[Phenacetin addiction and injurious effects; inclusion-body anemia an interstitial nephritis].
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Anemia↗
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Mortality from chronic interstitial nephritis and phenacetin consumption in Denmark.
After 1950, a pronounced increase in the mortality from chronic interstitial nephritis among women was registered in Denmark. This was suspected to be caused by a contemporary increase in the consumption of drugs containing phenacetin. Restrictions were therefore imposed on the sale of such drugs in 1961 and consumption decreased sharply. This report, based upon death certificates from 1941--76, shows that the mortality rate from chronic interstitial nephritis has decreased gradually among women in Denmark since 1960, and has now reached the same level in younger women as in the 1940's.
Chronic Disease↗
[Reversible renal failure in female patients with acute interstitial nephritis caused by cloxacillin].
Cloxacillin was not listed as one of the drugs causing the acute interstitial nephritis, yet. A case of a 50-year female patient treated with cloxacillin is presented. Therapy was followed by nausea, vomiting, myalgia and arthralgia, and the symptoms of the acute renal failure which completely diminished after prednisone therapy despite of co-existing peptic ulcer. Low doses of corticosteroids seem helpful in the treatment of the acute interstitial nephritis following therapy with cloxacillin even after a long time of the onset.
Acute Kidney Injury↗
Sarcoid tubulo-interstitial nephritis: long-term outcome and response to corticosteroid therapy.
Sarcoidosis is a chronic relapsing multi-systemic disorder characterized by the development of non-caseating granulomas. Granulomatous tubulo-interstitial nephritis is an uncommon manifestation of this condition. We identified 39 patients with sarcoidosis and renal disease from a single center of whom 17 patients had biopsy-proven tubulo-interstitial nephritis. They were analyzed with respect to demographic and clinical features, including response to corticosteroids and length of follow-up. They all presented with significant renal impairment. At presentation the mean+/-s.d. estimated glomerular filtration rate (eGFR) was 26.8+/-14 ml/min by modification of diet in renal disease (MDRD) equation 7. With treatment there was a significant improvement in renal function with eGFR 49.6+/-5.2 ml/min (P<0.01) at 1 year, and 47.9+/-6.8 ml/min (P<0.05) at the last review. The median follow-up was 84 months (range 6-284 months). Patients with chronic kidney disease (CKD) 3, the mean eGFR was 38.30+/-2.4 ml/min at presentation and 60.2+/-7.4 ml/min at 1 year (P=0.02) and in CKD 4 it improved from 19+/-2 to 38+/-6.6 ml/min at 1 year (P<0.05). After the 1st year, the change in eGFR was +0.8 ml/min/year for CKD 3 and -2 ml/min/year for CKD 4 (P<0.05). Three patients ceased their therapy either due to complications or poor compliance and experienced a worsening of renal function which was then reversed on re-commencing corticosteroids. Corticosteroids are effective in advanced tubulo-interstitial nephritis due to sarcoidosis. Long-term treatment is necessary to preserve renal function and to delay the onset of end-stage renal disease.
Adrenal Cortex Hormones↗
Proton pump inhibitors and acute interstitial nephritis.
BACKGROUND & AIMS: Proton pump inhibitors (PPIs) are a widely prescribed class of drugs, and their usage worldwide is increasing. Although well-tolerated, there have been case reports and a recent case series implicating these drugs in acute interstitial nephritis (AIN) and progression to acute renal failure (ARF). The aim of this study was to investigate how widespread this complication is in Australia, to identify which PPIs are implicated, and to establish whether PPI-induced AIN is a class effect. METHODS: We undertook a retrospective case review of potential cases at 2 teaching hospitals and a review of registry data from the Therapeutic Goods Administration of Australia (TGA). Parameters sought included the drug implicated, concurrent medications, symptoms, signs, serum creatinine, and time of onset after prescription. RESULTS: We identified 18 cases of biopsy-proven PPI-induced AIN causing ARF in the retrospective case review, which is the largest hospital-based case series to date. The TGA registry data identified an additional 31 cases of "biopsy proven interstitial nephritis." An additional 10 cases of "suspected interstitial nephritis," 20 cases of "unclassified acute renal failure," and 26 cases of "renal impairment" were also identified. All 5 commercially available PPIs were implicated in these cases. CONCLUSION: With the ever more widespread use of this class of medications, PPI-induced AIN is likely to become more frequent. There is now evidence to incriminate all the commercially available PPIs, suggesting there is a class effect. Failure to recognize this entity might have catastrophic long-term consequences including chronic kidney disease. Increased awareness might facilitate more rapid diagnosis and management of this potentially reversible condition.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Inherited interstitial nephritis in kdkd mice.
kdkd mice, a mutant subline of CBA/Ca mice, develop a progressive, T cell-mediated, autoimmune interstitial nephritis which leads to renal failure and death of all mice at 20-28 weeks of age. This disease is inherited in an autosomal recessive manner, with complete penetrance, and has been linked to grizzled and waltzer on mouse chromosome 10. Immunologic evaluation of this lesion has demonstrated that histologic disease is initiated by a population of CD8+, H-2Kk-restricted T cells, which recognize an antigen in collagenase-solubilized syngeneic renal tubules. These nephritogenic effector cells can also be demonstrated in non-disease prone CBA/Ca mice. Susceptibility to autoimmune nephritis correlates with distinct expression of regulatory, rather than effector, T cells. Interstitial nephritis in kdkd mice can be inhibited by protein-calorie restriction, infusions of CBA/Ca CD8+ T cells, or monoclonal antibodies of ICAM-1. This murine model most closely resembles medullary cystic disease in humans, which has not historically been considered an autoimmune disease. Mapping of the genes for both medullary cystic disease and the defect in kdkd mice should augment our understanding of mechanisms of organ-specific autoimmunity.
Animals↗
[Interstitial nephritis in urological practice].
The presented material consists of 9 postoperative patients' investigations. Interstitial nephritis was diagnosed in them after histological examination. Seven patients had a chronic disease, 2--acute disease. The revealed possible predisposing factors were: a prolonged use of analgetics, contact with formalin and typographical dyes, systematic alcohol usage, frequent catarrhal diseases with long-term fever, a history of acute renal destructive process. The clinical picture of patients with chronic interstitial nephritis was characterized by long periods of temperature elevation, small changes in blood counts, weakness, pain in the lumbar region. In urine analyses: moderate microhematuria, leukocyturia, proteinuria. There were signs of early damaged renal tubular functions. Antiinflammatory therapy was ineffective so the patients were operated on for various indications. During the operations there were severe macroscopic renal cirrhotic deteriorations. 2 patients underwent nephrectomy, 15 intraoperative biopsy. Histologically there were revealed: signs of interstitial tissue various cirrhotic changes in hydrops and lymphoplasmacytic infiltration with tubular compression and dystrophic changes. The following complex therapy including nonsteroid antiinflammatory agents, in some cases corticosteroids, desensitizing and antihistaminic remedy allowed one to achieve alleviation of the process.
Adult↗
Pantoprazole-induced acute interstitial nephritis.
Pantoprazole is a proton-pump inhibitor (PPI) that is commonly prescribed for the treatment of gastroesophageal reflux-related disorders. There are many documented side effects of PPIs. Here we report a case of acute interstitial nephritis, which developed after 6 weeks of treatment with pantoprazole. A 23-year-old man presented with acute renal failure requiring renal replacement therapy. Acute interstitial nephritis was diagnosed by renal biopsy and was successfully treated with corticosteroids and withdrawal of pantoprazole. Drug-induced acute interstitial nephritis can occur with PPIs such as pantoprazole and vigilance needs to be maintained.
2-Pyridinylmethylsulfinylbenzimidazoles↗
[Acute granulomatous interstitial nephritis with iritis. Possible induction by non-steroidal antiphlogistics].
A 49-year old woman developed non-oliguric acute renal failure accompanied by bilateral acute anterior uveitis, following a three weeks' period of lethargy, anorexia and temporary fever. Kidney biopsy revealed acute interstitial nephritis with interstitial infiltrations of lymphocytes and monocytes, as well as multiple perivascular epithelioid granulomas. A substantial improvement of renal function was achieved under treatment with systemic corticosteroids. The uveitis resolved completely under additional topical treatment. During a follow-up period of 9 months, there has been no relapse of nephritis or uveitis. The disease of this patient resembles the so-called TINU syndrome of unknown aetiology. Remarkable features of the present case are the histological diagnosis of granulomatous acute interstitial nephritis in the absence of systemic granulomatous disease, as well as a possible association with the administration of non-steroidal antiinflammatory drugs.
Acute Disease↗
[Ampicillin associated acute interstitial nephritis with renal insufficiency--case report].
It is reported on a 20-year-old male patient, in whom during the treatment of a streptococcal infection with ampicillin an exanthem and an acute interstitial nephritis with acute renal insufficiency appeared. The temporary connection between the application of the medicament and the occurrence of the clinical symptoms and the sensitization to ampicillin proved by the lymphocyte transformation test speak for an ampicillin-induced interstitial nephritis. The discontinuation of the treatment with ampicillin and the application of prednisolone led to a complete involution of the clinical picture. Since ampicillin is frequently used in the clinic one should take into consideration in the indication that possibly an acute renal insufficiency may appear due to an acute interstitial nephritis.
Acute Kidney Injury↗
Interstitial nephritis in rats produced by E. coli in adjuvant: immunological findings.
An increased incidence and severity of interstitial nephritis was produced in F344/fmai rats immunized with E. coli 022 in pertussis vaccine for 12-15 months. Migration of peritoneal exudate cells from immunized animals was inhibited by syngeneic kidney antigens. One out of twenty-eight immunized animals developed anti-TBM antibodies. In this model, interstitial nephritis develops in association with cell-mediated immunity to kidney tissue.
Adjuvants, Immunologic↗
Bilateral anterior uveitis and interstitial nephritis.
Five patients had bilateral anterior uveitis associated with renal disease. Interstitial nephritis was histologically confirmed in three cases. Fatigue, anorexia, abdominal pain, weight loss, and anemia were common systemic complaints or findings. In each case, the uveitis was anterior, eventually bilateral, and associated with minimal visual impairment. Complications of the uveitis included increased intraocular pressure, synechiae, keratic precipitates, macular edema, and intraretinal hemorrhage as well as cells in the anterior vitreous humor and an exudate over the pars plana. Sjögren's syndrome, systemic lupus erythematosus, sarcoid, and syphilis were excluded as diagnoses that could explain the association of renal and uveal disease.
Adolescent↗
Acute interstitial nephritis associated with cefotetan therapy.
We report a case of acute interstitial nephritis associated with cefotetan therapy. Cefotetan should be considered a potential cause of acute renal failure in patients who develop rash, eosinophilia, and fever in association with an acute deterioration of renal function.
Acute Disease↗
Acute interstitial nephritis due to nicergoline (Sermion).
We report a case of acute interstitial nephritis (AIN) due to nicergoline (Sermion). A 50-year-old patient admitted to our hospital for fever and acute renal failure. Before admission, he had been taking nicergoline and bendazac lysine due to retinal vein occlusion at ophthalmologic department. Thereafter, he experienced intermittent fever and skin rash. On admission, clinical symptoms (i.e. arthralgia and fever) and laboratory findings (i.e. eosinophilia and renal failure) suggested AIN, and which was confirmed by pathologic findings on renal biopsy. A lymphocyte transformation test demonstrated a positive result against nicergoline. Treatment was consisted of withdrawal of nicergoline and intravenous methylprednisolone, and his renal function was completely recovered. To our knowledge, this is the first report of nicergoline-associated AIN.
Acute Disease↗
[Acute interstitial nephritis and uveitis in the adult: apropos of 3 cases].
Acute renal failure due to tubulo-interstitial nephritis accompanied by uveitis has been observed in 3 young women (TINU syndrome). In these 3 cases, the nephropathy was preceded (1-3 months) by asthenia, anorexia, weight loss and a major inflammatory syndrome. Nonsteroidal anti-inflammatory drugs (NSAID) administration was noted. In 2 cases, uveitis appeared after the nephropathy had subsided. Renal biopsies performed in the 3 patients revealed mainly interstitial changes with mononuclear cell infiltration; immunofluorescence studies were negative. Although the severity of renal failure varied among patients, renal function recovered completely, returning to normal within 2, 3 and 24 months respectively, on corticosteroid therapy. The TINU syndrome is a rare situation compared to drug-induced acute interstitial nephritis, including NSAID related-nephritis. However, the real incidence of this syndrome might be underestimated since the uveitis can appear a few weeks later and its origin may not be related to the renal episode.
Acute Disease↗
Recurrent acute interstitial nephritis induced by azithromycin.
A 14-year-old girl is reported with recurrent, azithromycin-induced, acute interstitial nephritis. The second episode was more severe than the first; and although both were treated with intensive corticosteroid therapy, renal function remained impaired. Although most cases of antibiotic induced acute interstitial nephritis are benign and self-limited, some patients are at risk for permanent renal injury.
Acute Disease↗
Inhibition of inducible nitric oxide synthase intensifies injury and functional deterioration in autoimmune interstitial nephritis.
T lymphocytes are exquisitely sensitive to the antiproliferative effects of nitric oxide. We examined the effects of oral administration of two nitric oxide synthase inhibitors, Nw-nitro-L-arginine methyl ester (L-NAME) and L-N6-(1-iminoethyl)lysine (L-NIL), on the course of T cell-dependent autoimmune interstitial nephritis in Brown Norway rats. Kidneys from rats immunized to produce interstitial nephritis display a net generation of nitric oxide end products. By immunohistochemical staining, the cytokine-inducible nitric oxide synthase (iNOS) is expressed in cortical tubular epithelial cells. Treatment with either inhibitor results in markedly more severe disease following immunization. Animals receiving L-NAME were hypertensive, while those treated with L-NIL, a highly selective inhibitor of iNOS, were not. Evaluation of the expression of IFN-gamma, IL-2, and IL-4 in diseased kidneys by quantitative reverse transcriptase-PCR demonstrated that L-NAME-treated animals displayed significantly augmented levels of IFN-gamma and IL-2 with preserved ratios of IFN-gamma/IL-4 and IL-2/IL-4, while L-NIL-treated animals had augmented levels of IL-2 and IFN-gamma with augmented IFN-gamma/IL-4 and IL-2/IL-4 ratios. Animals treated with L-NAME or L-NIL both had augmented Ag-specific IgG responses. The L-NAME group demonstrated increases in both the IgG2a and IgG1 subtypes, with a constant IgG2a/IgG1 ratio, while the L-NIL group demonstrated an increase in the ratio of the IgG2a/IgG1 response. These Ab and cytokine data suggest that the L-NIL-treated animals had a skewing of their immune response toward a Th1-like response. We conclude that in autoimmune interstitial nephritis, generation of nitric oxide through the iNOS pathway has host-protective effects, and suggest that this may be broadly applicable to T cell-mediated pathologies.
Administration, Oral↗
Interstitial nephritis, proteinuria, and renal failure caused by nonsteroidal anti-inflammatory drugs. Immunologic characterization of the inflammatory infiltrate.
Nine patients with the unusual combination of renal failure, nephrotic-range proteinuria, and biopsy-proved interstitial nephritis are described. Six of these patients had received nonsteroidal anti-inflammatory agents (three fenoprofen, one ibuprofen, one zomepirac, and one tolmetin). The remaining three patients had no history of exposure to drugs known to cause interstitial nephritis. Immunologic characterization of the infiltrating cells with monoclonal antibodies showed that the majority of cells in most cases were cytotoxic T cells, although some B cells were present in all cases. Giant collecting duct cells were seen in half the patients with drug exposure but in none of the others. Otherwise, there were no conspicuous morphologic differences between patients with and without drug exposure. Many of the patients had associated glomerular abnormalities. Only the zomepirac and tolmetin recipients showed pure interstitial disease. The three fenoprofen recipients and the zomepirac and tolmetin recipients regained normal renal function after the drug was discontinued. The combination of renal failure, nephrotic range proteinuria, and interstitial nephritis is one form of nephrotoxicity observed in patients treated with nonsteroidal anti-inflammatory agents. However, this lesion, which may be mediated by cytotoxic T cells, may also be seen rarely in patients with no apparent drug exposure.
Adult↗