Cases reported "Nephritis, Interstitial"

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1/28. Tubulointerstitial nephritis associated with minimal self reexposure to rifampin.

    We report the case of a 27-year-old Asian man who self-medicated with two capsules of rifampin 1 year after completing a continuous course of chemotherapy for tuberculosis that included that drug. He developed flank pain and edema and presented with uremia requiring dialysis; despite this, he had a serum potassium of only 3.5 mEq/L. Renal biopsy showed interstitial infiltrate with inflammation of the tubules. Renal function began to improve after a 3-week course of prednisone. This case is remarkable for the severity of the renal failure despite such a minimal self-exposure.
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2/28. Rapidly progressive fibrosing interstitial nephritis associated with Chinese herbal drugs.

    Rapidly progressive fibrosing interstitial nephritis after a slimming regimen containing aristolochic acid has been identified as Chinese herbs nephropathy (CHNP). From 1995 to 1998, we observed 12 Chinese people from different areas of taiwan who underwent renal biopsy for unexplained renal failure. Medical history gave no clue to the causes of impaired renal function except for the ingestion of traditional Chinese herbs. Although these patients ingested herbal drugs from various sources for different purposes, their renal biopsy samples showed amazingly similar histological findings, with extensive hypocellular interstitial fibrosis and atrophy and loss of tubules in all cases. Glomeruli were apparently intact. They also had similar clinical features, such as normal or mildly elevated blood pressure, early and severe anemia, low-grade proteinuria, glycosuria, and insignificant urinary sediments. Renal function deteriorated rapidly in most patients despite discontinuation of the herbal medicines. Seven patients underwent dialysis, and the remainder experienced slowly progressive renal failure. Bladder carcinoma was found in one patient. Morphologically and clinically, the nephropathy in our patients was similar to CHNP, reported in belgium. Because of the complexity and unknown types of herbs used in different clinical situations, unidentified phytotoxins other than aristolochic acid might be responsible for this unique disease entity. We conclude that the relation of this nephropathy to the consumption of Chinese herbs is striking. Using uncontrolled herbal remedies carries a high risk for developing interstitial renal fibrosis and urothelial malignancy.
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3/28. nephrotic syndrome associated with fanconi syndrome. Immunopathogenic studies of tubulointerstitial nephritis with autologous immune-complex glomerulonephritis.

    The nature of renal lesions in a patient with simultaneous onset of the fanconi syndrome and nephrotic syndrome was investigated by immunologic studies of the patient's serum, cryoproteins, and renal tissue. Acute severe tubulointerstitial nephritis and generalized segmental glomerulonephritis were present. Renal tubular epithelial (RTE) antigen, IgG, and Clq were localized in the glomerull and proximal tubules. Cryoprecipitates containing RTE antigen and anti-RTE antigen were isolated from the patient's serum antibody to RTE antigen was detected in the serum of the patient. However, antibody to tubular basement membrane was not found in the cryoproteins or serum. The unusual simultaneous presentation of these two syndromes in our patient possibly represents a common etiology: tubular damage with release of RTE antigen and subsequent development of immune-complex glomerulonephritis mediated by renal tubular epithelial antigen and antibody to this antigen.
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4/28. carnitine palmitoyltransferase II deficiency due to a novel gene variant in a patient with rhabdomyolysis and ARF.

    adult patients deficient in carnitine palmitoyltransferase II (CPT II) cannot generate sufficient amounts of energy, which results in rhabdomyolysis and acute renal failure (ARF). Its genetic basis has been recognized; but histopathologic changes, especially electron microscopic changes, have scarcely been described. The study subject is a patient with ARF caused by repetitive nontraumatic rhabdomyolysis. The acylcarnitine profile of serum and enzyme assay on skin fibroblasts confirmed the diagnosis of CPT II deficiency. Renal biopsy specimens were examined microscopically and immunohistochemically. The histological diagnosis was interstitial nephritis with acute tubular necrosis caused by rhabdomyolysis. myoglobin in tubules was detected by means of immunohistochemistry and electron microscopy. The genetic structure of CPT II was analyzed in the patient and his family. Eight pairs of polymerase chain reaction (PCR) primers were designed to cover the coding region. Each PCR-amplified gene product was subjected to dna sequencing, which unveiled heterozygosity at the CPT II locus consisting of a deletion of cytosine and thymine at codon 408, resulting in a stop signal at 420, as well as a mutation of arginine to cysteine at codon 631. The frame shift at 408 has never been described before. dna sequencing of the family showed the deletion mutation from the mother and the point mutation from the father. We describe renopathological findings in a patient with CPT II deficiency associated with rhabdomyolysis, which suggested the pathological role of myoglobin casts in the development of tubular necrosis. Genetic analysis of the patient identified a novel variant of the CPT II gene.
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5/28. Karyomegalic tubulointerstitial nephritis--a case report.

    Karyomegalic tubulointerstitial nephritis is a rare disease of uncertain etiology, which leads to progressive renal failure. Here, we report on a 39-year-old patient who presented with asymptomatic progressive decline of renal function. Two sequential renal biopsies demonstrated chronic tubulointerstitial nephritis with bizarre and dramatic enlargement of proximal tubule epithelial cell nuclei - the hallmark of karyomegalic nephritis. Clinical and pathologic findings of this case are discussed in light of the available literature. The morphologic changes in this disease are highly characteristic if the pathologist is aware of this entity.
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6/28. hyperkalemia unresponsive to massive doses of aldosterone and renal tubular acidosis in a patient with chronic interstitial nephritis: clinical and experimental studies.

    A unique 53-year-old male patient is described in whom aldosterone-refractory hyperkalemia and renal tubular acidosis/RTA/ was due to chronic interstitial nephritis associated with peritubular hyaline deposits in the distal nephron. hyperkalemia was not caused by an adrenal disorder or acidosis and could not be abolished by interventions enhancing K clearance; saline infusions, high doses of furosemide, cortisone, cortisol, long-acting synthetic ACTH and excessive doses of aldosterone. glucocorticoids induced a marked decrease in sodium excreting capacity probably by an action on the ascending limb of Henle's loop while aldosterone elicited a paradoxical natriuretic response by unknown mechanism. The results of our experimental studies carried out on the hyperkalemic RTA patient as well as on various control subjects and patients suggest 1. a specific defect in renal K excretion associated with decreased aldosterone responsiveness of the tubules presumably due to the peritubular pathology, and 2. a disturbance in the cellular regulation of K distribution between fluid compartments of unknown origin.
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7/28. A case with renal tubular damage: differentiation of Na reabsorption function by lithium clearance.

    The recovery of the renal proximal and distal tubular sodium (Na) reabsorption was evaluated by analysis of the physiological metabolism of lithium reabsorbed by the renal tubules in a patient with toxic interstitial nephropathy. Administration of glucocorticoid facilitated the rapid recovery of the proximal tubular Na reabsorption (-0.63 to 3 mmol/min for 2 wk) followed by recovery of phosphate reabsorption (51 to 82% for 2 months). Distal Na reabsorption was not altered for 2 months. Although Li clearance has been previously performed in healthy volunteers, we could differentiate the recovery of the proximal and distal renal tubular function even in a diseased patient.
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8/28. Persistent nephrogenic diabetes insipidus, tubular proteinuria, aminoaciduria, and parathyroid hormone resistance following longterm lithium administration.

    We report a patient who developed persistent nephrogenic diabetes insipidus associated with renal tubular acidosis, renal resistance to parathyroid hormone, aminoaciduria and proximal tubule pattern proteinuria in the presence of a reduced glomerular filtration rate (19-24 ml/min). A review of the previous reports of persistent nephrogenic diabetes insipidus revealed that in all patients the glomerular filtration rate had been less than 60 ml/min at presentation. Chronic renal failure may therefore predispose to the development of persistent nephrogenic diabetes insipidus in patients receiving lithium.
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9/28. sodium wasting, acidosis and hyperkalemia induced by methicillin interstitial nephritis. Evidence for selective distal tubular dysfunction.

    A 61 year old male patient was studied who manifested dehydration, azotemia, acidosis and hyperkalemia six weeks after exposure to methicillin. Thyroid and adrenal glucocorticoid and mineralocorticoid function were normal. The dehydration was found to be caused by a profound sodium-losing nephropathy; urinary sodium ranged from 78 to 101 meq/day during a salt restricted diet. A distal renal tubular acidosis and a quantitively impaired ability to excrete potassium were also found. These defects were relatively unresponsive to mineralocorticoid or prednisone therapy. A renal biopsy specimen showed an interstitial nephritis which selectively affected distal tubules and was thought to be secondary to methicillin. The data suggest functional impairment specific for the distal tubule, but with only a modest decrease in the glomerular filtration rate.
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10/28. Granulomatous interstitial nephritis after a jejunoileal bypass: an ultrastructural and histochemical study.

    We present a case of granulomatous interstitial nephritis and renal failure after a jejunoileal bypass for obesity. Improvement of the renal function occurred after reversal of the intestinal bypass. The renal biopsy showed an interstitial nephritis, oxalate crystal deposition and several aggregates of multinucleated giant cells related to the crystal material (granulomatous reaction). By ultrastructural and histochemical studies we demonstrated mitochondrial alterations in the tubular epithelial cells, and we suggested the proximal tubule origin of the giant cells. The association of the oxalate crystals with damaged tubules and giant cells suggests that the oxalate crystals are responsible for these alterations. The possibility of an associated immunological process as the cause of the interstitial nephritis cannot be excluded.
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