median age of 69. Median calculated creatinine clearance at presentation was 14 ml/min. Two had raised serum calcium at presentation and three had a raised serum angiotensin-converting enzyme. All patients were treated with steroids and five out of seven had an improvement in their renal function. Two patients progressed to end-stage renal failure despite treatment with steroids. CONCLUSIONS: Idiopathic granulomatous interstitial nephritis may represent a renal-limited form of sarcoid. It may be associated with hypercalcaemia and a raised serum angiotensin-converting enzyme and usually responds to treatment with corticosteroids.

Adult↗
PubMed1999

Drug-induced acute interstitial nephritis in renal allografts: histopathologic features and clinical course in six patients.

Drug-induced acute interstitial nephritis is a common cause of dysfunction in native kidneys, but is rarely reported in renal allografts. This report describes six renal transplant recipients with acute renal allograft dysfunction or delayed allograft function in whom a renal transplant biopsy showed histopathologic features of drug-induced interstitial nephritis with no diagnostic evidence of acute rejection, cyclosporine or tacrolimus nephrotoxicity, or other lesion that could account for the graft dysfunction. In five of the six patients, interstitial nephritis occurred within 4 weeks of transplantation. All the patients were receiving trimethaprim-sulfamethoxazole and/or other drugs associated with interstitial nephritis. After discontinuation of these drugs and short-term corticosteroid treatment, all patients showed improvement in renal function, although the time course of this improvement varied considerably, with three patients showing a return to baseline serum creatinine level within 2 weeks and two patients showing a gradual improvement over 8 weeks. Four of the five patients followed up for more than 1 year (range, 14 to 33 months) after the episode of interstitial nephritis had good allograft function (serum creatinine level </= 1.6 mg/dL) at most recent follow-up, with one patient who had graft loss because of severe rejection 7.5 months after the development of interstitial nephritis. These findings suggest drug-induced interstitial nephritis may be an infrequent cause of graft dysfunction in kidney transplant recipients. Drug-induced interstitial nephritis is a reversible lesion that should be considered in the differential diagnosis of acute renal allograft dysfunction.

Acute Disease↗
PubMed1999

Tetracycline-induced acute interstitial nephritis as a cause of acute renal failure.

Acute interstitial nephritis with severe acute renal failure is reported following tetracycline treatment in a 22-year-old male medical student. Acute renal failure developed within 48 h of a single repeated tetracycline dose and presented 2 days after taking the drug when there was oliguria, nausea, vomiting and bilateral loin pain without rash and fever. The serum creatinine concentration was 8.6 mg/dl and blood urea nitrogen 84 mg/dl. Examination of the urinary sediment revealed 15-20 RBCs per high-power field, and occasional granular and hyaline casts. Percutaneous renal biopsy performed immediately after admission revealed acute interstitial nephritis with immune complexes along the tubular basement membrane and intact glomeruli and was consistent with type 2 interstitial nephritis. Within 4 days of commencement of steroid treatment and hemodialysis, the urine output started to increase with improvement in serum creatinine and BUN levels and after 2 weeks of therapy hemodialysis was discontinued. He remains well 1 year following his illness with complete normalization of his renal function. Although a number of renal side effects of tetracycline antibiotics have been reported, acute interstitial nephritis is rarely caused by tetracycline treatment having been reported just twice following systemic use of minocycline.

Acute Kidney Injury↗
PubMed1987

Interstitial nephritis and primary biliary cirrhosis: a new association?

Interstitial nephritis may be associated with a variety of auto-immune disorders, but there have been no reports among these of primary biliary cirrhosis. A patient presenting with sodium- and potassium-losing nephropathy due to interstitial nephritis was discovered to have primary biliary cirrhosis which was asymptomatic. Correction of the electrolyte abnormalities with sodium and potassium supplements had no effect on renal function, but creatinine clearance increased from 28 to 68 ml/minute during a seven-week course of prednisolone. The occurrence in primary biliary cirrhosis of other forms of renal tubular dysfunction, the frequent presence in both interstitial nephritis and primary biliary cirrhosis of multi-system involvement and the close temporal relationship in this patient, suggest that the two conditions were related.

Biopsy↗
PubMed2007

Multiple myeloma presented as acute interstitial nephritis and rheumatoid arthritis-like polyarthritis.

Acute interstitial nephritis and rheumatoid arthritis (RA) or RA-like polyarthritis are among the very rare paraneoplastic manifestations of multiple myeloma (MM). A 47-year-old man with acute renal failure due to interstitial nephritis was admitted to our university hospital and successfully treated with corticosteroid. He later developed a symmetric distal polyarthritis with morning stiffness mimicking RA. On follow-up, the patient had a rise in serum creatinine, hypercalcemia, anemia, and a monoclonal spike (Bence Jones protein) on the urine protein electrophoresis. Bone marrow biopsy demonstrated a diffuse neoplastic plasma cell infiltration. Diagnosis of MM was made and the patient received chemotherapy. After four-course chemotherapy, the patient's articular manifestations resolved, urine monoclonal spike disappeared, and serum creatinine returned to a near normal level. We hypothesize that in this case, immunologic hypersensitivity reactions to the light-chain molecules or other tumoral antigens deposited within the kidney or joint spaces, in the context of MM cytokine milieu may have resulted in this unusual presentation. Ultimately, clinicians and pathologists should consider MM in the differential diagnosis of the acute interstitial nephritis and RA-like polyarthritis.

Acute Kidney Injury↗
PubMed1984

[Acute interstitial nephritis with iridocyclitis].

One case with acute interstitial nephritis with undistinguished etiology, accompanied by iridocyclitis is described. Recently, numerous communications about similar cases have been reported which justify the differentiation of the syndrome "interstitial nephritis-iridocyclitis" among the acute interstitial nephritis. The case is of certain interest because of some characteristics: involvement of liver in the morbid process, immunemorphological finding from that described by other authors. Assumptions are presented about the pathogenetic mechanism of the disease. Conclusions are drawn in connection with the corticosteroid treatment, having induced a considerable improvement.

Acute Disease↗