. Noninvasive interrogation of microvasculature for signs of endothelial dysfunction in patients with chronic renal failure. Am J Physiol Heart Circ Physiol 287: H2687-H2696, 2004. First published August 5, 2004; doi:10.1152/ajpheart.00287.2004.-Endothelial cell dysfunction (ECD) has been demonstrated in patients with end-stage renal disease (ESRD) who have cardiovascular disease (CD) or diabetes mellitus (DM). While techniques to examine conduit arteries have been adapted to these patients, evaluation of microvascular function has lagged behind. Therefore, we used laser Doppler flowmetry (LDF) and scanned laser Doppler imaging (LDI) to quantify parameters of the postocclusion reactive hyperemia and thermal hyperemic responses (local heating to 43°C) in ESRD patients (n ϭ 63) and healthy individuals (n ϭ 33). Patients with ESRD were partitioned among those with either CD or DM or both (designated CDorDM, n ϭ 30), patients with both CD and DM (designated CDϩDM, n ϭ 12, statistically similar to CDorDM), and patients with neither CD or DM (designated ϳCDorDM, n ϭ 33). LDF during thermal hyperemia showed a decrease in the thermal peaks and plateau as well as a delay in plateau compared with control, consistent with ECD. LDF during reactive hyperemia showed a decrease in the pay-back area under the curve, also consistent with ECD. ϳCDorDM were heterogeneous: almost 50% contained flow abnormalities similar to CDorDM. There was also a reduction in the number of functional arterioles on LDI images. Fourier analysis of LDF oscillations showed that low-frequency oscillations characterizing endothelial function were impaired in CDorDM and in many ϳCDorDM. The data demonstrate that ESRD patients with expected ECD (CDorDM) are characterized by distinct abnormalities in LDF parameters. However, similar abnormalities are found in approximately one-half of ESRD patients without evidence for CD or DM. Postocclusive and thermal interrogation of the microvasculature with laser Doppler-resolved parameters of the microcirculation, followed by Fourier analysis of the very slow oscillations, may provide a valuable adjunct to early noninvasive diagnosis of ECD in ESRD, especially important in a subpopulation of ESRD patients with no known CD or DM, which could be at increased risk of impending clinical manifestations of vasculopathy.laser Doppler flowmetry; imaging; microcirculation; coronary artery disease; diabetes mellitus CARDIOVASCULAR COMPLICATIONS have emerged as the most serious life-threatening accompaniment of end-stage renal disease (ESRD) (23). Widespread macrovascular endothelial cell dysfunction (ECD), diagnosed in large conduit vessels as paradoxical vasoconstriction to acetylcholine occurring before angiographic stigmata of atherosclerosis are detectable, is believed to be ultimately responsible for the development of many cardiovascular complications (24,33,43). Patients with ESRD are at additional risk for ECD because the uniform and concomitant presence of hyperhomocystenemia, accumulation of asymmetric dimethylargi...

Prediction of cardiovascular (CV) complications represents the Achilles' heel of end-stage renal disease. Surrogate markers of endothelial dysfunction have been advocated as predictors of CV risk in this cohort of patients. We have recently adapted a noninvasive laser Doppler flowmetry (LDF) functional testing of endothelium-dependent microvascular reactivity and demonstrated that end-stage renal disease patients are characterized by profound alterations in thermal hyperemic responsiveness. We hypothesized that such functional assessment of the cutaneous microcirculation may offer a valid, noninvasive test of the severity of endothelial dysfunction and CV risk. To test this hypothesis, we performed a cross-sectional study, in which we compared LDF measurements to conventional risk factors, and performed a pilot longitudinal study. LDF studies were performed in 70 patients and 33 controls. Framingham and Cardiorisk scores were near equivalent for low-risk patients, but more divergent as risk increased. C reactive protein (CRP) levels and LDF parameters (amplitude of thermal hyperemia (TH), area under the curve of TH) showed significant abnormality in high-risk vs low-risk patients calculated using either Framingham or Cardiorisk scores. Patients who had abnormal LDF parameters showed increased CV mortality, however, had similar risk assessments (Framingham, Cardiorisk, CRP, and homocysteine) to those with unimpaired LDF tracings. In conclusion, LDF parameters of microvascular reactivity offer a sensitive characterization of endothelial dysfunction, which may improve CV risk assessment through incorporation into the Framingham or Cardiorisk algorithm.

SummaryPatient safety is the foundation of high-quality health care. More than 350,000 patients receive dialysis in the United States, and the safety of their care is ultimately the responsibility of the facility medical director. The medical director must establish a culture of safety in the dialysis unit and lead the quality assessment and performance improvement process. Several lines of investigation, including surveys of patients and dialysis professionals, have helped to identify important areas of safety risk in dialysis facilities. Among these are lapses in communication, medication errors, patient falls, errors in machine and membrane preparation, failure to follow established policies, and lapses in infection control. The quality assessment and performance improvement process should include a dedicated safety team to focus on specifically identified areas of risk and to establish outcome goals guided by best practices and agreed-upon measures of success. A safety questionnaire can be given to patients and staff and the responses evaluated to improve understanding of the prevailing attitudes and concerns about safety. By sharing these results, openly acknowledging the challenges, and using a blame-free root cause process to identify action plans, the facility can begin to establish a culture of safety.

Contrast-induced nephropathy, also referred to as contrast-induced acute kidney injury (CIAKI), is among the most common causes of AKI, especially in patients with underlying chronic kidney disease. In addition to the increased cost engendered by the development of CIAKI, several studies have suggested the occurrence of AKI after cardiac procedures is associated with an increase in both morbidity and mortality. This increase in morbidity and mortality occurs after both intravenous and intra-arterial studies. This review focuses on relevant proposed pathophysiological mechanisms, risk factors, and current prophylactic strategies, which may reduce the incidence of CIAKI during cardiac angiographic imaging studies.

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Cardiac disease is the leading cause of death in patients having end-stage renal disease (ESRD). Patients with ESRD have a higher risk for developing coronary artery disease (CAD) than one would estimate from the presence of traditional risk factors such as hypertension, diabetes, hyperlipidemia, and cigarette smoking. Patients with milder forms of renal dysfunction who do not require dialysis also appear to have an increased risk for CAD. ESRD is associated with anemia, hyperhomocystinemia, increased calcium-phosphate product, hypoalbuminemia, increased troponin, increased markers of inflammation, increased oxidant stress, and decreased nitric oxide activity, factors that could contribute to increased CAD risk. Patients with ESRD require aggressive management of traditional risk factors for CAD, which include hypertension, hyperlipidemia, hyperhomocystinemia, and hypercoagulability. Milder forms of renal dysfunction could also be predictors of occult CAD and should be screened for in assessing cardiac risk in asymptomatic individuals.

The most proximate defect responsible for the pathogenesis of Bartter’s syndrome remains uncertain. Although an abnormality in chloride reabsorption in the thick ascending limb of Henle has been postulated, renal clearance studies performed during oral water loading failed to disclose a reduction in fractional chloride reabsorption. We alternatively postulate that the underlying abnormality may reside in a generalized increase in cell sodium permeability. Elevated levels of cell sodium may secondarily stimulate Na-K-ATPase activity. In the cells of the distal nephron, stimulated Na-K-ATPase would lead to enhanced potassium secretion into the tubular fluid producing the characteristic potassium depletion. In addition, increased cell sodium influx may stimulate a sodium-calcium exchanger. If this process exists in vascular smooth muscle, it may result in reduction of cytosolic calcium activity. This effect and/or chronic potassium depletion may mediate the reduced vascular reactivity characteristic of this syndrome.