NKF 2015 Spring Clinical Meetings Abstracts
241 MIGRATION TO HEPARIN-FREE HEMODIALYSIS (HD) WITH STREAMLINE® AIRLESS BLOODLINES (SL) IN A LARGE INPATIENT PRACTICE Sami Safadi1, Mary Ann Ryan2, Amanda L Severson2 and Marie C. Hogan1. 1Nephrology and Hypertension, Mayo Clinic, Rochester, MN and 2Nursing, Mayo Clinic, Rochester, MN. Background: The development of the routine HD practice was facilitated by the introduction of extracorporeal circuit (EC) anticoagulation (AC) with heparin. However, EC-AC carries an increased risk of bleeding, a frequent concern in the hospitalized patients. Streamline® (SL) bloodlines eliminate blood-air contact, and reduce turbulence in dialysis circuit. Our inpatient HD unit moved to heparin-free dialysis with SL tubing with subsequent reductions in heparin use. Here we report our experience. Methods: All dialysis staff were trained and assessed in competence for correct setup-up of the air free tubing, spanning one month. Procedural guidelines for set up and critical assessment of the dialysis circuit were implemented across the inpatient practice. Staff underwent training in the assessment of circuit clotting. Fresenius 2008K HD Machines were calibrated to meet tubing specifications. Clotting during HD is now routinely assessed in all inpatient HD sessions through a post rinse-back visual guide. We validated the method showing good reproducibility across the HD nursing staff. Results: Our heparin prescription rates during hemodialysis dropped from an average of 15-25% before the introduction of SL tubing to <1% afterwards. There was no change in the clotting rate (around 28%) with the change to heparin-free dialysis with SL. Conclusions: We have successfully migrated from intermittent extracorporeal AC with heparin to heparin-free airless with SL tubing in a busy inpatient safely. Routine monitoring for extracorporeal circuit clotting should be a standard quality procedure in inpatient dialysis units.
242 MULTIPLE BILATERAL PULMONARY EMBOLISM FOLLOWING ANGIOPLASTY AND STENT PLACEMENT OF ARTERIOVENOUS GRAFT Gokul Samudrala1, David Levy1, Deerajnath Lingutla2, Michael DiSalle1, and Wajid Choudhry3 1Rochester Regional Health System, Unity Hospital, Department of Medicine, Rochester NY. 2Rochester Regional Health System, Unity Hospital, Hospitalist Program, Rochester NY. 3Department of Nephrology, University of Rochester Medical Center, Rochester NY Clinically insignificant pulmonary embolism (PE) following arteriovenous graft (AVG) manipulation has been previously documented and its incidence may be underestimated in the literature. However to the best of our knowledge only two cases of clinically significant PE have been reported. We present a case of symptomatic multiple PE in a patient with end stage renal disease (ESRD) following angioplasty and stent placement of her AVG. 79 year old female with hypertension, congestive heart failure, chronic obstructive pulmonary disease and ESRD on Hemodialysis was sent to the emergency department (ED) from the dialysis center after she was found to be hypotensive. One day prior to her presentation she had angioplasty of her AVG and a stent was placed. At presentation in the ED she was hypotensive and hypoxic. Chest radiograph at presentation was suggestive of pulmonary vascular congestion. Computerized tomographic angiogram of the chest showed multiple bilateral pulmonary emboli. Doppler of the lower extremities was negative for deep vein thrombosis and subsequent hypercoagulable workup was negative as well. Heparin drip was initiated, which was transitioned to Coumadin prior to discharge home. This case illustrates that physicians should be aware of the potential for clinically significant thromboembolic disease following mechanical manipulation of AV grafts. Future research directed at identifying risk factors for clinically significant PE would be helpful. Such factors may include underlying lung disease, number of AVG manipulations, and clot burden as measured by pre-angioplasty imaging.
Am J Kidney Dis. 2015;65(4):A1-A93
243 ACUTE INTERSTITIAL NEPHRITIS SECONDARY TO MONOCLONAL GAMMOPATHY: RAPID IMPROVEMENT IN RENAL FUNCTION WITH CHEMOTHERAPY Lindsay D. Sanders, Mira T. Keddis, Mayo Clinic, Phoenix, AZ, USA Acute interstitial nephritis is a rare complication of dysproteinemia and its management is not well defined in current practice. We describe a case of monoclonal gammopathy presenting with renal failure secondary to lambda restricted plasmocytic interstitial inflammation that responded to one cycle of bortezomib, cyclophosphamide, and dexamethasone. A 74-year-old Japanese female with 4-year history of monoclonal gammopathy of unknown significance developed progressive decline in renal function over 1 year (eGFR drop from 53ml/min to 28ml/min) prompting evaluation. Laboratory findings included anemia, monoclonal IgG lambda with M-spike of 6g/L and proteinuria. Bone survey was negative and bone marrow biopsy showed only 6% plasma cells. Kidney biopsy showed chronic active interstitial inflammation with predominant T cell lymphocytic infiltrate and lambda light chain restricted plasma cells and no evidence for crystals or cast nephropathy. In the setting of normal bone marrow biopsy, no treatment was pursued initially. Other causes for acute interstitial nephritis were not identified. GFR dropped to 18ml/min 2 months later. In the context of progressive renal failure, lambda restricted plasmocytic interstitial inflammation and IgG lambda monoclonal disease, monoclonal gammopathy of renal significance (MGRS) manifesting as interstitial nephritis was suspected. A multiple myeloma treatment regimen including bortezomib, cyclophosphamide, and dexamethasone for one month led to rapid recovery of renal function to eGFR of 38ml/min 4 months later with complete resolution of M-spike. This case highlights two important observations: 1) Interstitial nephritis may be the sole manifestation of MGRS, 2) Chemotherapy directed at the culprit clone led to significant improvement in renal function. This treatment approach should be considered for clear cases of dysproteinemia related renal disease even in the setting of normal bone marrow.
244 CORRELATION BETWEEN RENAL RESISTIVE INDEX, CENTRAL VENOUS PRESSURE, AND MEAN ARTERIAL PRESSURE IN SEPTIC ICU PATIENTS WITHOUT PRIOR RENAL DISEASE Sandipani Sandilya, Lewis Eisen, Ladan Golestaneh. Montefiore Medical Center, Bronx, NY, USA. The resistive index (RI) is a measure of renal blood flow by doppler ultrasound in the arcuate or interlobar arteries (systolic velocity-diastolic velocity)/systolic velocity) and is used as a marker of hemodynamic perturbation. The mean value in normals is 0.60. Studies have shown a correlation between acute kidney injury (AKI) in the intensive care unit (ICU) setting and RI values above 0.68. The relationships between RI, central venous pressures (CVP) and mean arterial pressures (MAP) has not been examined. We hypothesize that RI increases with decreases in MAP due to a reduction in diastolic velocity from hypoperfusion, and decreases with increasing CVP since the latter may be a sign of venous congestion. We enrolled patients under IRB approval as part of a larger study to correlate RI with septic AKI. RI was measured within 24 hours of ICU admission in patients above age 18, septic by SIRS criteria, and no prior renal disease. Mean MAP and CVP values within the first 24 hours were used for data analysis. 26 patients were included in the analysis: 13 were males, and the mean age was 53±16. 11 patients developed AKI by Acute Kidney Injury Network (AKIN) criteria. Spearman rank correlation showed a negligible correlation for RI vs CVP [0.0757 (P 0.71)] and for RI vs MAP [0.134 (P 0.515)]. For additional analyses, RI was dichotomized between elevated RI>=0.68 and not elevated RI<0.68. On chi-square analysis there was no relationship between elevated RI and vasopressor use (P 0.62). There was a strong trend for patients with elevated RI to have AKI which did not quite meet statistical significance. (P 0.057). Our analysis does not reveal a relationship between RI and MAP, CVP, and vasopressor use. Patients with an elevated RI had a strong trend toward having AKI. This supports a model where local mediators play a vital role in the fluctuation of RI. Elevations in RI cannot be explained by the global hemodynamic status of the patient.
A75