Acute Renal Failure

Thadhani, Ravi; Pascual, Manuel; Bonventre, Joseph V.

doi:10.1056/nejm199605303342207

Cited by 1,511 publications

(1,093 citation statements)

References 115 publications

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“…9e11 These events contribute to intraluminal aggregation of cells and proteins, causing tubular obstruction. 12,13 The loss of cell adhesion in injured cells proceeds changes in the distribution of actin and actin-binding proteins with altered structural characteristics and cytoskeletal changes 10 that lead to reduced sodium transport and other impairments. 14 Kidney epithelium has a remarkable regenerative capacity after ischemic/toxic injury.…”

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confidence: 99%

TMIGD1 Is a Novel Adhesion Molecule That Protects Epithelial Cells from Oxidative Cell Injury

Arafa

Bondzie

Rezazadeh

et al. 2015

The American Journal of Pathology

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Oxidative damage to renal tubular epithelial cells is a fundamental pathogenic mechanism implicated in both acute kidney injury and chronic kidney diseases. Because epithelial cell survival influences the outcome of acute kidney injury and chronic kidney diseases, identifying its molecular regulators could provide new insight into pathobiology and possible new therapeutic strategies for these diseases. We have identified transmembrane and immunoglobulin domain-containing 1 (TMIGD1) as a novel adhesion molecule, which is highly conserved in humans and other species. TMIGD1 is expressed in renal tubular epithelial cells and promotes cell survival. The extracellular domain of TMIGD1 contains two putative immunoglobulin domains and mediates self-dimerization. Our data suggest that TMIGD1 regulates transepithelial electric resistance and permeability of renal epithelial cells. TMIGD1 controls cell migration, cell morphology, and protects renal epithelial cells from oxidative-and nutrient-deprivationeinduced cell injury. Hydrogen peroxide-induced oxidative cell injury downregulates TMIGD1 expression and targets it for ubiquitination. Moreover, TMIGD1 expression is significantly affected in both acute kidney injury and in deoxy-corticosterone acetate and sodium chloride (deoxy-corticosterone acetate salt)-induced chronic hypertensive kidney disease mouse models. Taken together, we have identified TMIGD1 as a novel cell adhesion molecule expressed in kidney epithelial cells that protects kidney epithelial cells from oxidative cell injury to promote cell survival. (Am J Pathol 2015 http://dx

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mentioning

confidence: 99%

TMIGD1 Is a Novel Adhesion Molecule That Protects Epithelial Cells from Oxidative Cell Injury

Arafa

Bondzie

Rezazadeh

et al. 2015

The American Journal of Pathology

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“…In conclusion, Nlrp3 shows a tissue-specific role in which leukocyte-associated Nlrp3 is associated with tubular apoptosis, whereas renal-associated Nlrp3 impaired wound healing. Ischemia/reperfusion (IR) injury is a major cause of acute kidney injury 1 and increases the risk of developing chronic kidney disease (CKD). 2 After injury, wounded tissue organizes an efficient response that aims to combat infections, clear cell debris, re-establish cell number, and reorganize tissue architecture.…”

mentioning

confidence: 99%

A Tissue-Specific Role for Nlrp3 in Tubular Epithelial Repair after Renal Ischemia/Reperfusion

Bakker

Butter

Claessen

et al. 2014

The American Journal of Pathology

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“…Thus, in patients with HRS, intermittent hemodialysis should only be used in selected cases, mainly in patients with life-threatening complications of uremia: pulmonary edema, hyperkalemia and acidemia. 8,9 The effectiveness of other renal replacement therapies such as continuous venovenous hemofiltration, continuous venovenous hemodialysis and slow lowefficient daily dialysis, 24 are unknown in patients with HRS. Clearly, randomized studies are needed to evaluate the effects of MARS and other renal replacement therapies on the recovery of renal function and survival in patients with HRS.…”

Section: Renal Replacement Therapymentioning

confidence: 99%

Hepatorenal syndrome in patients with cirrhosis

Moreau

2002

J of Gastro and Hepatol

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Type 1 hepatorenal syndrome (HRS) is a severe complication of end-stage cirrhosis. Type 1 HRS is an acute functional renal failure (i.e. glomerular hypofiltration) with no other explanation than the presence of the circulatory and neurohumoral alterations associated with severe chronic liver disease. Plasma volume expansion does not improve renal function. In contrast, administration of the vasopressin analog terlipressin, a splanchnic and systemic vasoconstrictor, may improve renal function and be used while awaiting liver transplantation. © 2002 Blackwell Publishing Asia Pty LtdKey words : cirrhosis, renal failure, vasoconstrictors. DEFINITIONS AND DIAGNOSISHepatorenal syndrome (HRS) is a renal failure which complicates end-stage cirrhosis with ascites. [1][2][3][4][5] There are two clinical types of HRS: type 1 and 2. 2 Type 1 HRS is characterized by the development of acute renal failure; that is, a doubling of initial serum creatinine to levels above 130 µ mol/L or a 50% decrease in the initial 24-h creatinine clearance to below 20 mL/min in less than 2 weeks. 2 Patients with type 1 HRS are in poor condition. Type 2 HRS is characterized by moderate and stable renal failure in patients who have a better condition than those with type 1 HRS. 2 This review will focus on the mechanisms, diagnosis, prognosis and treatment of type 1 HRS, and the term HRS will be used instead of type 1 HRS.Information on the frequency of HRS is controversial. In a large North American study of 3860 patients with ascites, HRS was diagnosed in less than 1% of patients. 6 Another study of 234 non-azotemic patients with ascites showed that the probability of developing HRS was 20% and 40% at 1 and 5 years, respectively. 7

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Acute Renal Failure

Cited by 1,511 publications

References 115 publications

TMIGD1 Is a Novel Adhesion Molecule That Protects Epithelial Cells from Oxidative Cell Injury

TMIGD1 Is a Novel Adhesion Molecule That Protects Epithelial Cells from Oxidative Cell Injury

A Tissue-Specific Role for Nlrp3 in Tubular Epithelial Repair after Renal Ischemia/Reperfusion

Hepatorenal syndrome in patients with cirrhosis

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