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PubMed2003

Urinary retinol binding protein in Indo-Asian patients with idiopathic interstitial nephritis.

BACKGROUND: Idiopathic interstitial nephritis (IIN) is common in the UK Indo-Asian population. Lack of systemic involvement and unremarkable urinalysis on stick testing suggest that it may underlie some cases of end-stage renal failure of undetermined cause. If IIN is diagnosed early, prompt initiation of treatment can improve long-term outcome. AIMS: To investigate whether urinary retinol binding protein (RBP) is elevated more commonly than urinary albumin in IIN, and might be useful in the early detection of renal disease in Indo-Asian patients. DESIGN: Preliminary observational study METHODS: We measured urinary RBP and urinary albumin in 19 Indo-Asian patients in whom a renal biopsy had shown IIN, 10 of whom had already been treated with corticosteroids at the time of specimen collection. A further 28 Indo-Asian patients with glomerular disease, and six with normal light-microscopic renal biopsy, were assessed in parallel. RESULTS: Urinary RBP/creatinine ratio (RCR) was elevated in all 19 cases of IIN, compared to 12/19 in whom the albumin/creatinine ratio (ACR) was elevated. Elevated urinary RBP was thus significantly more common than albuminuria in this group (p<0.01). Twelve of the 19 cases also satisfied the criteria for tubular proteinuria. RCR was elevated to >30 times the upper limit of normal in 7/9 who had not previously received corticosteroids, of whom four had normal ACR; none had ACR >5 times the upper limit of normal. DISCUSSION: These data suggest that measurement of urinary RBP should be explored as an adjunct to albuminuria, if screening for renal disease in the Indo-Asian population is contemplated.

Adult↗

PubMed1975

[Water-electrolyte re-equilibration in chronic interstitial nephritis].

In chronic interstitial nephritis there is a salt-losing syndrome. The reduction in the number of nephrons provides an experimental model for a study of the effects of a sodium load on the kidney. Partial restoral of renal function follows administration of sodium chloride and permits one to consider the main mechanisms of the regulation of sodium balance.

Adult↗

PubMed1988

Acute interstitial nephritis: immunologic and clinical aspects.

Acute interstitial nephritis is a common renal syndrome that may be associated with a variety of infections and drug therapies or may develop without an identified cause. Three cases are presented to illustrate the three types of acute interstitial nephritis--drug related, infection related, and idiopathic. Cell-mediated immune mechanisms seem to be more important than humorally mediated mechanisms in the pathogenesis of acute interstitial nephritis. Frequently, eosinophils are identified as a component of the interstitial cellular infiltrate, and eosinophiluria and eosinophilia have been claimed to be helpful in the diagnosis of acute interstitial nephritis, especially the drug-induced type. Neither eosinophiluria nor the presence of increased urinary levels of eosinophil major basic protein, however, is specific for the diagnosis of acute interstitial nephritis. Patients with drug-induced interstitial nephritis frequently have symptoms and signs suggestive of a hypersensitivity syndrome and rarely have more dramatic anaphylactic manifestations. Systemic glucocorticoids have been shown to be beneficial in this type of acute interstitial nephritis.

Acute Disease↗

PubMed1980

Interstitial nephritis.

There are many causes of interstitial nephritis other than pyelonephritis. The term interstitial nephritis does not connote a single etiologic or pathogenetic mechanism; it rather arbitrarily places together a wider variety of renal diseases that have a predilection for early and major involvement of the renal interstitium. The prototype of acute interstitial nephritis is acute pyelonephritis. In addition, there is a drug-related acute interstitial disease that is probably of immunological nature and usually reverses with discontinuance of the offending drug. Chronic interstitial nephritis includes many diverse illnesses. Nonobstructive pyelonephritis occurs but its prevalence is debated. Analgesic abuse nephropathy is not rare and is potentially reversible. Papillary necrosis has many causes and a wide spectrum of clinical presentations. Heavy metals, such as lead, cause interstitial nephritis. Balkan nephropathy occurs in an endemic area and although not bacterial in origin is of unknown cause.

Diagnosis, Differential↗

PubMed1985

Impaired potassium and magnesium homeostasis in acute tubulo-interstitial nephritis.

Although acute tubulo-interstitial nephritis is increasingly recognized as a cause of acute renal failure, little is known about renal tubular function in this disease. We report on two patients with acute tubulo-interstitial nephritis who demonstrated abnormalities in proximal and distal tubular function. The first patient developed hyperkalemia presumably from a potassium secretory defect in the distal nephron. The second patient developed an incomplete Fanconi's syndrome with glycosuria and aminoaciduria and two heretofore unreported complications of acute interstitial nephritis: hypokalemia and hypomagnesemia secondary to urinary losses of these cations. Careful monitoring of renal tubular function is indicated in patients with acute tubulo-interstitial nephritis.

Acute Disease↗

PubMed1981

Characterization of renal tissue lymphocytes in patients with interstitial nephritis.

Five patients with interstitial nephritis who presented with a variety of clinical profiles were studied with particular emphasis on documentation of the cellular types of potentially immunocompetent lymphocytes and mononuclear cells present within interstitial renal infiltrates. Immunohistologic studies coupled with conventional light and electron microscopic observations indicated that most mononuclear cells making up renal interstitial infiltrates were T cells. Some chronic inflammatory cell foci within renal interstitium were characterized by clusters of Ia antigen-positive T cells considered to be markers for activated lymphocytes. B cells were present in very small proportions (5 percent or less). The profile of immunocompetent cells present in lesions of interstitial nephritis suggests a major role for cell-mediated immunity in this disorder. Increase in tissue lymphocytes of the T gamma subclass with receptors for the Fc portion of immunoglobulin G (IgG) also suggests local activation of intrinsic suppressor cell mechanisms.

Adolescent↗

PubMed1976

Interstitial nephritis. A brief review.

Interstitial nephritis is a common condition, which in spite of a relatively constant pathologic picture has different etiologic agents and pathogenetic mechanisms. Failure to appreciate this, particularly in the chronic group, has led to considerable confusion and has been largely responsible for the overdiagnosis of chronic pyelonephritis. Although we are still largely ignorant of the causes of interstitial nephritis, it is now possible to define many of them. While experimental studies have not made spectacular contributions to our understanding, an attempt is now being made to develop appropriate models, and we hope these will enable us to still further clarify our understanding of other entities.

Adult↗

PubMed1985

Interstitial nephritis of acute onset.

Interstitial nephritis was diagnosed at renal biopsy in 10 previously healthy children. All had identical clinical symptoms: anaemia, raised sedimentation rate, low glomerular filtration rate, protein and leucocytes in the urine, but no bacteria; nine also had glycosuria. Six of the children had a history of recent ingestion of drugs or a serologically proved infection, or both. One child later developed uveitis. After the acute phase all made at least partial recovery, but after a mean follow up of two years and eight months only four were without any signs of disease, three had equivocal findings, two definite renal disease, and one renal failure. Interstitial nephritis, therefore, seems to be a clinical entity often occurring without known cause or triggering factor, its prognosis is variable, and some patients may develop chronic renal failure.

Acute Disease↗

PubMed1985

Tolerance to parenchymal self. Regulatory role of major histocompatibility complex-restricted, OX8+ suppressor T cells specific for autologous renal tubular antigen in experimental interstitial nephritis.

BN rats develop interstitial nephritis after immunization with rabbit, but not rat renal tubular antigen. Using RT1n rat strains that differentially express tubular antigen, we investigated the unresponsiveness of BN rats to BN tubular antigen (BN-TBM) using delayed-type hypersensitivity (DTH) responses to BN-TBM as a measure of cell-mediated immunity. Our results indicate that rat strains expressing tubular antigen respond to immunization with BN-TBM with the clonal expansion of antigen-specific, cyclophosphamide-sensitive, OX8+, MHC-restricted suppressor T cells. Such suppression appears to be relevant to the maintenance of tolerance to parenchymal self, since chronic cyclophosphamide therapy abrogates suppression and results in significant interstitial nephritis.

Animals↗

PubMedDate not supplied

[Chronic interstitial nephritis caused by analgesics].

Interstitial nephritis secondary to analgesic ingestion is apparently an uncommon subject in pediatric literature. Two cases are reported in this article: case 1 is a girl followed for the last fifteen years when she had lipoid nephrosis which was treated initially with corticosteroids; she responded satisfactorily, but presented frequent relapses. After 8 years, she was given cyclophosphamide plus prednisone and lately, she responded and has remained well. Further on, her urinalysis showed specific gravity of 1,033 and no proteinuria. Five years ago, because of protracted headache due to psychological disturbance, she started to ingest a variety of analgesics in progressively increasing doses. For the last 2 years, abdominal pains, paleness, polydipsia and polyuria have been observed; at present, her blood pressure, serum chemistry, and urine sediment are normal, but there is a marked failure in the renal concentration capacity, as well as marked sodium urinary losses. A percutaneous renal biopsy showed tubulo-interstitial fibrosis and edema with normal glomeruli. Case 2 is a girl with rheumatoid arthritis which appeared 3 years ago; for over one year, the patient was given 15 mg/day prednisone plus 1.5 g. acetylsalycilic acid. She was admitted to the hospital because her osteoarticular problem did not improve. Her blood pressure, blood chemistries and urinary sediment were also normal. LE tests were negative. Renal concentrating capacity was reduced and the renal biopsy showed tubular atrophy; there was intestinal edema and mononuclear infiltration. Chronic interstitial nephritis, secondary to analgesics is supported in both cases; polyuria and a marked defect of renal concentrating capacity are the earliest and most characteristic features. Normal urinary sediment is a common finding leading to erroneous assessment of a lack of renal involvement. Pathological lesions are located in the interstice of the renal medulla and sometimes in the papilla. Early arrest of analgesic ingestion may stop and even reverse the renal lesion and the renal insufficiency.

Adrenal Cortex Hormones↗

PubMed1994

Severe low back pain secondary to acute interstitial nephritis following administration of ranitidine.

Acute interstitial nephritis is a disease characterized by renal inflammation and is thought to be secondary to a hypersensitivity reaction. Although the causes of acute interstitial nephritis are numerous, adverse reactions to many common drugs, particularly antibiotics and nonsteroidal anti-inflammatory agents, are important etiological factors. Acute interstitial nephritis has many clinical manifestations, most notably fever and rash. Flank pain is an uncommon presentation. A case of acute, severe, low-back pain and rash in a healthy woman found to be secondary to acute interstitial nephritis is reported. The etiology of acute interstitial nephritis in this patient's case is suspected to be ranitidine (Zantac; Glaxo Pharmaceuticals, Research Triangle Park, NC), which has not been previously associated with this syndrome.

Acute Disease↗

PubMed1975

Chronic interstitial nephritis: etiologic factors.

Whether chronic interstitial nephritis (pyelonephritis) mainly results from kidney infection is widely debated. We studies 101 patients with interstitial nephritis, selected from 320 patients with newly diagnosed chronic renal disease, for frequency of etiological factors. Eleven had no etiologic factor(s) identified; 89 had clearcut factor(s): anatomic abnormalities 31, analgesic abuse 20, hyperuricemia 11, nephrosclerosis 10, stones 9, sickle cell disease1, tuberculosis 1, multiple causes7. Bacterial infection (present in 27%) was found only with another preceding primary cause of renal damage. Analgesic abusers frequently denied drug ingestion; 15% had urinary tract infection and 20% classical papillary necrosis. Two had family histories of analgesic abuse with nephropathy. We conclude that interstitial nephritis is a common form of chronic renal disease, is seldom idiopathic, rarely results from bacterial infection alone in adults, and frequently results from analgesic abuse in the United States.

Adolescent↗

PubMed1995

[Adult uveitis: apropos of 1 case with acute idiopathic interstitial nephritis].

The association of acute interstitial nephritis and uveitis is rare. In 1975, Dobrin reported a new syndrome in two children presenting acute interstitial nephritis, anterior uveitis and marrow-lymph node granulomas. We report one case of this association in the adult. A 35-year-old man was admitted to the hospital for acute renal failure, arthralgia and anterior uveitis. The infectious and the immunological investigations were negative. The ocular examination shows bilateral anterior uveitis. The renal biopsy revealed acute tubulo-interstitial nephritis. He was treated by prednisone (0.5 mg/Kg/day). His clinical course was favorable. Seven years later, the renal function is normal and we not observed a relapse of his uveitis.

Acute Disease↗

PubMed1957