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Central vein stenosis: current concepts.

Adv Chronic Kidney Dis. 2009 Sep;16(5):360-70

Authors: Agarwal AK

Central vein stenosis (CVS) is a common complication of the central venous catheter (CVC) placement. The prevalence of CVS has mostly been studied in those who present with symptoms such as swelling of the extremity, neck and breast. CVS compromises arteriovenous access and can be resistant to treatment. A previous history of CVC placement is the most important risk factor for the development of CVS later. Pacemaker and defibrillator wires are associated with a high incidence of CVS. Increasingly liberal use of peripherally inserted central catheters (PICC) is likely to increase the incidence of CVS. The trauma and inflammation related to the catheter placement is thought to result in microthrombi formation, intimal hyperplasia and fibrotic response, with development of CVS. Treatment of CVS by endovascular procedures involves angioplasty of the stenosis. An elastic or recurrent stenosis may require a stent placement. The long-term benefits of the endovascular procedures, although improved with newer technology, remain modest. Surgical options are usually limited. Future studies to explore the pathogenesis and the use of novel therapies to prevent and treat CVS are needed. The key to reducing the prevalence of CVS is in reducing CVC placement and placement of arteriovenous accesses prior to initiating dialysis. Early referral of the patients to the nephrologists by the primary care physicians is important. Timely vein mapping and referral to the surgeon for fistula creation can obviate the need for a CVC and decrease incidence of CVS.

PMID: 19695504 [PubMed - indexed for MEDLINE]

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Acute kidney injury: definitions and new paradigms.

Adv Chronic Kidney Dis. 2008 Jul;15(3):213-21

Authors: Endre ZH

Changes in terminology and new consensus definitions of acute kidney injury (AKI) and stages of severity have simplified some of the problems in the clinical approach to this complex syndrome. Nevertheless, new proactive approaches to the diagnosis of kidney injury instead of kidney failure are required to allow clinical translation of successful therapies developed for experimental AKI. The recent development of novel urinary and plasma biomarkers, which predict kidney failure, has allowed the development of new paradigms for detection, prevention, and stage-specific treatment.

PMID: 18565473 [PubMed - indexed for MEDLINE]

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Biomarkers of acute kidney injury.

Adv Chronic Kidney Dis. 2008 Jul;15(3):222-34

Authors: Edelstein CL

The diagnosis of acute kidney injury (AKI) is usually based on measurements of blood urea nitrogen (BUN) and serum creatinine. BUN and serum creatinine are not very sensitive or specific for the diagnosis of AKI because they are affected by many renal and nonrenal factors that are independent of kidney injury or kidney function. Biomarkers of AKI that are made predominantly by the injured kidney have been discovered in preclinical studies. In clinical studies of patients with AKI, some of these biomarkers (eg, interleukin-18, neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1) have been shown to increase in the urine before the increase in serum creatinine. These early biomarkers of AKI are being tested in different types of AKI and in larger clinical studies. Biomarkers of AKI may also predict long-term kidney outcomes and mortality.

PMID: 18565474 [PubMed - indexed for MEDLINE]

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Pulmonary complications after acute kidney injury.

Adv Chronic Kidney Dis. 2008 Jul;15(3):284-96

Authors: Faubel S

The development of respiratory failure in patients with AKI is a particularly devastating consequence that greatly increases patient mortality. When respiratory failure and AKI occur together, the mortality is greater than 80%. A clear understanding of the mechanisms leading to respiratory failure is of great clinical relevance to patients with AKI in order to prevent and treat this life-threatening complication. Pulmonary edema leading to respiratory failure has been a recognized complication of kidney failure since 1901. Remarkably, the pathogenesis of this complication remains elusive, despite over 100 years of clinical and experimental debate in the literature. A review of this literature suggests that there are 4 causes of pulmonary edema leading to respiratory failure in patients with AKI: (1) volume overload (cardiogenic edema), (2) left ventricular dysfunction (cardiogenic edema), (3) increased lung capillary permeability (noncardiogenic edema), and (4) acute lung injury (noncardiogenic edema with inflammation). In this review, these mechanisms are presented in historical context including the original descriptions of pathology and pathophysiology, recent epidemiologic data, and experimental studies in animals. Although volume overload is a well-accepted mechanism of pulmonary edema in patients with AKI, the purpose of this review was to highlight the evidence showing that noncardiogenic edema and acute lung injury also occur. By recognizing that the pulmonary complications of AKI are not simply from volume overload, specific treatment strategies may be discovered and used to improve outcomes in patients with the ominous and life threatening combination of AKI and respiratory failure.

PMID: 18565479 [PubMed - indexed for MEDLINE]

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Long-term outcomes of acute kidney injury.

Adv Chronic Kidney Dis. 2008 Jul;15(3):297-307

Authors: Goldberg R, Dennen P

Acute kidney injury (AKI) is common in the intensive care unit and is associated with significant morbidity and mortality. Based on the RIFLE criteria, AKI occurs in up to 67% of patients in the intensive care unit (ICU), with approximately 4% of critically ill patients requiring renal replacement therapy (RRT). It is well known that this subset of AKI patients who require RRT have an in-hospital mortality rate exceeding 50%. However, long-term outcomes of survivors of AKI requiring RRT remain poorly described. Long-term mortality is greater in those patients who survived AKI when compared with critically ill patients without AKI. Long-term morbidity, renal and extrarenal, is a frequent and underappreciated complication of AKI. Among survivors of AKI at long-term follow-up (1-10 years), approximately 12.5% are dialysis dependent (wide range of 1%-64%, depending on the patient population) and 19% to 31% have chronic kidney disease. According to the United States Renal Data System, “acute tubular necrosis without recovery” as a cause of end-stage kidney disease increased from 1.2% in 1994 to 1998 to 1.7% in 1999 to 2003. The incidence will likely continue to rise with the aging population, increase in comorbidities, and expansion of intensive care unit capabilities. AKI is an underrecognized cause of chronic kidney disease (CKD) and patients who survive should be followed closely for new CKD and/or progression of underlying CKD.

PMID: 18565480 [PubMed - indexed for MEDLINE]

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