Echocardiographic strain and mortality in Black Americans with end-stage renal disease on hemodialysis.

End-stage renal disease (ESRD) presents a significant health burden and is associated with high cardiovascular morbidity and mortality. This is particularly true in African Americans who generally have higher rates of cardiovascular mortality. Outcomes in ESRD are related to extent of cardiovascular disease, but markers for outcome are not clearly established. Global longitudinal strain (GLS) has emerged as an important measure of left ventricular systolic function that is additive to traditional ejection fraction (EF). It can be measured on routine digital echocardiography and is reproducible. This study tested the hypothesis that GLS is associated with mortality in black Americans with ESRD and preserved EF. Forty-eight outpatients undergoing hemodialysis, 59.4 ± 13.3 years, with EF ≥50% were prospectively enrolled. GLS, measured by an offline speckle tracking algorithm, ranged from -8.6% to -22.0% with a mean of -13.4%, substantially below normal (-16% or more negative). The prevalence of left ventricular systolic dysfunction, as determined by GLS, was 89%. Patients were followed for an average of 1.9 years; all-cause mortality was 19% (9 deaths). GLS was significantly associated with mortality (hazard ratio 1.15, 95% confidence interval 1.02 to 1.30, p = 0.02), whereas EF was not. After adjustment for multiple potential confounders (age, gender, race, smoking, hypertension, diabetes, hyperlipidemia, coronary disease, heart failure, and EF), GLS remained strongly associated with mortality (hazard ratio 1.30, 95% confidence interval 1.10 to 1.56, p = 0.002). In conclusion, GLS is an important index in patients with ESRD, which is additive to EF as a marker for mortality in this high-risk group.

Improving care coordination between nephrology and primary care: a quality improvement initiative using the renal physicians association toolkit.

BACKGROUND: Individuals at risk for chronic kidney disease (CKD), including those with diabetes mellitus and hypertension, are prevalent in primary care physician (PCP) practices. A major systemic barrier to mitigating risk of progression to kidney failure and to optimal care is failure of communication and coordination among PCPs and nephrologists. STUDY DESIGN: Quality improvement. Longitudinal practice-level study of tool-based intervention in nephrology practices and their referring PCP practices. SETTING & PARTICIPANTS: 9 PCP and 5 nephrology practices in Philadelphia and Chicago. QUALITY IMPROVEMENT PLAN: Tools from Renal Physicians Association toolkit were modified and provided for use by PCPs and nephrologists to improve identification of CKD, communication, and comanagement. OUTCOMES: CKD identification, referral to nephrologists, communication among PCPs and nephrologists, comanagement processes. MEASUREMENTS: Pre- and postimplementation interviews, questionnaires, site visits, and monthly teleconferences were used to ascertain practice patterns, perceptions, and tool use. Interview transcripts were reviewed for themes using qualitative analysis based on grounded theory. Chart audits assessed CKD identification and referral (PCPs). RESULTS: PCPs improved processes for CKD identification, referral to nephrologists, communication, and execution of comanagement plans. Documentation of glomerular filtration rate was increased significantly (P=0.01). Nephrologists improved referral and comanagement processes. PCP postintervention interviews documented increased awareness of risk factors, the need to track high-risk patients, and the importance of early referral. Final nephrologist interviews revealed heightened attention to communication and comanagement with PCPs and increased levels of satisfaction among all parties. LIMITATIONS: Nephrology practices volunteered to participate and recruit their referring PCP practices. Audit tools were developed for quality improvement assessment, but were not designed to provide statistically significant estimates. CONCLUSIONS: The use of specifically tailored tools led to enhanced awareness and identification of CKD among PCPs, increased communication between practices, and improvement in comanagement and cooperation between PCPs and nephrologists.

Calcification of the mitral valve and annulus: systematic evaluation of effects on valve anatomy and function.

BACKGROUND: Mitral annular calcification (MAC) is common in chronic kidney disease. It is associated with cardiovascular events and can cause valvular dysfunction, but it has not been systematically characterized. The aim of this prospective study was to assess the prevalence and distribution of MAC, its effects on leaflet motion, and its association with mitral stenosis and mitral regurgitation (MR) in a hemodialysis population. METHODS: Echocardiograms were obtained in 75 consecutive hemodialysis outpatients. MAC extent and distribution were graded semiquantitatively using two-dimensional and three-dimensional echocardiography. Associations with the presence and severity of mitral stenosis and MR were explored. RESULTS: The mean age was 60 ± 14 years; 60% were men, and 87% were African American. MAC was present in 64% (moderate to severe in 48%). Calcium extended more than halfway onto the leaflet in 37% and beyond the annulus in 40%. Leaflet motion was restricted in 37%. Mitral stenosis was present in 28%, and the extent of calcification was associated with mean mitral valve gradient (P < .0001). MR was prevalent (present in 81%) but was severe in none. The severity of MAC was greater in patients with moderate MR than in those with no or mild MR (P = .04). Three-dimensional analysis suggested an uneven distribution of annular calcium; the middle and lateral anterior segments were less often calcified than the anterior-medial or posterior segments. Calcification in any annular segment was highly associated with restricted motion of the attached leaflet segment. CONCLUSIONS: MAC is common and often extensive in hemodialysis patients. Calcium may be unevenly distributed among the annular segments. When present, annular calcification reduces the angle of leaflet opening and can cause valvular dysfunction.

Warfarin-induced pulmonary metastatic calcification and calciphylaxis in a patient with end-stage renal disease.

Patients with end-stage renal disease (ESRD) receiving hemodialysis (HD) suffer from a number of metabolic derangements. Ectopic deposition of calcium in the skin, soft tissues, blood vessels, and viscera is a potentially devastating consequence of disorders of calcium and phosphorus homeostasis. We report the case of a patient with ESRD and secondary hyperparathyroidism receiving HD who developed metastatic pulmonary calcification and calciphylaxis following initiation of warfarin therapy after mechanical valve replacement. Because not all patients with ESRD receiving HD develop ectopic calcification, there appears to be a complex cascade of metabolic interactions that predispose patients to this process. Warfarin is a vitamin K antagonist with inhibitory effects not only on proteins of the coagulation cascade, but also on other important protein systems. Its role in ectopic calcium deposition has been the subject of theories and has been reported in the literature, but no link with metastatic pulmonary calcification has been made. Patients receiving HD have an increased incidence of conditions that require chronic anticoagulation with warfarin, such as VTE, atrial fibrillation, and valvular heart disease requiring valve replacement surgery. Bioprosthetic valves should be considered in these patients because of the potential risk of metastatic calcification when warfarin is used in the setting of mechanical valve replacement.

Contrast-induced translocational hyponatremia and hyperkalemia in advanced kidney disease.

BACKGROUND: In patients with advanced kidney disease, administration of effective osmolar agents may lead to hyponatremia, hyperkalemia, metabolic acidosis, and intravascular expansion. To our knowledge, osmolar effects of contrast agents in patients with advanced kidney disease have not been previously elucidated. METHODS: This retrospective case series includes 5 patients with advanced kidney disease who underwent diagnostic and/or therapeutic cardiac catheterization and developed hyponatremia. Blood chemistry tests were performed before and after the procedure. Hyponatremia is defined as a plasma sodium concentration less than 135 mEq/L (mmol/L). RESULTS: Mean precontrast and postcontrast sodium levels were 138.6 mEq/L (mmol/L) and 122.6 mEq/L (mmol/L), respectively. Plasma potassium levels increased after contrast exposure. There was no difference in degree of hyperkalemia between patients with and without diabetes. Plasma bicarbonate levels were noted to decrease after contrast exposure in 4 of 5 patients, with the exception of a patient undergoing continuous ambulatory peritoneal dialysis. There was a strong correlation between dose of contrast administered and change in sodium level, with a correlation coefficient of 0.91. CONCLUSION: These data suggest that large volumes of contrast may result in hypertonic hyponatremia through a dual effect of exogenous fluid dilution and translocation. The fluid translocated from intracellular to extracellular spaces may lead to a decrease in sodium, chloride, and bicarbonate levels. All patients developed hyperkalemia, which may be caused by solvent drag and/or passive diffusion, in addition to impaired excretory capacity. Patients with advanced kidney disease exposed to large volumes of contrast should be monitored for osmolar-induced chemical changes so that timely postcontrast dialytic therapy can be instituted.