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Cystitis and interstitial nephritis related to the use of tiaprofenic acid (Surgam).

We describe a case of concurrent presentation of severe haemorrhagic cystitis and acute interstitial nephritis with eventually lethal outcome, associated with the use of tiaprofenic acid (Surgam), a propionic acid-derived non-steroidal anti-inflammatory drug (NSAID). Although interstitial nephritis and haemorrhagic cystitis are caused by all types of NSAIDs, a higher incidence of interstitial nephritis and especially haemorrhagic cystitis has been described related to propionic acid derivatives. Awareness of this serious adverse effect is important.

Aged↗

[Acute hematogenic interstitial nephritis of urinary origin: an unrecognized factor in the exacerbation of chronic kidney failure].

Hypertension, phosphate retention, hyperfiltration hyalinosis and the natural course of the underlying are well known factors leading to progression of chronic renal failure. Acute bacterial interstitial nephritis occurring in a previously diseased kidney, although well documented in experimental animals, has not been shown to aggravate chronic renal failure in man. We report on 3 cases of acute suppurative interstitial nephritis, due to E. coli urinary infection complicated by septicemia. All had rapid aggravation of previously mild renal failure secondary to chronic interstitial nephritis. Sepsis originated from the urinary tract which in 2 instances had been temporarily obstructed. Renal biopsy disclosed a diffuse interstitial infiltrate containing numerous polymorphonuclear leukocytes. This was superimposed on chronic tubular and interstitial lesions. In 1 case there were glomerular lesions with crescents and mesangial C3 deposits. A 2nd biopsy performed in 2 cases was of prognostic interest. In one case it showed active lesions and the necessity of continuing the treatment and in the other a satisfactory healing allowing cessation of therapy. Treatment was guided by antibiograms, the clinical and urinary signs of activity, renal biopsy findings and antibiotics known to be concentrated in renal tissue. The duration of treatment seemed important for the regression of acute renal lesions. Hematogenous bacterial interstitial nephritis should be considered as a possible cause of aggravation in chronic renal failure.

Acute Disease↗

Immunologically mediated tubulo-interstitial nephritis in children.

14 children with proven or presumably immunologically mediated tubulo-interstitial nephritis are presented. In 2 patients anti-tubular basement membrane antibodies were detected. In 6 immunofluorescence microscopy showed granular deposits of immunoglobulin and/or complement likely representing interstitial location of immune complexes. The findings by immunofluorescence were not significant in the remaining 6 patients. However, the association of renal disease to extra-renal disorders, namely chronic active hepatitis and ulcerative colitis, or uveitis or the presence of an epithelioid granuloma with multinucleated giant cells suggests that in such patients an immunologic disorder might be responsible for the tubulo-interstitial nephritis.

Animals↗

Acute interstitial nephritis associated with salmonellosis.

Acute interstitial nephritis (AIN) is a common cause of acute renal failure. We report a case of AIN, confirmed by renal biopsy, that developed in a patient with typhoid fever due to a Salmonella hadar infection. AIN secondary to Salmonella infection is a rare complication that has only been described twice in the literature. Salmonella should be added to the list of possible causes of AIN.

Journal Article↗

Interstitial nephritis, the nephrotic syndrome, and chronic renal failure secondary to nonsteroidal anti-inflammatory drugs.

Nonsteroidal anti-inflammatory drugs (NSAIDs) may induce a variety of acute and chronic renal lesions. Acute interstitial nephritis can follow the use of nearly all NSAIDs, but the number of reported cases is low. Most of these patients are elderly and develop a nephrotic syndrome with acute renal failure while taking NSAID for months. Renal biopsy shows acute tubulo-interstitial lesions with minimal changes in the glomeruli. The renal signs usually improve after discontinuing the drug, with or without steroid therapy, but chronic renal insufficiency or even end-stage renal disease (ESRD) are possible hazards. There is evidence that interstitial nephritis results mainly from a delayed hypersensitivity response to NSAID, and nephrotic syndrome results from changes in glomerular permeability mediated by prostaglandins and other hormones. Nephrotic syndrome without interstitial nephritis may occur, as well as immune-complex glomerulopathy, in a small subset of patients receiving NSAIDs. Patients taking NSAID for months or years may develop papillary necrosis, chronic interstitial nephritis, or even ESRD. Case-control studies suggest that patients at risk are older men who suffer from chronic heart disease and renal hypoperfusion. Impaired medullary circulation and direct toxicity due to a drug metabolite seem to play a critical role in inducing interstitial fibrosis, which can be facilitated by a sustained production of some growth factors and cytokines.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗

The diagnosis and racial origin of 394 patients undergoing renal biopsy: an association between Indian race and interstitial nephritis.

BACKGROUND: There is a high incidence of renal disease in the ethnically Indian population in the United Kingdom, the pathological basis for which is only partly understood. This study attempted to define associations between renal biopsy diagnosis and race. The aim was thereby to identify types of renal disease which may contribute to the observed predisposition to renal failure in the Indian population served by our centre. METHOD: A single-centre-based retrospective analysis of the final diagnosis and corresponding ethnicity in 394 consecutive patients undergoing native renal biopsy for the investigation of abnormal renal function or urinary sediment. RESULTS: A highly significant association between a diagnosis of interstitial nephritis and Indian race was observed. There were 30 cases of interstitial nephritis, of whom 17 were Indian. In 15 of the Indian patients no aetiology could be established. The clinical features, outcomes, and the effect of steroid therapy in the Indian patients with idiopathic interstitial nephritis are described. CONCLUSION: Idiopathic interstitial nephritis is associated with Indian racial origin. This pathology may significantly contribute to the high incidence of end-stage renal failure in Indian patients resident in the United Kingdom.

Adult↗

Acute interstitial nephritis: a clinical and morphological study in 27 patients.

The clinical presentation, the morphological findings, and the clinical outcome of 27 patients with biopsy-proven acute interstitial nephritis were studied. All patients except one presented with acute renal failure. Typical clinical findings were often absent. Only four patients showed the classical triad of pyrexia, rash and arthralgia. In more than half of the patients an increased blood eosinophil count was not present. Kidney biopsy is therefore needed to establish the diagnosis of acute interstitial nephritis. In many patients acute interstitial nephritis was diagnosed in the biopsy when clinically this type of kidney disease was not expected. In 17 patients renal function improved spontaneously after withdrawal of the drug responsible or treatment of the infection. In ten patients who showed further deterioration of renal function in the first 2 weeks after admission, prednisone therapy was instituted. In all of them improvement of renal function was observed, with six returning to normal.

Acute Disease↗

Detection of carp interstitial nephritis and gill necrosis virus in fish droppings.

Carp interstitial nephritis and gill necrosis virus (CNGV) is an unclassified large DNA virus that morphologically resembles members of the Herpesviridae but contains a large (ca. approximately 280-kbp) linear double-stranded DNA. This virus has also been named koi herpesvirus, koi herpes-like virus, and cyprinid herpesvirus 3. CNGV is the cause of a lethal disease that afflicts common carp and koi. By using immunohistochemistry, molecular analysis, and electron microscopy we previously demonstrated that this virus is present mainly in the intestine and kidney of infected fish. Based on these observations, we postulated that viruses and/or viral components may appear in droppings of infected carp. Here we report that (i) by using PCR we demonstrated that fish droppings contain viral DNA, (ii) fish droppings contain viral antigens which are useful for CNGV diagnosis, and (iii) fish droppings contain active virus which can infect cultured common carp brain cells and induce the disease in naïve fish following inoculation. Thus, our findings show that CNGV can be identified by using droppings without taking biopsies or killing fish and that infectious CNGV is present in the stools of sick fish. The possibility that fish droppings preserve viable CNGV during the nonpermissive seasons is discussed.

Animals↗

Antibiotics-induced acute interstitial nephritis in 6 children.

INTRODUCTION: Antibiotics-induced acute interstitial nephritis (AIN) is a rare disorder in children, and the diagnosis is often delayed. However, many commonly prescribed antibiotics seem to be implicated. PATIENTS AND METHODS: We reviewed the medical records of 6 children, age range from 10 months to 14 years, with biopsy-confirmed antibiotics-induced AIN. Clinical presentation, morphological findings, and outcomes are reported. RESULTS: Symptoms of AIN started 2-4 weeks after antimicrobial therapy with beta-lactam antibiotics in 5 children and with gentamicin in 1 child. All patients presented with acute renal failure and fever. The glomerular filtration rate was dramatically reduced in 2 cases and mildly reduced in 4 patients. Two of our patients had supportive treatment, 2 received corticosteroid therapy, and 2 children remained under peritoneal dialysis for 12 and 22 days, respectively. Five patients had a full recovery of their renal function, and 1 child, 2 years later, still presented impairment of the renal function. CONCLUSION: AIN should be considered in case of acute renal failure in children, mostly when other common causes have been excluded, and there is a history of drug exposure.

Acute Disease↗

Idiopathic necrotising granulomatous interstitial nephritis.

We report a case of idiopathic necrotising granulomatous interstitial nephritis seen as an incidental autopsy finding in a 65 years female. The unusual features were the presence of necroses, with a florid, bizarre giant cell reaction. There were varying degrees of tubular damage, with relative sparing of glomeruli. There was no history of drug ingestion; Mycobacteria, fungi or crystals were not identified.

Aged↗

[Idiopathic interstitial nephritis induced acute renal failure: clinical and pathological analysis].

OBJECTIVE: To understand idiopathic interstitial nephritis (IIN) and its relationship with acute renal failure as well as its clinical and pathological characteristics for avoiding misdiagnosis and missing diagnosis. METHOD: A detail clinical and pathological analysis was performed on 7 patients with idiopathic interstitial nephritis. RESULTS: The major manifestations were acute non-oliguric renal insufficiency combined with mild proteinuria (< 2 g/d), microscopic hematuria and obvious disorder of renal tubular function (for example, glycosuria). Three patients had high gamma-globulinemia and 2 were associated with uveitis. Renal biopsy showed typical tubulointerstial nephritis but glomeruli, and the renal vasculature was almost normal. All patients were treated with prednison. Renal function recovered in 5 patients. CONCLUSION: When a patient has renal insufficiency especially non-oliguric renal failure with disorder of tubular function without definite causes, IIN should be considered. The diagnosis and treatment should be done immediately.

Acute Kidney Injury↗

Cimetidine-induced acute interstitial nephritis.

Cimetidine is responsible for changes in serum creatinine. Previously reported, this has been thought to be related to an alteration in the manner in which the kidney handles creatinine. Herein a case of acute interstitial nephritis attributable to the ingestion of routine doses of cimeditine is detailed. Review of the changes in serum creatinine and renal function in patients taking cimetidine reveals that as many as 60% of the patients taking cimetidine may have changes in serum creatinine. In none of those series, however, have changes in urinary protein excretion or urinary sediment been followed. Recently several reports have been published in which patients have developed acute interstitial nephritis while taking cimetidine. However, in no previously reported case has the diagnosis been proved by rechallenging the patient with that drug. In our study the patient had moderate to severe renal insufficiency with acute interstitial nephritis while on cimetidine. Rechallenging the patient with cimetidine resulted in prompt return of clinical signs and symptoms as well as changes in serum creatinine and urinary sediment characteristics diagnostic of interstitial nephritis.

Aged↗

Relapsing steroid-responsive idiopathic acute interstitial nephritis.

A 49-year-old woman developed acute renal failure secondary to interstitial nephritis. Her clinical history, complementary studies and two renal biopsies could not establish the etiology. She showed signs of incomplete Fanconi syndrome. Treatment with corticosteroids was very effective, though she tended to relapse. We comment briefly on some aspects of idiopathic acute interstitial nephritis.

Acute Kidney Injury↗

[Chronic interstitial nephritis and mesalazine: 3 new cases?].

We report three new cases of chronic interstitial nephritis occurring in two patients with Crohn's disease and one patient with ulcerative colitis treated with mesalazine. In the three cases asymptomatic renal disease was revealed by an increase in serum creatinine which was normal before treatment. Renal biopsy showed features of severe chronic interstitial nephritis. Mesalazine withdrawal and administration of steroids in two cases led to partial improvement of renal function. Mechanism of renal toxicity of mesalazine is unknown. These observations stress the need for monitoring renal function in patients with inflammatory bowel disease treated with mesalazine.

Adult↗