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PubMed1993

Ranitidine-associated interstitial nephritis and Fanconi syndrome.

Ranitidine is an H2 blocking agent widely used in the treatment of peptic ulcer disease. Although acute interstitial nephritis has been described in association with a related drug, cimetidine, this complication secondary to ranitidine has been reported only once before. We describe a patient who presented with acute renal failure and features of Fanconi syndrome in association with the use of ranitidine. Renal biopsy showed acute interstitial nephritis. The patient had renal tubular acidosis with alkaline urine, aminoaciduria, renal glycosuria, uricosuria, and phosphaturia. There was a marked disparity between the degree of elevation of urea nitrogen and creatinine concentrations in the serum that was attributable to diminished urea generation, since simultaneous measurement of inulin, creatinine, and urea clearances showed that they were comparably reduced. Urinary nitrogen loss in the form of aminoaciduria contributed significantly to decreased urea generation. Both acute renal failure and Fanconi syndrome resolved after treatment with prednisone.

Adult↗

PubMedDate not supplied

Idiopathic acute interstitial nephritis associated with uveitis.

A case of acute interstitial nephritis associated with uveitis is presented, An 18-year-old man developed uveitis followed by renal dysfunction. Moderate renal dysfunction (sCr 3.0 mg/dl), and increased levels of urinary beta 2 microglobulin (over 8,000 micrograms/I) were observed. Renal tissue obtained by open renal biopsy revealed severe infiltration of mononuclear cells in the tubulo-interstitial area. The majority of infiltrating cells were CD4-positive T cells demonstrated by immunoperoxidase staining, suggesting the involvement of T cell-mediated delayed hypersensitivity. Corticosteroid was effective against both uveitis and renal dysfunction. The possible pathogenesis of this syndrome is reviewed from the literature.

Adolescent↗

PubMed1988

[Acute interstitial nephritis caused by drug hypersensitivity. Current controversies].

Acute interstitial nephritis (AIN) due to drug hypersensitivity represents 0.8 to 8 p. 100 of all causes of acute renal failure. Two thirds of cases are due to antibiotics, mainly beta-lactamines, and to non-steroidal anti-inflammatory drugs. Blood hypereosinophilia, fever, arthralgias and/or hepatocellular damage are suggestive of an allergic drug reaction in patients with AIN, with a sensitivity of 0.75 and a specificity of 0.76. Examination of an early renal biopsy specimen is a clue to the diagnosis of AIN due to drug hypersensitivity if it discloses a diffuse or focal interstitial infiltration with lymphocytes, plasma cells, and mainly by eosinophils and/or epithelioid cell granulomas. These findings suggest a delayed hypersensitivity reaction, although many cases seem to be also mediated by humoral immune factors. Renal recovery is frequent when the responsible drug is promptly withdrawn. The value of steroid therapy in preventing residual renal damage has to be assessed by controlled studies.

Anti-Bacterial Agents↗

PubMedDate not supplied

An etiology of nephrotic syndrome in chronic interstitial nephritis (pyelonephritis); an electron microscopic study.

Renal tissues were studied using electron microscopy (EM) and immunofluorescence microscopy (IFM) from three patients who were found to have chronic interstitial nephritis (pyelonephritis) by light microscopy (LM). By LM, 90% of the glomeruli in two patients and all glomeruli in one patient were normal. By EM, glomerular capillaries in all patients revealed generalized fusion of epithelial foot processes. In two patients, IFM for immunoglobulins, third component of complement and fibrinogen were negative. These two patients received corticosteroids for 6 to 12 weeks. In one, proteinuria markedly decreased (from 17.9 to 1.1 gm) in four weeks and in the other follow-up studies of renal histology revealed normal glomeruli and partial restoration of foot processes by LM and EM respectively. Thus, this study offers evidence for lipoid nephrosis (or minimal lesion disease) as an etiology of nephrotic syndrome in chronic interstitial nephritis (pyelonephritis). The impaired renal function in these patients is attributed to tubulo-interstitial disease rather than glomerular pathology. It remains to be determined whether the two disparate pathological conditions have coexisted or chronic interstitial nephritis had led to the appearance of lipoid nephrosis through an unidentified mechanism.

Adult↗

PubMed1989

Acute interstitial nephritis associated with uveitis and primary hypoparathyroidism.

In a study of a patient with acute renal failure and uveitis, renal biopsy showed acute interstitial nephritis. Serum calcium and parathyroid hormone concentrations were persistently low during the acute phase and after the resolution of renal failure. Clinical history was negative for intake of drugs capable of inducing acute interstitial nephritis.

Acute Disease↗

PubMed1987

Effector T cell differentiation in experimental interstitial nephritis. I. The development and modulation of effector lymphocyte maturation by I-J+ regulatory T cells.

Because mice susceptible to interstitial nephritis use different effector T cells than nonsusceptible mice, we analyzed the differentiation process of the effector T cell repertoire by using an in vitro culture technique. In the presence of helper T lymphocytes, accessory cells, IL 2, tubular antigen, and precursor effector cells, both Lyt-2+ nephritogenic effector cells and L3T4+ nonnephritogenic effector cells can be initially induced in both susceptible and nonsusceptible strains within 3 days of culture. In nonsusceptible mice, however, the Lyt-2+ nephritogenic cell is inhibited from further development and disappears, whereas in susceptible mice, its presence is preserved with a resulting effect of tissue destruction. This selection of effector T cell preference is regulated by I-J+ T lymphocytes which are co-functionally expressed with effector cell expansion. Unlike precursor effector lymphocytes, however, the maturation of the regulatory process requires a subset of I-J+ accessory cells and structurally intact tubular antigen. Our findings indicate, therefore, that both susceptible and nonsusceptible mice have the potential for the expression of interstitial nephritis, but nonsusceptible mice are formally protected from autoimmunity by the regulation of lymphocyte preference.

Animals↗

PubMed1991

Acute interstitial nephritis and uveitis syndrome: activated immune cell infiltration in the kidney.

Infiltrating cells were analysed in renal biopsy tissue obtained from a 15-year-old girl with acute interstitial nephritis and uveitis using monoclonal antibodies specific for mononuclear cell surface markers. The interstitial infiltrates consisted mainly of T cells and monocytes/macrophages. A considerable proportion of the infiltrating cells were identified by a monoclonal antibody against the interleukin-2 receptor, indicating that a majority of those immune cells are activated. This observation documents the participation of cell-mediated immune injury in interstitial nephritis associated with uveitis.

Acute Disease↗

PubMed1987

Contrasuppression in autoimmunity. Abnormal contrasuppression facilitates expression of nephritogenic effector T cells and interstitial nephritis in kdkd mice.

We have used the murine model of spontaneous autoimmune interstitial nephritis in kdkd mice to examine the importance of abnormal immunoregulation in the expression of disease. T cells from naive congenic CBA/Ca mice suppress both histologic renal injury in the kdkd strain as well as the DTH reactivity to CBA/Ca renal tubular antigens mediated by lymphocytes from nephritic kdkd mice. These antigen-specific suppressor T cells are Lyt-2+, L3T4+, I-Jk+, genetically dominant and I-Jk restricted. Unfractionated spleen cells from young, prenephritic kdkd mice also demonstrate such suppressor function. Shortly preceding disease onset, however, net suppression is functionally bypassed by emergent contrasuppressor T cells. These regulatory cells are also Lyt-2+ and I-Jk+, and adhere both to the Vicia Villosa lectin and CBA/Ca TBM. By admixing these contrasuppressor cells with spleen cells from non-disease-prone CBA/Ca mice we were able to demonstrate the presence of DTH-reactive and nephritogenic effector cells in the latter population. Such nephritogenic effector cells could also be simply demonstrated after depletion of the suppressor cells with anti-I-Jk mAbs and complement. These findings support a role for contrasuppressor cells in the abrogation of tolerance to parenchymal self-antigens.

Age Factors↗

PubMed1999

Acute interstitial nephritis following amoxicillin overdose.

Antibiotics are commonly prescribed medications for pediatric infections. Acute interstitial nephritis has been reported with B-lactam antibiotics. We report the case of a 4-year-old boy who ingested 240 mg/kg of amoxicillin and developed acute oliguric renal failure with hematuria and crystalluria. The patient was hospitalized for serial renal function and electrolyte evaluation. Although he developed hyperkalemia, full recovery was obtained with conservative management. This case emphasizes that medications considered to be non-toxic even with overdose can have serious adverse effects which may require therapeutic intervention.

Acute Disease↗

PubMed2003

[Immunoallergic interstitial nephritis vs. cholesterol atheroembolism. Differentiating characteristics].

The commonest clinical presentation of both immunoalergic interstitial nephritis (IIN) and atheroembolic renal disease (ATD) is an acute renal failure accompanied by skin lesions and eosinophilia. As a consequence, differential diagnosis between both entities is often very difficult. We have performed a comparative retrospective study of those patients diagnosed as having IIN or ATD in our Hospital in the period 1980-2000. A total of 42 patients have been diagnosed of IIN and 16 of ATD. Demographic data, as well as clinical and laboratory parameters and outcomes of every studied patient were analysed. We found a significantly higher prevalence of male sex (100% vs 57%, p < 0.01), previous history of hypertension (100% vs 55%, p < 0.01), chronic renal insufficiency (56% vs 17%, p < 0.01), ischemic heart disease (56% vs 14%, p < 0.001), peripheral ischemic disease, endovascular procedures (87% vs 7%, p < 0.001) and anticoagulant treatments (25% vs 5%, p < 0.001) among patients with ATD as compared with IIN, respectively. On the contrary, previous infections (45% vs 12%, p < 0.01) and exposure to new drugs (100% vs 40%, p < 0.001) were significantly more frequent among IIN patients in compare with ATD. ATD patients showed skin lesions consisting of livedo reticularis and digital infarcts (63% vs 31%, p < 0.05) accompanied by blood pressure increase (100% vs 24%, p < 0.001), whereas IIN patients showed fever (41% vs 19%, p < 0.05) and cutaneous rash as significant clinical manifestations, respectively. The number of ATD patients with proteinuria > 1 g/24 h was significantly higher, but no differences between both groups in the prevalence of urinary sediment abnormalities were observed. The prevalence of absolute eosinophilia was high in both groups (88% among ATD patients, 64% among IIN patients; pNS). Prognosis of both entities was clearly different: Almost all patients with ATD died (69%) or evolved to end-stage renal failure, whereas most patients with IIN showed a recovery of renal function after withdrawal of responsible drugs and steroid treatment. In summary, the analysis of clinical and laboratory data allows an initial differential diagnosis in patients suspected as having IIN or ATD.

Acute Kidney Injury↗

PubMed1990

Acute interstitial nephritis in adolescents and young adults.

We have reviewed our experience with acute interstitial nephritis (AIN) in pediatric patients over the 3-year period from 1985 to 1988. We encountered 7 new cases of AIN in this interval and it was seen in 7% of kidney biopsies performed during this time of study. The clinical presentation was very nonspecific and included fever (100%), gastrointestinal complaints (57%) and rash (28%). Laboratory findings on admission included elevated erythrocyte sedimentation rate (100%), anemia (70%), pyuria (57%) and abnormal renal ultrasound (86%). Associated systemic diseases were observed in 4 patients. AIN was severe enough to necessitate treatment with hemodialysis in 42% of the cases. Corticosteroid therapy was used in 6 patients with a favorable response in all but 1 case. While 6/7 patients manifested complete recovery, 1 adolescent who may have had pre-existing renal disease had persistent chronic renal failure (estimated GFR, 25 l/min/1.73 m2). We have concluded that: (1) AIN is a relatively common disease in pediatric practice; (2) it can be severe enough to necessitate dialysis therapy, and (3) AIN often occurs in children with systemic disorders that may be associated with immunologic disorders.

Adolescent↗

PubMed1996

Pathological and biochemical modifications of renal function in ibuprofen-induced interstitial nephritis.

Use of ibuprofen in patients with asymptomatic renal failure is known to produce acute renal toxicity. One of the manifestations is interstitial nephritis of which the pathogenic mechanism remains unclear. In the present study, this nephrotoxic syndrome was induced in rabbits by giving a single dose of uranyl nitrate, followed by consecutive doses of ibuprofen. This animal model thus allowed the assessment of renal functional and pathological changes associated with ibuprofen use in renal insufficiency. In these rabbits, the major abnormality appeared to be confined to the tubulointerstitial compartment. Microscopic examinations of the renal necropsy specimens showed tubular necrosis and interstitial lymphocytic infiltration. The histological finding of lymphocytic aggregation suggests that this nephrotoxic effect stems from a cytotoxic immune reaction in the interstitium. Moreover, levels of renal 2-arylpropionyl-CoA epimerase, a key enzyme involved in the metabolic inversion of ibuprofen, showed a significant reduction, which may result from the massive destruction of the tubular cells in these animals. These results support the premise that renal insufficiency is a prerequisite factor for ibuprofen-induced interstitial nephritis.

Animals↗

PubMed1994

Acute interstitial nephritis with renal failure associated with propylthiouracil therapy.

Propylthiouracil therapy is associated with a variety of adverse reactions. Renal involvement, although rare, has occurred, but neither acute interstitial nephritis nor severe acute renal failure has been reported previously. We report a case of fulminant acute interstitial nephritis with renal failure following treatment with propylthiouracil.

Acute Disease↗

PubMed1997

Oral feeding of renal tubular antigen abrogates interstitial nephritis and renal failure in Brown Norway rats.

We have examined whether oral feeding of antigen can regulate the expression of autoimmune interstitial nephritis induced by antigen-in-adjuvant (RTA/CFA) immunization of Brown Norway rats. Male rats were divided into six experimental groups: Group I, RTA/CFA immunization alone; Groups II, III, and IV were pretreated with 1 mg (Group II), 5 mg (Group III), and 25 mg (Group IV) of oral tubular antigen every other day for ten days, followed by RTA/CFA immunization; Group V was pretreated with a control antigen, followed by RTA/CFA immunization; and Group VI was immunized with CFA alone. Renal histology, inulin clearance, DTH responses to RTA, and IgG antibody responses to RTA were monitored as endpoints of the study. Our results demonstrated that Group III and IV animals had significantly less severe renal injury, as assessed by inulin clearance and extent of renal cortical involvement by mononuclear cells. Group II and IV animals had suppressed DTH responses, and only Group IV animals had significantly depressed antigen-specific IgG serum titers. Group III animals had neither suppressed DTH responses or IgG titers. We conclude that oral administration of tubular antigen can modulate the intensity of interstitial nephritis produced by immunization, but that the regulatory mechanism is not dependent (at all doses of fed antigen) on suppressed DTH reactivity to RTA or suppressed antigen-specific IgG.

Administration, Oral↗

PubMed2003

Zopiclone-induced acute interstitial nephritis.

Zopiclone, a relatively new nonbenzodiazepine short-acting hypnotic medication is prescribed frequently for insomnia. The authors report a case of zopiclone-induced acute interstitial nephritis in a young, otherwise healthy man. The patient presented with anuric acute renal failure requiring hemodialysis. Kidney biopsy results showed acute interstitial nephritis with a prominent eosinophilic infiltrate in the interstitium. He recovered his renal function after stopping the medication and receiving corticosteroids.

Acute Disease↗

PubMed1993

Acute renal failure in patients with drug-induced acute interstitial nephritis.

The clinical features, laboratory evaluation, and outcome were analyzed in 23 patients with acute renal failure (ARF) and drug-induced acute interstitial nephritis (21 proven with biopsy). The groups of drugs implicated were: antibiotics (20 cases), nonsteroidal anti-inflammatory drugs (2 cases), and other drugs (phenobarbitone, 1 case). The clinical and laboratory signs of the disease appeared 3 to 28 days after exposure to the drug. Fever, skin rash, and flank tenderness were the most common clinical features observed (87%); and hematuria (100%), sterile pyuria (83%), and eosinophilia (39%) were established by laboratory tests. Hemodialysis (HD) was performed in 7 patients. Complete normalization of kidney function was observed in 3 patients; improvement to basal level in 3 patients (this group had preexisting renal disease); and CRF, requiring HD, in 1 patient. Renal function improved in all patients with mild to moderate renal insufficiency regardless of the therapy involved. Statistical evaluation could not confirm any significant differences between status of renal function at presentation, treatment (corticosteroids versus symptomatic and supportive measures only), and outcome of drug-induced acute interstitial nephritis (AIN). In summary, ARF due to drug-induced AIN has a favorable course with good prognosis regardless of the use or nonuse of corticosteroids in management strategy.

Acute Kidney Injury↗

PubMed1984

[Acute immunoallergic interstitial nephritis due to noramidopyrine].

A 46-year old patient under noramidopyrine treatment was admitted for acute renal failure. Renal biopsy was performed and showed acute interstitial nephritis without staining at immunofluorescent microscopy. In vitro and in vivo immunological tests using noramidopyrine as antigen were all negative. Abnormal serum creatinine levels were still present 4 months later. To our knowledge, noramidopyrine has rarely been the cause of interstitial nephritis (only one other case has been published), but it has frequently been responsible for drug-induced blood diseases, and noramidopyrine-related drugs have previously been involved in drug-induced nephritis. As the renal damage can probably be explained by a delayed hypersensitivity reaction, an early corticosteroid treatment would help in improving renal function.

Acute Disease↗

PubMed1981

Acute interstitial nephritis. A case characterized by increase in serum IgG, IgM, and IgE concentrations. Eosinophilia, and IgE deposition in renal tubules.

A case of acute interstitial nephritis with a distinct immunopathologic pattern was seen. The relevant findings included elevated levels of serum IgG, IgM, and IgE; persistent eosinophilia; prominent granular and electron-dense depositions of IgE and C3 in renal tubules, as demonstrated by direct immunofluorescent and electron microscopic procedures; persistent failure to demonstrate anti-basement membrane antibodies (both glomerular and tubular); and hypocomplementemia. The findings in our case suggest a type of acute interstitial nephritis with a somewhat different clinical outlook. In this respect, serial assays of complement components and IgE in serum and kidney tissue and determinations of circulating anti-basement membrane antibodies (both glomerular and tubular) may be of particular importance.

Acute Disease↗