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The disease course and prognosis of work fitness were studied in 66 patients with acute interstitial nephritis (AIN). In 68 patients, the disease onset was preceded by antibiotic treatment. The main disease symptom consisted in creatininemia of varying degree, disappearing on the 5th-10th day of the disorder. Prognosis in AIN is favourable. The working capacity gets restored 2-4 months after the disease onset.
The discovery of glycosuria with normal glycemia is generally interpreted as a consequence of a congenital tubular defect. Nevertheless it may be also the result of an acute interstitial nephritis. This conclusion is supported by the clinical and biochemical picture observed in two children, presenting with apparently unexplained fever and significant increase of inflammatory blood indices, in whom euglycemic glycosuria represented the critical finding for diagnosis of acute interstitial nephritis.
Immunosuppressive effects of E-series prostaglandins have been demonstrated in many in vitro assays of immune responsiveness as well as in autoimmune diseases. To explore the mechanisms underlying prostaglandin E1 (PGE1)-associated immunosuppression in autoimmunity, we treated SJL mice immunized to produce immune-mediated interstitial nephritis with PGE1, PGF2 alpha, or vehicle alone. Mice receiving PGE1 treatment do not develop interstitial nephritis, nor do they display delayed-type hypersensitivity (DTH) to the immunizing renal tubular antigen preparation. The observed immunosuppression is critically dependent on PGE1 administration during the period of effector T cell induction. We therefore investigated the effect of PGE1 on the in vitro induction of DTH effector T cells reactive to renal tubular antigens (SRTA). PGE1 inhibits effector T cell induction in a dose-dependent, reversible manner, but has no inhibitory effect on fully differentiated DTH effector cells or SRTA-reactive cell lines. The PGE1 effect is indirect and mediated via nonspecific suppressor lymphokines. This suppression can be overcome by recombinant interleukin 1 (IL-1), which suggests a mechanism related to either diminished IL-1 secretion or target cell sensitivity to IL-1.
A 49-year-old woman, who had been diagnosed as sarcoidosis based on bilateral hilar lymphadenopathy and lung biopsy, presented increased serum creatinine and calcium concentrations. Renal biopsy showed the presence of interstitial nephritis with non-caseating epithelioid granuloma and focal membranous transformation. Therapy with prednisolone was effective in normalizing serum creatinine, serum calcium, serum angiotensin converting enzyme, and urine beta2 microglobulin, but these abnormalities reappeared after rapid withdrawal of prednisolone. This is a rare case of sarcoidosis manifested by both membranous nephropathy and granulomatous interstitial nephritis, and indicates the necessity of long-term treatment of corticosteroid.
BACKGROUND: Acute interstitial nephritis (AIN) is a recognized cause of reversible acute renal failure characterized by the presence of an interstitial inflammatory cell infiltrate. METHODS: In order to evaluate the clinical characteristics and management of this disorder, we performed a retrospective study of all cases of AIN found by reviewing 2598 native renal biopsies received at our institution over a 12 year period. Presenting clinical, laboratory and histological features were identified, as was clinical outcome with specific regard to corticosteroid therapy response. RESULTS: AIN was found in 2.6% of native biopsies, and 10.3% of all biopsies performed in the setting of acute renal failure during the period analysed (n = 60). The incidence of AIN increased progressively over the period observed from 1 to 4% per annum. AIN was drug related in 92% of cases and appeared to be idiopathic in the remainder. The presenting symptoms included oliguria (51%), arthralgia (45%), fever (30%), rash (21%) and loin pain (21%). Median serum creatinine at presentation was 670 micromol/l [interquartile range (IQR) 431-1031] and 58% of cases required acute renal replacement therapy. Corticosteroid therapy was administered in 60% of cases. Serum creatinine at baseline was similar in the corticosteroid-treated and conservatively managed groups; 700 micromol/l (IQR 449-1031) vs 545 micromol/l (IQR 339-1110) P = 0.4. In this, the largest retrospective series to date, we did not detect a statistically significant difference in outcome, as determined by serum creatinine, between those patients who received corticosteroid therapy and those who did not, at 1, 6 and 12 months following presentation. CONCLUSION: The results of this study do not support the routine administration of corticosteroid therapy in the management of AIN.
We report a case of the deliberate inhalation of a toluene-containing adhesive which caused acute renal failure and hepatic damage. Renal biopsy disclosed a severe tubulo-interstitial nephritis, renal function recovered after 14 days' haemodialysis. The literature on renal complications of toluene exposure is reviewed, this is the only case of acute renal failure due to interstitial nephritis after toluene exposure with subsequent recovery. Recovery in this case may have been related to the avoidance of further toluene exposure.
Rifampin is a widely used antimicrobial agent, most commonly administered in the treatment of tuberculosis. Since its introduction in the late 1960s, rifampin has become a standard agent in the treatment of tuberculosis, especially with the acceptance of short-course chemotherapy in the U.S. Rifampin also is being used with increasing frequency in the treatment of nontuberculous infections, especially serious staphylococcal infections. While rifampin usually is well tolerated in most patients, adverse effects, including serious forms of toxicity, have been reported. Some of these adverse effects include liver toxicity and various immunologic reactions such as skin rashes, eosinophilia, and interstitial nephritis. This report documents a case of acute interstitial nephritis, most likely secondary to intermittent rifampin administration.
In experimental tubulo-interstitial (anti-basement membrane) nephritis of the rat, granulomatous inflammation develops around immunologically altered tubular basement membranes. The present light- and electron microscopic studies indicate that in the course of the granulomatous reaction, tissue monocytes evolve from blood monocytes and pursue two independent pathways of differentation. On the one hand they may differentiate into macrophages ("distant from tubules") or, alternatively, into epitheloid cells ("adjacent to tubules"). The latter, through cell fusion, develop into multinucleated giant cells of the Langhans' type. The cytoplasmic components of the epitheloid cells and the multinucleated giant cells should be interpreted as an activation of cellular biosynthesis. Its products, upon being secreted at the immunodefective basement membrane, will obviously serve immune defense mechanisms.
A 49-year-old male was admitted to our hospital because of acute renal failure. He had been treated by a local doctor for rheumatoid arthritis (RA) during the past eight years. We treated him with steroid pulse therapy, because of suspected acute interstitial nephritis. We confirmed this diagnosis by renal biopsy and steroid pulse therapy markedly improved his renal dysfunction. Immunohistochemical studies revealed that interstitial infiltrating leukocytes consisted mainly of polymorphonuclear leukocytes (PMNs), macrophages and B lymphocytes, while T lymphocytes were less predominant. ELAM-1 and GMP-140 were expressed in the peritubular capillaries. These findings suggest that endothelial activation of the peritubular capillaries may cause interstitial infiltration of PMNs and macrophages, resulting in the development of acute interstitial nephritis. Four months later, he developed severe interstitial pneumonitis, and his symptoms were not improved by high-dose steroid pulse and cyclophosphamide pulse treatment. Eight weeks after the second admission, cyclosporin A (Cy A) was started. Three weeks after starting Cy A, he was free from symptoms and his chest radiograph was normalized. Renal function was also improved by Cy A. These observations suggest that endothelial activation by adhesion molecules may play an important role in RA-related autoimmune diseases and that Cy A might be efficacious in such cases.
Nephrotic syndrome (NS) secondary to drug-induced acute interstitial nephritis (AIN) is well described in adult but is very rare in children. We report an unusual case of AIN mimicking prototypical childhood minimal change NS. A 2-year-old girl on long-standing amoxicillin therapy for vesicoureteral reflux presented with the acute onset of generalized edema, proteinuria, hypoalbuminemia, hypercholesterolemia, and an inactive urinary sediment. She was placed on empiric steroid therapy for presumed minimal change NS. When she did not respond to steroids, a renal biopsy was performed and revealed AIN. Her NS resolved completely with cessation of her amoxicillin therapy and concomitant tapering of her steroids. This patient demonstrates that the association of AIN with NS should be carefully considered in children on antimicrobials who develop NS, even in the absence of the classic clinical features of AIN. In addition to the usual work-up and care of a child with NS, in these patients consideration may also need to be given to withdrawal of the potential precipitating agent.
UNLABELLED: A new case of tubulo-interstitial nephritis and uveitis (TINU) syndrome in a 14-y-old girl is described. In this patient unilateral mastitis was an associated feature. The aetiology of this rare syndrome, the prognosis for which is usually good, is still unknown. The most common theory supports a cell-mediated immune response induced by infectious/antigenic stimuli. CONCLUSION: The presence of acute unilateral mastitis in this patient may represent an additional localization in TINU syndrome.
We report a case of biopsy-proven acute interstitial nephritis (AIN) in a 50-year-old diabetic woman, who had been treated with celecoxib for 4 weeks before presentation. She presented with clinical findings of renal proximal tubulopathy, aseptic leukocyturia and acute renal failure. A kidney biopsy specimen showed AIN with intense tubuli and eosinophilic infiltrate in the interstitium. She recovered normal renal function two weeks after cessation of celecoxib and use of a corticosteroid. A review of the literature yielded eight cases of COX-2 inhibitor-associated AIN with a biopsy-proven diagnosis. Among the reported cases, AIN was diagnosed after an average of 8.3 months of therapy (SD 12 months, range 3 days - 3 years) with 25 mg rofecoxib or 200 mg celecoxib daily. Common symptoms included asthenia, anorexia, nausea and vomiting. The classic triad of fever, rash and eosinophilia was uncommon. Typical laboratory features included hematuria, proteinuria, eosinophilia. Renal failure was common at the time of diagnosis. Mean serum creatinine levels were 0.86 +/- 0.11 mg/dl, 5.66 +/- 3.50 mg/dl and 1.15 +/- 0.24 before treatment, at time of diagnosis and 1 - 2 months after COX-2 inhibitor withdrawal, respectively. Three patients required emergency hemodialysis. After cessation of COX-2 inhibitor treatment, patients recovered completely with a normalized serum creatinine level after one to two months. Management consisted of withdrawal of the COX-2 inhibitor drug and in four patients, corticosteroid therapy was well-tolerated and may have been beneficial.
The first case of favorable evolution under conservative treatment for acute renal failure caused by megalocytic interstitial nephritis and the ongoing transitory impairment of the polymorphonuclear bactericidal ability are described. This case report has been included in a critical overview of the cases previously reported.
We are reporting the clinical and pathologic features of severe acute renal failure which developed in a patient after the institution of cimetidine (Targamet) therapy. A renal biopsy specimen revealed an acute interstitial nephritis with numerous plasma cells and eosinophils suggestive of an immunologic reaction. Marked improvement of renal function occurred within three weeks after cessation of the drug therapy. Our clinical and pathologic data strongly suggest an association between acute interstitial nephritis and cimetidine, a suggestion which should be confirmed by additional case studies.
Concomitant renal and ocular lesions have been described in a few systemic diseases. The association of acute interstitial nephritis (AIN) and anterior uveitis without determined cause was first described in children. Recently, the same clinical association has been reported in adults. We report 3 cases of this association and present a review of the literature. Including our 3 patients, 7 cases of this association have been reported in adults. All patients were females aged 27-74 years. Initial symptoms were either ocular, or pseudoviral (fever, myalgia and fatigue). Histological renal studies revealed acute interstitial nephritis with tubular lesions. Immunofluorescence and electron microscopy were not contributive. Ocular prognosis was always good. In 5 patients, the evolution of renal function was excellent with complete resolution of acute renal failure within a few weeks. Chronic renal failure developed in two of the four patients who did not receive systemic steroid therapy (with evolution towards terminal renal failure in one patient). Three of the patients received 60 mg per day of prednisone and none of them developed chronic renal failure. Despite the small number of patients reported and the possibility of spontaneous regression, these data suggest a beneficial effect of systemic steroid therapy to prevent or reduce interstitial inflammation and subsequent fibrosis.
We examined the T cell receptor (TCR) repertoire of infiltrating T cells in the kidney, labial salivary glands (LSGs) and peripheral blood lymphocytes (PBLs) in Sjögren's syndrome (SS) patients with interstitial nephritis. The TCR V beta gene repertoire in kidney was more restricted compared with that in LSGs and PBLs. The TCR V beta 2 gene was predominantly expressed in six of seven kidneys (86%). Junctional sequence of TCR V beta 2 gene shows that some of these cells expanded clonally. The identical TCR clones in the kidneys were not detected in LSGs and the amino acid (Arg96) in the CDR3 region of V beta 2 gene was conserved specifically in kidneys. These findings suggest that T cells infiltrating in the kidneys from SS patients with interstitial nephritis identify different autoantigens from LSGs rather than superantigen.
We describe an unusual complication of acute pyelonephritis in a 45-year-old diabetic female. She was admitted to our hospital due to fever and flank pain which had developed 10 days earlier. Urinalysis showed many WBC and urine culture revealed Escherichia coli. After adequate antibiotic treatment, clinical symptoms abated but renal failure and leukocyturia persisted. Abdominal CT showed bilateral focal bacterial nephritis and renal biopsy disclosed chronic granulomatous interstitial nephritis. On the 80th hospital day she was discharged with a serum creatinine of 299 mumol/l. In the outpatient clinic, renal dysfunction and leukocyturia persisted up to 1 year. In conclusion, this case raises the possibility of a chronic interstitial process of acute pyelonephritis.
We examined the effect of daily cyclosporin A administration on the development and extent of tubulointerstitial nephritis produced in rats immunized with tubular basement membranes in adjuvant. Six mg/kg/day of cyclosporin A, given from the time of immunization, completely blocked the development of interstitial lesions and renal insufficiency. The administration of cyclosporin A after the development of interstitial nephritis also arrested the progression of the histological lesions. Both T cell-mediated and humoral immunity were markedly reduced by the administration of cyclosporin A, as evidenced by the near absence of delayed-type hypersensitivity responses and by the reduced production of anti-tubular basement membrane antibodies. Cell admixture experiments indicated that impairment of the delayed-type hypersensitivity response to tubular antigen was probably not the result of active suppression, and suggested that the protective effect of cyclosporin A might be secondary to its direct inhibitory action on the activation of nephritogenic T and B cells. Finally, the treatment of control rats with cyclosporin A, in the doses used, did not produce any detectable kidney damage nor did it impair renal function. We conclude that cyclosporin A can be an effective prophylactic and therapeutic agent in autoimmune interstitial nephritis in rats.