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At least 199 records · Page 11Linked to original sources
PubMed2006

Acute immuno-allergic interstitial nephritis caused by fluindione.

Fluindione is a vitamin K antagonist that is commonly prescribed for the treatment of cardiovascular disease and venous thromboembolism in France. Bleeding is the most common side effect of fluindione, whereas hypersensitivity reactions are rare. We describe here a patient with acute immuno-allergic interstitial nephritis caused by fluindione. Initial symptoms included fever, eosinophilia, low albuminuria, microscopic hematuria, eosinophiluria and acute renal failure. Kidney biopsy showed severe interstitial nephritis with interstitial edema, inflammatory infiltrates and tubulorrhexis. Fluindione withdrawal and corticosteroid treatment resulted in rapid recovery of renal function. A review of the literature revealed a very low incidence of fluindione-induced interstitial nephritis, with variable renal and extra-renal signs. Early recognition of this rare complication may prevent the development of severe chronic renal injury.

Aged↗
PubMed2005

Acute interstitial nephritis due to mesalazine.

A case of mesalazine-induced acute interstitial nephritis (AIN) in a 41-year-old patient with ulcerative colitis (UC) is reported here. Clinical symptoms such as fever and arthralgia, and laboratory findings such as eosinophilia and renal failure suggested AIN, which was confirmed by biopsy. With withdrawal of mesalazine and intravenous methylprednisolone the patient's renal function was recovered. It is observed that early discontinuation of mesalazine is associated with amelioration of interstitial nephritis in most patients, so the recommendation is that patients receiving mesalazine should undergo routine monitoring of renal function. Delayed diagnosis may lead to permanent renal function impairment.

Acute Disease↗
PubMed2003

Renal allograft loss as the result of polyomavirus interstitial nephritis after simultaneous kidney-pancreas transplantation: results with kidney retransplantation.

BACKGROUND: Polyomavirus (PV) infection in kidney transplant patients has been reported to cause interstitial nephritis and subsequent graft loss. The cornerstone of current therapy is a reduction in immunosuppression, which can subsequently lead to kidney allograft rejection. This dilemma becomes even more challenging in the setting of simultaneous kidney-pancreas transplantation, because a reduction in immunosuppression may result in rejection of the pancreas allograft. Antiviral therapy has not been shown to be clinically successful in decreasing the risk of graft loss secondary to PV infection. Furthermore, because of limited experience, the decision to perform retransplantation in patients who lost their primary kidney grafts to PV interstitial nephritis becomes a difficult one. METHODS: Retrospective review and case studies. RESULTS: We report two successful living donor kidney retransplants in simultaneous kidney-pancreas transplant patients who lost their first kidney grafts to PV infection. Both patients are receiving rimantadine therapy and performing well, with functioning kidney and pancreas grafts and no evidence of recurrent PV interstitial nephritis 22 and 37 months after retransplantation. CONCLUSIONS: Although follow-up is limited, our initial experience would indicate that graft loss secondary to PV interstitial nephritis is not an absolute contraindication for kidney retransplantation.

Adult↗
PubMed1983

Drug-induced granulomatous interstitial nephritis.

Among 22 cases of drug-induced acute interstitial nephritis (AIN), noncaseating interstitial granulomas were found in eight cases (36%). Acute renal failure (ARF), oliguric in three patients, appeared within 1-20 days after the beginning of therapy. Clinical symptoms suggesting a hypersensitivity reaction were unusual, marked blood eosinophilia was absent, and immunologic tests were inconstantly positive. The discovery of interstitial granulomas may be a clue to the diagnosis of drug-induced AIN, especially when the inflammatory infiltrates do not contain eosinophils. Since significant residual renal impairment may be observed the benefit of early steroid therapy must be debated.

Adolescent↗
PubMed1986

Drug-induced acute interstitial nephritis: report of 10 cases.

Between January 1979 and June 1985, 10 patients with acute allergic interstitial nephritis were seen in a clinical nephrology service at a large regional hospital. The onset of renal failure was temporally related to the use of a drug: a nonsteroidal anti-inflammatory agent (NSAID) (in four patients), cimetidine (in three), antibiotics (in two) or allopurinol (in one). The onset of renal failure was acute in three patients and insidious in seven. Two patients also exhibited marked proteinuria. Clinical features such as fever, rash, hematuria, pyuria with or without eosinophiluria, and mild to marked proteinuria had led to suspicion of the disease. The diagnosis was confirmed by renal biopsy findings of inflammatory cells, predominantly lymphocytes, plasma cells and eosinophils. Three patients required hemodialysis; two of them received steroids as well. Steroid therapy was also used in two patients with NSAID-induced proteinuria. Renal function improved in nine patients by 35 days, but one patient continued to have slow but progressive deterioration of renal function. Acute interstitial nephritis can be distinguished from other forms of acute renal failure by heavy renal uptake of gallium 67, maximal 48 hours or more after injection. The improvement in renal function after discontinuation of the implicated drug, the characteristic histopathological findings of allergic interstitial nephritis, and the presence of eosinophils and sometimes IgE in the blood suggest a hypersensitivity reaction.

Acute Disease↗
PubMed2005

Acute interstitial nephritis predisposed a six-year-old girl to minimal change nephrotic syndrome.

A six-year-old girl was admitted to our hospital with acute renal failure. We made a clinical diagnosis of acute interstitial nephritis and oral corticosteroid therapy was started. Her renal failure soon recovered, and renal biopsy showed acute interstitial nephritis by light microscopy with glomerular foot process effacement by electron microscopy. Although her proteinuria was not heavy at the time of biopsy, her proteinuria subsequently increased to show nephrotic syndrome. We continued to give corticosteroids and her nephrotic syndrome went into remission 13 days after biopsy. Serological and bacteriological examination showed no evidence of known pathogen or drug hypersensitivity. The time changes in proteinuria were monitored by fractional total protein excretion (FETP) and fractional beta2 microglobulin excretion (FEbeta2MG) in order to evaluate the severity of proteinuria under different glomerular filtration rates and different proximal tubular functions. The results revealed that nephrotic syndrome had occurred during recovery from acute interstitial nephritis. This is the first case report to show the sequential occurrence of acute interstitial nephritis and nephrotic syndrome based on evidence from fractional protein excretion.

Acute Disease↗
PubMed1993

Immune-related potassium-losing interstitial nephritis: a comparison with distal renal tubular acidosis.

Six patients with immune-related potassium-losing interstitial nephritis (IRPLIN) are described, and compared with 34 patients with immune-related distal renal tubular acidosis (IRdRTA) and 24 with familial distal renal tubular acidosis (FdRTA). Close similarities were found between IRPLIN and IRdRTA. In our experience, both syndromes are confined to postpubertal women, and are characterized by systemic features of autoimmune disease and a chronic interstitial nephritis which is probably immune-mediated and responsible for the functional tubular defects of the two syndromes. In IRPLIN, a renal potassium-losing state is the main consequence (probably mediated at least in part by renin and aldosterone hypersecretion secondary to renal sodium-losing), and urinary acidification is normal or minimally disturbed; consequently there is no systemic acidosis, and the syndrome is not complicated by nephrocalcinosis or renal bone disease. In IRdRTA, the renal tubular lesion also usually causes potassium depletion, but the most prominent tubular fault is a defect in urinary acidification, which commonly causes metabolic acidosis and often leads to nephrocalcinosis and bone disease. Familial dRTA, in contrast, is equally prevalent in the two sexes and presents at an earlier age than IRPLIN and IRdRTA. Patients with FdRTA and IRdRTA have a similar urinary acidification defect and propensity to acidosis, nephrocalcinosis and bone disease. FdRTA is frequently complicated by renal potassium-losing, but hypokalaemia is less common and less profound than in IRdRTA and IRPLIN, suggesting that immune-related interstitial nephritis has a particular tendency to cause renal potassium-losing.

Acidosis, Renal Tubular↗
PubMed1987

Allergic interstitial nephritis due to diazepam.

A 56-year-old man developed allergic interstitial nephritis and deterioration of preexisting chronic renal failure after receiving diazepam. On discontinuation of diazepam, kidney function returned to the baseline level and itching, eosinophilia, and eosinophiluria subsided. A causative correlation between allergic interstitial nephritis and diazepam is suggested.

Diazepam↗
PubMed1989

Interstitial nephritis related to nonsteroidal anti-inflammatory agents and beta-lactam antibiotics: a comparative study of the interstitial infiltrates using monoclonal antibodies.

Acute interstitial nephritis (AIN) is a common pattern of renal injury induced by therapeutic agents. In order to characterize the types of mononuclear leukocytes infiltrating the kidney in drug-induced interstitial nephritis, a panel of monoclonal antibodies (Leu1, Leu3a, OKT8, OKM1, Leu14, OKT17, IL-2) was applied to cryostat sections of 13 renal biopsies (five non-steroidal anti-inflammatory agents (NSAID) (Group I); five beta-lactam antibiotics (Group II), 3 miscellaneous (Group III]. The majority of infiltrating mononuclear leukocytes were Leu1-positive T cells (71.7 +/- 18.7%), followed by monocytes (15.2 +/- 7.7%) and B cells (7.4 +/- 9.1%). Leu3a/OKT8 ratio was 0.954 +/- 0.341. Rare cells reacted with antibody to the interleukin-2 receptor (1.4 +/- 1.2%). No statistically significant differences could be found in the percentages of T lymphocytes, B lymphocytes, monocytes, activated (IL-2+) T cells or Leu3a/OKT8 (helper/suppressor) ratios in the three groups. In Group II, the following pathologic correlations were seen: Leu3a/OKT8 versus interstitial inflammation (R = -0.848), percent Leu3a versus interstitial inflammation (R = -0.818), percent OKT17 versus tubulitis (R = 0.785), percent Leu14 versus tubular atrophy (R = -0.891), and interstitial edema (R = 0.965). Our findings support a role for cellular immune mechanisms in the pathogenesis of AIN related to both NSAIDs and beta-lactam antibiotics.

Adult↗
PubMed1988

Sodium-valproate-induced interstitial nephritis.

A 5-year-old Chinese girl had had absence seizures and received sodium valproate (VPA) treatment which provided good control. Six months later, she developed interstitial nephritis with proteinuria and microhematuria. Renal biopsy revealed interstitial nephritis with granular deposition of immunoglobulin G (IgG) and C3 in the renal tubular basement membrane (TBM). Ultrastructurally, dilated smooth endoreticular cisternae with mitochondrial degeneration in the tubular cells and scattered electron-dense deposits within the TBM were also noted. Serum circulating immune complexes were detectable, ACH50 and properdin factor B increased. Mononuclear cells (MNC) from the patient after in vitro incubation with VPA (100 micrograms/ml) induced interleukin-2 (IL-2) production and lymphoproliferative response. However, there was no response in controls. The serum VPA level ranged from 84 to 92 micrograms/ml. After VPA was stopped, the microhematuria and proteinuria disappeared. These observations indicate that VPA-induced interstitial nephritis represents a sequence of interrelationships among multiple immunologic factors.

Child, Preschool↗
PubMed2006

[Chronic interstitial nephritis in an 18-year-old due to intake of a compound analgesic].

BACKGROUND: Renal side effects of nonsteroidal anti-inflammatory drugs (NSAIDs) are acute renal failure due to an impaired perfusion caused by inhibition of prostaglandin synthesis, acute allergic interstitial nephritis as well as acute toxic tubular necrosis. Moreover, chronic renal failure may occur due to a chronic interstitial nephritis or an analgesic nephropathy that is characterized by capillary sclerosis and papillary necrosis in addition to chronic interstitial nephritis. In contrast to acute renal insufficiency that may already occur after a single NSAID dose, analgesic nephropathy is a disease caused by long-term intake of NSAID compound analgesics and predominantly affects the middle and old age. CASE REPORT: An 18-year-old patient with a 4-year history of NSAID compound analgesic intake presented to the urology department with right-sided flank pain and increased serum creatinine. An obstruction as well as nephrolithiasis were ruled out and the patient was referred to the medical department. Urinalysis showed leukocyturia, mild microhematuria as well as proteinuria of 2.2 g/day whereupon a diagnostic kidney biopsy was performed. Histology revealed a chronic nonpurulent destructive interstitial nephritis. After cessation of analgesic intake, the serum creatinine level fell to the normal range; however, a reduced creatinine clearance persisted indicating chronic renal damage. CONCLUSION: The present case is remarkable in that chronic renal damage due to intake of a compound analgesic was already observed in an 18-year-old patient. In this context, the permission of NSAID compound analgesics and their free over-the-counter sale to adolescents need to be critically questioned.

Acetaminophen↗
PubMed2006

Karyomegalic interstitial nephritis: report of 3 new cases and review of the literature.

Karyomegalic interstitial nephritis is a rare, but perhaps an "underdiagnosed" condition. Peculiar nuclear changes characterize it, involving mainly tubular cells along with glomeruli and blood vessels. Herein, 3 bioptically proven new cases of patients with chronic renal failure are discussed. The first case had a recently diagnosed karyomegalic nephritis which, to date, still does not require dialysis. The other 2 (brother and sister) required dialysis 4 and 1 years after diagnosis. Karyomegalic changes were found not only in the skin and duodenal biopsies of the male, in skin and liver biopsies of the female and in the urine cells of both patients, but also in several organs (brain, thyroid, lung, esophagus, arteries) as shown at the autopsy of the female. There was a fatal outcome for both patients. The data reported in this study emphasize the usefulness of pathologic investigation of both tissue and urine samples in the identification of this disease. Moreover, as karyomegalic interstitial nephritis is strongly suspected to have a genetic background, its identification may well not only be of clinical relevance, due to its ominous outcome, but may also bear eugenetic value.

Adult↗
PubMed2005

Granulomatous interstitial nephritis associated with bone marrow transplantation.

We describe two brothers with severe combined immunodeficiency, who presented with systemic granulomatous disease, with granulomatous interstitial nephritis as the main feature, several years following bone marrow transplantation. Neither brother had an apparent drug-induced, infectious disease or autoimmune source for the granulomatous interstitial nephritis. Both patients' renal function improved following treatment with corticosteroids. This report implicates granulomatous interstitial nephritis as a complication of bone marrow transplantation for severe combined immunodeficiency.

Adolescent↗
PubMed2000

[Streptococcal infection, acute kidney failure and interstitial nephritis].

The relationship between streptococcal infection and renal disease has been object of multiple studies. Streptococcal infection may induce acute glomerulonephritis or interstitial nephritis. We report a patient with a streptococcal infection who developed acute renal failure. The renal biopsy showed an acute interstitial nephritis, with an interstitium infiltrate with a significant number of eosinophils. We review the causes of acute renal failure associated with streptococcal infection, specially acute interstitial nephritis.

Acute Kidney Injury↗