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PubMed1985

Acute tubulo-interstitial nephritis and uveitis syndrome (TINU syndrome).

Acute renal failure due to tubulo-interstitial nephritis developed in a 15-year-old girl. The disease was accompanied by uveitis and an inflammatory syndrome, consisting of a markedly increased erythrocyte sedimentation rate and high serum gamma globulin levels. The nephropathy as well as the inflammatory syndrome subsided spontaneously. A topical antiphlogistic treatment healed the ocular disease, which has not relapsed so far. The association of acute tubulo-interstitial nephritis and acute uveitis observed in several patients has led to the identification of a specific syndrome with a very particular symptomatology and course, the so-called TINU syndrome, the interest of which resides in the predictability of the complete reversibility of the nephropathy either spontaneously or after steroid treatment, contrasting with the marked tendency towards relapse of the uveitis. The demonstration of circulating immune complexes in the serum during the acute phase of the illness, as in our patient, further points to the involvement of immune processes in the syndrome, but the origin and pathogenesis remain as yet unknown.

Acute Disease↗
PubMed2001

Isolated sarcoid granulomatous interstitial nephritis: review of five cases at one center.

AIMS: To identify any clinical or biochemical parameters which determine prognostic outcome in isolated sarcoid granulomatous interstitial nephritis presenting with renal failure. METHODS: A review of five cases of renal failure due to isolated sarcoid granulomatous interstitial nephritis, which presented to Hope Hospital over the 7-year period 1994 to 2000. Follow-up averaged 35 months with a range of 11 to 73 months. RESULTS: Only one patient had an elevated serum ACE at presentation, reflecting the suboptimal sensitivity of this test as a marker in sarcoidosis and the limited extent of disease in these patients. Four of the five cases had a marked improvement in creatinine clearance within 10 days of starting oral prednisolone. Two patients required acute hemodialysis on presentation. Their renal failure responded to treatment with steroids, enabling withdrawal of dialysis within 10 days. All patients remained dialysis-independent although serum creatinine levels rose during follow-up. One patient experienced a relapse that responded to an increased dose of steroid. CONCLUSIONS: Serum ACE is not reliable in the diagnosis of renal failure due to sarcoid interstitial nephritis and the diagnosis can only be made on renal biopsy. First-line treatment with oral prednisolone results in a rapid improvement in creatinine clearance although prolonged treatment may be needed to prevent a relapse.

Aged↗
PubMed1999

Cynomolgus polyoma virus infection: a new member of the polyoma virus family causes interstitial nephritis, ureteritis, and enteritis in immunosuppressed cynomolgus monkeys.

Polyoma virus infection causes acute interstitial nephritis and ureteral stenosis in humans but has rarely been noted in other species. In the present study, a hitherto unknown polyoma virus was detected in 12 of 57 cynomolgus monkeys after 3 to 11 weeks of immunosuppression given to promote acceptance of renal allografts or xenografts. This virus, termed cynomolgus polyoma virus (CPV), is antigenically and genomically related to simian virus 40 (SV40). The tubular epithelial nuclei of the collecting ducts in the medulla and cortex reacted with an antibody for the SV40 large T antigen and by electron microscopy contained densely packed paracrystalline arrays of 30- to 32-nm diameter viral particles. A polymerase chain reaction analysis of DNA extracted from affected kidneys detected polyoma virus sequences using primers for a highly conserved region of the large T antigen of polyoma virus. Sequence analysis showed 7 base substitutions and 3 to 5 deletions in the 129-nucleotide segment of amplified products, compared with the corresponding portion of SV40, yielding 84% homology at the amino acid level. CPV caused interstitial nephritis in six renal allografts, a xenograft kidney, and six native kidneys. Infected animals showed renal dysfunction and had tubulointerstitial nephritis with nuclear inclusions, apoptosis, and progressive destruction of collecting ducts. CPV was detected in the urothelium of graft ureters, associated with ureteritis and renal infection. Viral infection was demonstrable in smooth muscle cells of the ureteric wall, which showed apoptosis. One animal had diarrhea and polyoma virus infection in the smooth muscle cells of the muscularis propria of the intestine. Spontaneous resolution occurred in one case; no animal had virus detected in tissues more than 3 months after transplantation. Thus, immunosuppression predisposes cynomolgus monkeys to a polyoma virus infection with clinical consequences quite similar to BK virus infection in humans, including renal dysfunction. We also suggest that this may be the pathogenetic basis for the significant incidence of late onset, isolated ureteral stenosis observed in these recipients.

Animals↗
PubMed2001

Acute renal failure from hemoglobinuric and interstitial nephritis secondary to iodine and mefenamic acid.

Mefenamic acid ingestion, usually in excess and over prolonged period is known to produce interstitial nephritis, or less commonly papillary necrosis, with acute renal failure. However, it is not dose-dependent for the induction of tubulointerstitial damage. Excess iodine ingestion is known to produce toxicity and possible death, but acute renal failure is rare. There is evidence from clinical and experimental data that iodine has toxic effect on tubular epithelial cells. Iodine has not been documented to produce red cell hemolysis and hemoglobinuria. We present a unique case of acute renal failure from hemoglobinuric and acute interstitial nephritis secondary to suicidal ingestion of potassium iodide solution and also ingestion of a few mefenamic acid tablets. These agents led to potentiation of the renal injury from hemoglobinuric tubulopathy, probably from the iodine, and renal dysfunction from alteration of renal perfusion by selective COX-1 inhibition of prostaglandin production, and induction of acute interstitial nephritis from mefenamic acid, leading to acute renal failure which was reversible by hemodialysis and supportive therapy.

Acute Disease↗
PubMed2002

Genetic polymorphisms of renin-angiotensin system and progression of interstitial nephritis.

Genes of the renin-angiotensin system (RAS) are involved in the progression of renal failure. Among them, the angiotensin-converting enzyme (ACE), angiotensinogen (AGT) and angiotensin II type 1 receptor (AT1R) genes are of particular interest. We examined polymorphisms of these three genes for association with the development of interstitial nephritis and progression to end-stage renal failure. The allele frequency and genotype distribution were compared in 90 patients with interstitial nephritis and 200 healthy controls. DNA samples were genotyped by polymerase chain reaction (PCR). We did not find statistically significant differences between groups in the insertion/deletion polymorphism of the ACE gene. An involvement of M235T polymorphism of the AGT gene in renal disease was observed in our study. The frequency of the T allele was higher in patients than in controls (32% vs. 24%). In the A1166C AT1R polymorphism the homozygous CC genotype was also more frequent in interstitial nephritis patients (7% vs. 3.5%). In patients carrying the C allele, an average time to ESRD was significantly shorter than in subjects with the AA genotype. Our study shows the association of the AGT and AT1R gene polymorphisms with the development and progression of interstitial nephritis. The C allele of the A1166C polymorphism appears to be a risk factor for faster disease progression.

Adult↗
PubMed1976

Chronic renal failure in dogs: a comparative clinical and morphological study of chronic glomerulonephritis and chronic interstitial nephritis.

Chronic renal disease is an important clinical problem in dogs. Until recently, diffuse renal fibrosis with chronic renal failure has been attributed mainly to chronic interstitial nephritis, itself considered to be the end stage of acute leptospiral nephritis. A clinical and morphological analysis of eight cases of chronic glomerulonephritis is described and a comparison made with eight dogs suffering from severe chronic interstitial nephritis. Clinically and biochemically, the two diseases were virtually indistinguishable, both resulting in uraemia. A possible distinguishing feature of chronic interstitial nephritis was the anaemia which was absent from chronic glomerulonephritis cases. Morphologically, the two diseases appeared to be distinguishable on three grounds; the pattern and severity of fibrosis, the degree of fibrin deposition and the immunofluorescence findings.

Animals↗
PubMed1995

Acute interstitial nephritis associated with loracarbef therapy.

We describe a biopsy-confirmed case of acute interstitial nephritis associated with the use of loracarbef in an 18-month-old boy, which resulted in end-stage renal failure. This complication has been documented with the use of beta-lactam antibiotics, and it seems likely the loracarbef was responsible for acute interstitial nephritis in this patient.

Acute Disease↗
PubMed1989

The prevalence of leptospirosis and its association with multifocal interstitial nephritis in swine at slaughter.

An abattoir survey was undertaken to determine the prevalence of leptospirosis and its association with lesions of multifocal interstitial nephritis (so-called "white spotted kidneys") in swine at slaughter. Both cross-sectional and case-control study designs were used. Of 197 kidneys from hogs randomly selected at slaughter, 11 (5.6%) had generalized grey-white foci typical of multifocal interstitial nephritis (MFIN). Antibody titers greater than or equal to 1:80 against Leptospira pomona were detected in nine (4.6%) hogs and against L. bratislava in 63 (32%) of these hogs. Leptospira pomona (kennewicki) was detected by immunofluorescence in 5/197 (2.5%) of randomly selected hogs. Leptospires identified as genotype kennewicki were isolated from six (9.8%) of 61 kidneys cultured. Leptospira bratislava was not detected by immunofluorescence or culture. There was a highly significant (p = 0.00) and strong association (odds ratio (OR) = 195) between high L. pomona titer (greater than or equal to 1:80) and the presence of leptospires in the kidneys, as detected by culture. There was also a significant (p = 0.046) and strong (OR = 8.10) association between multifocal interstitial nephritis and the presence of renal leptospires as detected by culture. The association between leptospiral titer and MFIN lesions in the prevalence survey group of animals was statistically significant (p = 0.031), but this association was not significant in the case-control study group (p = 0.071) The failure to identify L. bratislava despite serological evidence of infection suggests that some of these seropositive animals may have been transiently infected at an early age, that serological findings were falsely positive, or that immunofluorescence and isolation attempts failed to detect L. bratislava if they were indeed present in the kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Interstitial nephritis and glomerulonephritis in visceral leishmaniasis in a dog. A case report.

Renal involvement characterized by interstitial nephritis and glomerulonephritis is reported in a case of visceral leishmaniasis in a dog. Focal interstitial inflammatory infiltrates including lymphocytes and plasma cells together with collections of histiocytes containing Leishmania donovani organisms were found in the renal cortex. The glomeruli showed diffuse mesangial cell proliferation, thickening of the capillary wall and focal, segmental glomerulosclerosis. By electron microscopy, finely granular electron dense deposits were shown in subendothelial, intramembranous as well as subepithelial locations. It is suggested that the interstitial nephritis was caused by the presence of parasitic elements in the renal interstitium, whereas the glomerular involvement may have been due to deposition of antigen-antibody complexes.

Animals↗
PubMed1988

Drug hypersensitivity causing granulomatous interstitial nephritis.

In association with treatment for pharyngitis, a 47-year-old white man developed a systemic illness with fever, myalgia, episcleritis, hemoptysis, pleurisy, eosinophilia, and renal impairment. Renal biopsy revealed granulomatous interstitial nephritis, which resolved due to no specific treatment other than withdrawing all medication. Both the severe systemic manifestations and spontaneous recovery are unusual in association with drug-induced granulomatous nephritis. The drugs that may have caused the reaction included dihydrocodeine, phenylpropanolamine, erythromycin, and amoxycillin. Although the latter three drugs have been previously implicated in the development of interstitial nephritis, there have been no previous reports of granulomatous interstitial nephritis with any of these drugs.

Amoxicillin↗
PubMed1992

[A case report of chronic tubulo-interstitial nephritis].

We report a case of 10-year-old boy with chronic tubulo-interstitial nephritis (TIN). He had febrile convulsion and received sodium valproate (VPA) treatment. 18 months later, he had developed Fanconi syndrome. On admission, he also had evidence of tubular and glomerular dysfunction. Renal biopsy revealed interstitial nephritis with linear tubular-basement-membrane deposition of IgG and C3 and dominant infiltration of CD4 positive cells in interstitium. Although there is not a positive proof of the etiology in the relationship between TIN and VPA, it is likely that VPA is a possible cause of chronic TIN from his past history.

CD4 Antigens↗