Cases reported "Nephritis, Interstitial"

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11/28. Unexpected severe reversible cyclosporine A-induced nephrotoxicity in a patient with systemic lupus erythematosus and tubulointerstitial renal disease.

    We describe a patient with systemic lupus erythematosus and impaired renal function probably mainly due to tubulointerstitial disease. After a six-week course of low-dose cyclosporine A, she developed a severe but reversible loss of glomerular filtration rate and effective renal plasma flow despite of low cyclosporine A plasma levels. Based upon the observed fall of the filtration fraction, the rise in the relative clearance of 99Tc-dimercaptosuccinic acid and the increase in proteinuria, we suggest that in this case the tubules and/or interstitium are the main targets for cyclosporine A nephrotoxicity. Neither our patient's clinical symptoms nor her serologic parameters improved possibly because of the low dosage and/or short duration of cyclosporine A treatment. We conclude that one should be cautious when treating patients with systemic lupus erythematosus and pre-existing renal disease with cyclosporine A especially when tubulointerstitial abnormalities are present and/or other nephrotoxic drugs are used.
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12/28. Acute tubulo-interstitial nephritis from candida albicans with oliguric renal failure.

    A patient developed candidemia after receiving steroids and antibiotics. Subsequently, acute oliguric renal failure occurred. Renal biopsy showed multiple cortical microabscesses. These contained encapsulated ovoid Candida, budding organisms, short hyphae, and polymorphs. Adjacent tubules showed disruption of the basement membrane, infiltration by polymorphs and necrosis. There was no evidence of pelvic-calyceal obstruction by bezoar. The acute renal failure was attributed to acute candidal tubulo-interstitial nephritis, and was successfully reversed with Amphotericin.
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13/28. Idiopathic acute interstitial nephritis: characterization of the infiltrating cells in the renal interstitium as T helper lymphocytes.

    A previously healthy 39-year-old man presented with acute renal failure. There was no history of exposure to drugs nor was there any infection. Renal biopsy revealed interstitial nephritis with extensive acute degenerative changes in the tubules and extensive interstitial infiltration with mononuclear cells and no eosinophils. Monoclonal antibody staining studies identified the cells in the renal interstitium to be a helper/inducer subset of T lymphocytes. We suggest that a delayed hypersensitivity mechanism played a pathogenetic role in this patient's idiopathic acute interstitial nephritis.
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14/28. Red blood cell casts in acute interstitial nephritis.

    A 45-year-old woman receiving hydralazine and hydrochlorothiazide therapy was found to have a reduced glomerular filtration rate, a positive antinuclear antibody reaction, and RBC casts in the urinary sediment. Glomeruli with normal morphology (light, immunofluorescence, electron microscopy) were found on renal biopsy; however, a mild interstitial nephritis was observed that predominantly involved the distal tubules. The etiology of this inflammatory process is unknown. Changes in distal tubular function correlated with the morphology: acidification was impaired whereas concentrating ability was normal. Although RBC casts have been thought to be diagnostic of glomerular diseases, the present case demonstrates that tubulointerstitial disease can be responsible for RBC cast formation.
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15/28. Chronic interstitial nephritis. Its occurrence with oxalosis and anti-tubular basement membrane antibodies after jejunoileal bypass.

    A 38-year-old woman suffered rapid onset of renal failure between 11 and 15 months after undergoing a jejunoileal bypass for morbid obesity. Microscopic examination of renal biopsy specimens revealed oxalosis and severe tubulointerstitial nephritis. Immunofluorescence microscopy disclosed linear staining of tubular basement membranes with antisera to IgG and C3, which suggests antitubular basement membrane disease, a side effect not previously recognized with jejunoileal bypass. Possible mechanisms leading to the formation of these antibodies include (1) oxalate damage to renal tubules with release of tubular basement membrane antigens, and (2) bacterial overgrowth in the bypass segment, with mucosal damage and release of intestinal mucosal antigens that share antigenetic determinants with renal proximal tubules. Anti-tubular basement membrane disease may be an additional mechanism that produces or enhances renal damage in patients with jejunoileal bypass.
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16/28. Tubular basement membrane antibody-induced interstitial nephritis in systemic lupus erythematosus.

    Interstitial nephritis characterized by linear staining for human immunoglobulin G (IgG) along the tubular basement membrane of proximal renal tubules is described in a child with systemic lupus erythematosus (SLE). autoantibodies reacting with the tubular basement membrane of the proximal renal tubules and bowman capsule of glomeruli were present in serum. The autoantibodies were specific and could be absorbed with a normal human renal cortical fraction. The findings suggest that in addition to the well-known, immune complex-mediated injury, autoantibody-induced interstitial nephritis can also rarely occur in SLE.
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17/28. Neutral lipid storage with acid lipase deficiency: a new variant of Wolman's disease with features of the Senior syndrome.

    A girl presented with small stature, obesity, tapetoretinal degeneration, deafness, psychomotor regression, seizures, acanthosis nigricans, hepatomegaly, and chronic tubulointerstitial nephropathy. She died at age ten with renal insufficiency and uncontrolled seizures. Histochemistry showed lipid storage in hepatocytes, histiocytes, smooth muscles and, to a much lesser extent, kidney tubules and cortical neurons. The liver had increased cholesterol esters (5-fold) and triacylglycerols (8-fold), and decreased phospholipids (50%). Methyllumbelliferyl-oleate, oleylcholestrol, trioleylglycerol, and tripalmitylglycerol lipase activities were markedly reduced in the liver, in the range found in Wolman's disease. In cirrhotic fatty livers these activities ranged from 7-87% of the normal mean. The patient's brain had limited neutral lipid storage and normal methyllumbelliferyl-oleate lipase. Trioleylglycerol lipase activity was 14-60% of controls; tripalmitylglycerol lipase activity 14-25% of controls; and oleylcholestrol lipase activity 12-33% of controls.
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18/28. Acute interstitial nephritis. A case characterized by increase in serum IgG, IgM, and IgE concentrations. eosinophilia, and IgE deposition in renal tubules.

    A case of acute interstitial nephritis with a distinct immunopathologic pattern was seen. The relevant findings included elevated levels of serum IgG, IgM, and IgE; persistent eosinophilia; prominent granular and electron-dense depositions of IgE and C3 in renal tubules, as demonstrated by direct immunofluorescent and electron microscopic procedures; persistent failure to demonstrate anti-basement membrane antibodies (both glomerular and tubular); and hypocomplementemia. The findings in our case suggest a type of acute interstitial nephritis with a somewhat different clinical outlook. In this respect, serial assays of complement components and IgE in serum and kidney tissue and determinations of circulating anti-basement membrane antibodies (both glomerular and tubular) may be of particular importance.
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19/28. Interstitial nephritis caused by methicillin. Studies in a case complicating staphylococcal sepsis with acute glomerulonephritis.

    A 16-year-old student was admitted with acute, oliguric renal failure complicating staphylococcal sepsis. During treatment with methicillin drug hypersensitivity was suspected, and antibiotic was changed to vancomycin; by day 19 hemodialysis was discontinued. Renal biopsy showed two pathologic processes: acute exudative glomerulonephritis and widespread tubulointerstitial nephritis. In addition to glomerular immunoglobulin and C'3 deposits, interstitial and focal tubular basement membrane deposits of IgG were seen. Antiserum to DPO (methicillin) haptens localized apparently to the same tubular sites, as did fluorescein-conjugated antibodies from the patient's serum. The data suggest that interstitial nephritis was caused by serum antibodies to methicillin which bound to sites in renal tubules to which methicillin also had fixed. The acute tubulointerstitial nephritis complicated acute oliguric glomerulonephritis of staphylococcal sepsis.
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20/28. Karyomegalic interstitial nephritis: further support for a distinct entity and evidence for a genetic defect.

    Karyomegalic interstitial nephritis was first described in 1979 by Mihatsch, who was reporting three such cases. We report here four additional cases as well as two family investigations. Our findings support the association of karyomegaly and interstitial nephritis as a distinct entity. Typical clinical features are asymptomatic progressive renal failure in the third decade of life and recurrent infections, mostly of the upper respiratory tract. Histologic alterations consist of markedly enlarged and hyperchromic nuclei in many tubular epithelial cells throughout the nephron accompanied by interstitial fibrosis in the surrounding atrophic tubules. Karyomegaly is not limited to the kidneys. In one case, autopsy revealed karyomegaly in epithelial and mesenchymal cells of many other organs. However, no association of karyomegaly with further histologic damage is evident except in the kidneys. Because of the familial clustering, karyomegalic interstitial nephritis seems to be an inherited disease. Examination of the nuclear proliferation-associated structures proliferating cell nuclear antigen/cyclin, Ki 67, and p53 suggests an inhibition of mitosis in karyomegalic cells. The finding of the same HLA haplotype, A9/B35, in four of six HLA-typed cases suggests the possibility of a genetic defect on chromosome 6, which is inherited and linked to the HLA locus.
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