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1/13. Thin basement membrane disease and acute renal failure secondary to gross hematuria and tubular necrosis.

    A patient with thin basement membrane disease (TBMD), macroscopic hematuria, and acute renal failure is described. A renal biopsy showed massive occlusion of renal tubules by red blood cells and casts. This was accompanied by tubular cell damage consistent with acute tubular necrosis. The patient was receiving warfarin because of a history of deep venous thrombosis at the time he developed the acute renal failure. The possible relationship of the warfarin therapy to the TBMD, intratubular hemorrhage, and acute renal failure are discussed.
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2/13. 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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3/13. Unusual radiographic presentation of IgA nephropathy.

    An adolescent male presented with hematuria and flank pain. Transient focal renal parenchymal defects were demonstrated by ultrasonography, radionuclide scintigraphy and computed tomography. Renal biopsy revealed IgA nephropathy with acute tubular necrosis. This peculiar radiographic pattern has not, to our knowledge, been previously described in IgA nephropathy and may relate to tubule cell damage by red blood cell casts or patchy renal ischemia.
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4/13. light and electron microscopical changes seen in acute tubular necrosis in renal allografts.

    Seven renal biopsy specimens taken from three renal-allografted patients clinically suspected of having acute tubular necrosis were examined by light microscopy and five of these specimens were also examined by electron microscopy. The common findings in these three patients were as follows: The tubular lumina in all parts were dilated and the tubular epithelia were flat. Large vacuoles were occasionally observed within the tubular epithelial cell cytoplasm. These alterations were prominent in proximal convoluted tubules. Electron microscopically, the microvilli of the brush border of proximal convoluted tubules were loose and relatively short. The basal infoldings of proximal convoluted tubules were reduced or had disappeared. It could not be confirmed whether the large intracytoplasmic vacuoles apparent by light microscopic observation were intracytoplasmic or widened lateral intercellular spaces upon electron microscopy. In the most markedly damaged allograft of the three, a grayish hematoxylinophilic substance, which corresponded to autophagosomes with electron-dense round bodies upon electron microscopy, was often observed in the tubular epithelia. In addition, immature or regenerative tubular epithelia were observed. Most of these alterations were similar to those of acute ischemic change seen in non-renal transplantation.
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5/13. Analysis of urinary sediment by transmission electron microscopy. An innovative approach to diagnosis and prognosis in renal disease.

    Urinary sediment TEM is capable of unequivocally demonstrating renal tubule cells and distinguishing them from urinary tract epithelial cells. The renal tubule cells and the accompaniments including myeloid bodies, inflammatory cells, or fibrin permit, in a particular clinical setting, synthesis of a meaningful renal diagnosis. Sequential TEM sediment studies can clarify ambiguities in diagnosis. Precisely, when much difficulty is experienced in distinguishing ATN from aminoglycoside nephrotoxicity in a patient with sepsis who has received aminoglycoside, urinary sediment TEM can facilitate the differential diagnosis with confidence. In another clinical setting, such as hypersensitivity acute interstitial nephritis, TEM urinary sediment has an irrevocable place by exhibiting the characteristic eosinophil granules that will confirm the above diagnosis, or deny it when they are absent. The morphologic features in the renal tubule cells in the sediment reflect similar changes in the tubular cells in renal tissue. Therefore, the severity of tubular changes are commensurate with the clinical outcome in terms of renal function recovery, need of dialysis, and mortality. The degree of correlation is significant. Thus, slight or no TEM sediment tubular changes signifies a good prospect for renal function recovery and low or no mortality. Conversely, severe tubular changes in the TEM sediment denote persistent renal failure accompanied by high mortality. Furthermore, the most severe tubular changes, found in hepatorenal syndrome, are consistent with its dismal prognosis.
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6/13. Rapidly progressive silicon nephropathy.

    Rapidly progressive renal failure developed in four patients with silica exposure. Three presented with manifestations of a connective tissue disorders. All had abnormal proteinuria, hypoalbuminemia and active urinary sediments. Histologically, a distinct constellation of findings was present, consisting of glomerular hypercellularity and sclerosis, crescents, interstitial cellular infiltrates and tubular necrosis with red cell casts as seen on light microscopy. On electron microscopy there was foot process obliteration, characteristic cytoplasmic dense lysosomes, microtubules and dense deposits. Despite vigorous treatment, two patients died of the systemic illness and one is on hemodialysis. The fourth is improved after pulse methylprednisolone therapy. We propose that silica induced this multisystem disease through activation of the immune system and a direct tissue toxic effect.
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7/13. Acute tubular necrosis in hepatorenal syndrome: an electron microscopy study.

    This report describes light and transmission electron microscopy (LM and EM, respectively) studies of kidneys from five cases of hepatorenal syndrome. The kidneys were removed and fixed for LM and EM between 30 and 120 min after death. All patients had progressive renal failure after admission to the hospital. All cases were jaundiced, had ascites, and exhibited features of hepatic encephalopathy. LM study revealed severe acute tubular lesions (ATL) or, more conventionally, acute tubular necrosis (ATN). EM study demonstrated necrosis of the proximal tubules characterized by swelling, disorganization of the cristae and appearance of dark bodies in the mitochondria, coalescence, fragmentation or displacement of the microvilli, loss of plasma membranes, rupture of the basement membranes, and separation of the cells from the basement membranes. rupture of tubular basement membranes (tubulorrhexis) and mitochondrial dark bodies suggest an ATN due to ischemia or induced by vasoconstrictor substance(s). Glomerular lesions were infrequent (one in five) and therefore, do not seem to have contributed to renal failure. All cases terminally had extremely low urinary sodium (11 mEq/liter), high urinary potassium (50 mEq/liter), a remarkably low urinary sodium/potassium ratio (0.26, normal = 4.27), and a low urinary osmolality (less than 400 mOsm/kg). From this study we conclude that an ATN of variable severity may be associated with the hepatorenal syndrome. Since this ATN developed without preceding shock, sepsis, or hypotension it is possible that this ATN like that in ischemic acute renal failure may be due to reduced renal blood flow and intense cortical vasoconstriction which has been reported in hepatorenal syndrome. Finally, our data imply that low urinary sodium is consistent with this pathologic lesion in this clinical setting.
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8/13. Acute tubular necrosis in kidney transplant patients treated with enalapril.

    We report two cases of acute renal failure in renal transplant patients using cyclosporine-A (CsA) after the introduction of angiotensin-converting enzyme inhibitor (ACEI) to control arterial hypertension. They had no renal artery stenosis or acute rejection. Both patients presented severe acute tubular necrosis (ATN), which subsided after discontinuation of the ACEI. Synergistic toxic effect of ACEI and CsA on the renal tubules might explain ATN in these two cases.
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9/13. Rapidly progressive acute renal failure due to acyclovir: case report and review of the literature.

    acyclovir nephrotoxicity has been described since the inception of the drug's use more than a decade ago. Acute renal failure mediated by this compound is characterized by abrupt elevations in serum creatinine and a gradual return to baseline renal function on discontinuation of the drug. Drug crystal formation in collecting tubules resulting in an intraparenchymal form of obstructive nephropathy has been suggested as the mechanism for acyclovir nephrotoxicity. The patient we present developed rapidly progressive acute renal failure with concomitant mental status changes in the setting of treatment with high-dose parenteral acyclovir. acyclovir therapy was discontinued and an open renal biopsy was obtained to further evaluate our patient's diminishing renal function. Pathologic examination of the biopsy specimen revealed loss of proximal tubule brush border and dilated proximal and distal tubules with flattening of lining cells and focal nuclear loss. No crystals were noted. These changes were consistent with acute tubular necrosis with regeneration. Over the next 4 days our patient's renal and neurologic levels recovered to their prehospitalization statuses. It appears that our patient was affected by acyclovir-mediated nephrotoxicity that manifested on biopsy by acute tubular necrosis and the absence of crystalluria or crystal deposition. Intravenous acyclovir treatment can therefore produce rapidly progressive acute neurologic and renal toxicity that is usually reversible. The pathologic changes of acute tubular necrosis must now be included as part of the spectrum of renal damage associated with acyclovir therapy.
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10/13. Acute tubulointerstitial nephritis: phenotype of infiltrating cells and prognostic impact of tubulitis.

    The prognostic impact of tubulitis and the phenotype of the infiltrating cells in the tubules were studied in ten percutaneous renal biopsies from six patients with acute tubulointerstitial nephritis (ATIN). The inflammatory cell subsets in the tubules and interstitium (CD3 , CD4 , CD8 , CD20 , CD45RO , CD56 , CD57 , CD68 and TIA-1 cells), the expression of vimentin and the proliferation-associated antigen Ki-67 by cortical tubular cells, and the grade of tubulitis, interstitial infiltration and fibrosis were analysed. Cytotoxic injury to tubular cells in the vicinity of tubular-wall-localized lymphocytes was studied ultrastructurally. ATIN was drug-induced in three patients, related to legionella infection in two and idiopathic in one patient. Four patients recovered, one with reduced renal function. Two patients developed end-stage renal disease. CD8 and CD4 lymphocytes, and a smaller number of macrophages, infiltrated the tubules. The predominant lymphocyte subset in the tubules was the same as in the interstitium. Cytotoxic injury to tubular cells was not seen electron microscopically. The tubular cells exhibited increased proliferative activity and expressed vimentin, indicating non-specific tubular damage. The cell subset, the severity of tubulitis, and the tubular expression of vimentin were not related to outcome. The main prognostic factor was the severity of the interstitial fibrosis. Tubulitis in ATIN may be a harmless non-immune reaction, mediated by tubular expression of cytokines, together with adhesion and other molecules.
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