Diagnosis and Treatment of Acute Tubular Necrosis

Esson, Matthew; Schrier, Robert W.

doi:10.7326/0003-4819-137-9-200211050-00010

Cited by 230 publications

(161 citation statements)

References 99 publications

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“…Acute tubular necrosis (ATN) is a common cause of ARF (Esson and Schrier, 2002), and is observed in hypoxic conditions such as hemorrhagic shock or sepsis (Mehta, 2003). The transcriptional response to hypoxia can be adaptive or infl ammatory (Taylor and Colgan, 1999).…”

Section: Introductionmentioning

confidence: 99%

Cyclooxygenase-2 and hypoxia-regulated proteins are modulated by basic fibroblast growth factor in acute renal failure

et al. 2012

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Acute renal failure (ARF) can be caused by injuries that induce tissue hypoxia, which in turn can trigger adaptive or infl ammatory responses. We previously showed the participation of basic fi broblast growth factor (FGF-2) in renal repair. Based on this, the aim of this study was to analyze the effect of FGF-2 signaling pathway manipulation at hypoxia-induced protein levels, as well as in key proteins from the vasoactive systems of the kidney. We injected rat kidneys with FGF-2 recombinant protein (r-FGF) or FGF-2 receptor antisense oligonucleotide (FGFR2-ASO) after bilateral ischemia, and evaluated the presence of iNOS, EPO and HO-1, in representation of hypoxiainduced proteins, as well as COX-2, renin, kallikrein, and B2KR, in representation of the vasoactive systems of the kidney. A reduction in iNOS, HO-1, EPO, renin, kallikrein, B2KR, and in renal damage was observed in animals treated with r-FGF. The opposite effect was found with FGF-2 receptor down-regulation. In contrast, COX-2 protein levels were higher in kidneys treated with r-FGF and lower in those that received FGFR2-ASO, as compared to saline treated kidneys. These res ults suggest that the protective role of FGF-2 in the pathogenesis of ARF induced by I/R is a complex process, through which a differential regulation of metabolic pathways takes place.

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Section: Introductionmentioning

confidence: 99%

Cyclooxygenase-2 and hypoxia-regulated proteins are modulated by basic fibroblast growth factor in acute renal failure

et al. 2012

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“…Kidney biopsy demonstrated two distinct types of renal injury, MPGN, and ATI, with the latter primarily contributing to acute kidney injury. At the time of biopsy, the patient had several risk factors for ATI including underlying nephrotic syndrome, hypotension, and sepsis [8,9]. The biopsy finding of MPGN explained the patient's nephrotic syndrome which preceded his episode of AKI.…”

Section: Discussionmentioning

confidence: 99%

Mixed cryoglobulinemia and secondary membranoproliferative glomerulonephritis associated with ehrlichiosis

et al. 2014

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Ehrlichiosis is a tick-borne disease with diverse clinical presentations, ranging in severity from a flu-like illness with fever and myalgias to a serious systemic disease with multisystem organ failure. Nephrotic syndrome has been reported previously in two cases of human ehrlichiosis. A kidney biopsy revealed minimal change disease in one of those patients. Herein, we present the case of a 40-year-old man with ehrlichiosis who developed nephrotic syndrome, cryoglobulinemia, and secondary membranoproliferative glomerulonephritis (MPGN). The patient originally presented with shortness of breath, diffuse myalgias, headache, and lower extremity edema. He subsequently developed acute kidney injury and underwent kidney biopsy which showed MPGN and acute tubular injury. A tick-borne disease panel was positive for IgM and IgG to Ehrlichia chaffeensis. Serum testing revealed type 3 mixed cryoglobulinemia with no evidence of hepatitis C infection. The cryoprecipitate contained IgM and IgG antibodies to E. chaffeensis. Cryoglobulinemia is frequently associated with infections, particularly hepatitis C; however, our case is the first to describe ehrlichiosis associated with cryoglobulinemia and secondary MPGN.

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“…As to the first point, in general, ischemic acute tubular necrosis is a common complication of ischemia (due to prolonged hypotension), major surgery or sepsis, particularly in combination with underlying comorbidities (such as chronic kidney disease, atherosclerosis, diabetes mellitus, advanced malignancy and poor nutrition) (7,8). Since the patient had hypertension and the biopsy findings showed significant glomerulosclerosis and hyaline changes in arterioles, ischemic acute tubular necrosis was likely to occur even if his blood pressure decreased only slightly (9).…”

Section: Discussionmentioning

confidence: 99%

Ischemic Acute Tubular Necrosis due to Diltiazem Overdose

et al. 2016

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Diltiazem overdose has a high mortality rate due to cardiotoxicity associated with bradycardia and hypotension. A previous article reported that this type of overdose can cause acute tubular necrosis, which was not pathologically, but rather clinically, diagnosed. We herein report the case of a 55-year-old man who sustained nonoliguric acute kidney injury after taking 60 diltiazem tablets. A kidney biopsy performed six days after admission showed ischemic, not toxic, acute tubular necrosis. The patient's kidney function improved spontaneously. In this case report, we clarify the cause of renal impairment caused by diltiazem overdose pathologically. Physicians should therefore consider ischemic acute tubular necrosis as a cause of kidney injury in patients with diltiazem overdose.

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Diagnosis and Treatment of Acute Tubular Necrosis

Cited by 230 publications

References 99 publications

Cyclooxygenase-2 and hypoxia-regulated proteins are modulated by basic fibroblast growth factor in acute renal failure

Cyclooxygenase-2 and hypoxia-regulated proteins are modulated by basic fibroblast growth factor in acute renal failure

Mixed cryoglobulinemia and secondary membranoproliferative glomerulonephritis associated with ehrlichiosis

Ischemic Acute Tubular Necrosis due to Diltiazem Overdose

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