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1/31. Spontaneous renal allograft rupture attributed to acute tubular necrosis.

    A renal allograft recipient receiving triple immunosuppressive therapy developed spontaneous allograft rupture 5 days after her second cadaveric renal transplantation. Renal biopsy showed interstitial edema with severe acute tubular necrosis (ATN). There was no evidence of acute rejection or renal vein thrombosis. The ruptured renal graft was salvaged by an aggressive fluid resuscitation therapy and surgical hemostasis. The renal function was satisfactory on discharge. We conclude that renal allograft rupture can be the result of interstitial edema solely attributed to ATN in the absence of graft rejection. The ruptured graft kidney is potentially salvageable for those patients whose hemodynamic status can be stabilized by appropriate supportive therapy.
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ranking = 1
keywords = interstitial
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2/31. The role of technetium-99m MAG3 renal imaging in the diagnosis of acute tubular necrosis of native kidneys.

    The differential diagnosis for patients with acute renal failure of their native kidneys, as a result of primary intrarenal disease, includes acute tubular necrosis, glomerulonephritis, and interstitial nephritis. The role of MAG3 renography has not been studied in this setting. The authors describe four patients with acute renal failure in whom MAG3 renal imaging reliably identified acute tubular necrosis, as confirmed by follow-up kidney biopsies. In contrast to the poor parenchymal uptake observed in glomerulonephritis and interstitial nephritis, MAG3 shows a distinctive pattern in patients with acute tubular necrosis. For patients with acute renal failure, a renal scan can facilitate decision-making regarding the initiation of therapy.
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ranking = 77.609348119828
keywords = interstitial nephritis, nephritis, interstitial
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3/31. Unexplained acute renal failure in a toddler: a rare complication of Epstein-Barr virus.

    A previously healthy toddler developed severe acute renal failure with nephromegaly and peripheral atypical lymphocytosis. Profound interstitial nephritis with acute tubular necrosis was diagnosed by renal biopsy, and both the clinical picture and serological evaluation suggested Epstein-Barr virus (EBV) as the etiological agent. The previous reports of EBV-induced renal failure and the clinical and pathological presentations of interstitial nephritis in children are reviewed.
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ranking = 55.861941690113
keywords = interstitial nephritis, nephritis, interstitial
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4/31. Acute renal failure in patients with glomerular diseases: a consequence of tubular cell damage caused by haematuria?

    We describe three patients with acute renal failure after the onset of gross haematuria. In all patients a presumptive diagnosis of rapidly progressive glomerulonephritis was made and immunosuppressive therapy initiated. A renal biopsy was performed in two patients, which showed evidence of IgA nephropathy. Extracapillary proliferation was seen in a few glomeruli. The most notable abnormality was acute tubular necrosis with intraluminal erythrocytes and cell debris. In the third patient, who was known to have longstanding glomerular haematuria, acute tubular necrosis was considered likely after review of the urinary sediment. Despite the fact that immunosuppressive therapy was stopped, renal function rapidly returned to normal in all these patients. We feel that our patients and additional literature data demonstrate that in patients with glomerular disease a reversible acute renal failure can occur that is caused by acute tubular necrosis mediated by haematuria. Recognition of this entity will prevent unnecessary long-term immunosuppressive therapy.
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ranking = 10.873703214857
keywords = nephritis
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5/31. Renal allograft rupture caused by acute tubular necrosis.

    Renal allograft rupture is a rare but potentially lethal complication of kidney transplantation. A renal allograft recipient receiving quadruple immunosuppressive therapy developed a spontaneous allograft rupture 13 days after kidney transplantation. Warm ischaemia time during the transplant was 80 minutes. The ruptured kidney graft could not be salvaged because of the patient's haemodynamic instability. The histopathological examination showed interstitial oedema with severe acute tubular necrosis with no signs of acute rejection. The most common causes of renal graft rupture are acute rejection and vein thrombosis, while acute tubular necrosis may only rarely be responsible for this complication. Renal graft rupture may be the result of interstitial damage attributed both to the prolonged warm ischaemia time during the transplant and to post-transplant acute tubular necrosis in the absence of graft rejection. In those patients whose haemodynamic status cannot be stabilized by appropriate aggressive haemodynamic support therapy, graft nephrectomy should be considered the only definitive treatment.
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ranking = 1
keywords = interstitial
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6/31. IgA nephropathy: acute renal failure, acute tubular necrosis, and features of postinfectious acute glomerulonephritis.

    From 1976 to 1987 on our Nephrological Unit, 57 patients with IgA nephropathy (IgAN) proven by renal biopsies were found. Three of those presented with acute tubular necrosis (ATN) and glomerulitis, without extrarenal predisposing cause in two; and showed, as prominent manifestation, a severe acute renal failure syndrome (ARFS), needing dialytic treatment. All three had hematuria, which was macroscopic in two and microscopic in one. Thus the prevalence of the association of glomerulitis and ATN was about 5.2%. There was complete recovery of renal functions in all three patients, but the usual symptomatology of IgAN. Two patients presented polymorphonuclear neutrophils infiltration of glomerular capillaries and in one of them, electron-dense deposits on the epithelial side of glomerular basement membrane ("humps") were observed, as well as those identified in the mesangial area. The glomerular polymorphonuclear neutrophils infiltration and endothelial cells proliferation (cases 1 and 3), the presence of "humps" (case 1), high antistreptolysin O (ASO) titers (cases 1 and 2), and low serum complement levels (case 1), suggest the possibility that antigens able to cause postinfectious glomerulonephritis (streptococcal or not) could induce in some individuals, by another immunopathogenetic route, mixed histopathological and clinical features of IgAN and postinfectious glomerulonephritis.
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ranking = 65.242219289144
keywords = nephritis
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7/31. Pamidronate-induced nephrotoxic tubular necrosis--a case report.

    Few cases of pamidronate (bisphosphonate class of drugs) nephrotoxicity in humans have been previously reported in the literature. In 7 patients, the pamidronate-related nephrotoxicity was attributed to focal collapsing glomerulosclerosis [Markowitz et al. 2001], and in 1 patient was related to tubulo-interstitial inflammatory nephritis [Van Doom et al. 2001]. We report herein on a 65-year-old Caucasian female patient who presented with acute chronic renal failure due to pamidronate-induced toxic proximal tubular necrosis without immunologic or inflammatory tubulo-interstitial involvement. The acute pattern of renal failure resolved following cessation of pamidronate administration in this patient for osteoporosis; the patient also had a monoclonal gammopathy of unspecific origin (MGUS).
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ranking = 11.873703214857
keywords = nephritis, interstitial
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8/31. cephalexin-induced acute tubular necrosis.

    A 24-year-old woman with a history of penicillin allergy developed reversible acute renal failure after receiving cephalexin for 4 days. The patient experienced nausea, vomiting, diarrhea, pruritus, cough, and an elevated creatinine level of 2.2 mg/dl. The patient's creatinine level continued to rise, peaking at 5.3 mg/dl on hospital day 3. Nephrotoxic acute tubular necrosis was confirmed by electron microscopy. Within 1 month of discharge from the hospital, the patient's creatinine level decreased to 0.6 mg/dl. Although the renal injury most commonly associated with the cephalosporin class of antibiotics is allergic interstitial nephritis, currently available cephalosporins infrequently can cause direct tubular toxicity.
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ranking = 27.930970845057
keywords = interstitial nephritis, nephritis, interstitial
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9/31. 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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ranking = 27.930970845057
keywords = interstitial nephritis, nephritis, interstitial
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10/31. Adenovirus tubulointerstitial nephritis presenting as a renal allograft space occupying lesion.

    This report describes a case of adenovirus infection in a renal allograft 36 days after transplantation that presented with transient macroscopic hematuria, prominent systemic features and acute renal dysfunction. The patient had persistent high fevers despite broad antibiotic cover. A CT scan demonstrated a new discrete space occupying lesion in the allograft, which was devoid of blood flow on Doppler sonography. A targeted renal biopsy showed florid and focal necrotizing interstitial nephritis with intranuclear tubular viral inclusions. Treatment with ganciclovir and reduction in immunosuppression resulted in a rapid improvement. immunohistochemistry and electron microscopy confirmed adenovirus infection. This case demonstrates an uncommon presentation of necrotizing adenoviral nephropathy, which should be considered in cases of renal allograft mass lesions.
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ranking = 218.04862803538
keywords = interstitial nephritis, tubulointerstitial, nephritis, tubulointerstitial nephritis, interstitial
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