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Management of hemodialysis patients with central venous stenoses or occlusions
A16
TENTH ANNUAL CLINICAL NEPHROLOGY MEETING ABSTRACTS
21 MODULATION OF VASOPRESSIN-V2 RECEPTOR SIGNALING AND ADENYLYL CYCLASE VI WITH CHRONIC VASOPRESSIN EXPOSURE 1N RAT KIDNEY. Carolyn'A. Ecelbar~er, Crystal A. Bickel, and Joseph G. Verbalis. Division of Endocrinology and Metabolism, Department of Medicine, Georgetown University, Washington, DC. Previous studies have shown that vasopressin V2 receptor mRNA and binding is down-regulated by chronically elevated circulating vasopressin. Nevertheless, these changes coincide with increased water reabsorptive capacity of the renal collecting duct, primarily as a result of increased relative abundance of aquaporins -2 and -3. Therefore, the aim of these studies was to examine the impact of high circulating vasopressin levels on cyclic AMP production in inner medullary collecting duct (1MCD) suspensions and on relative adenylyl cyclase VI (ACVI) abundance as assessed by semi-quantitative immunoblotting. Water restriction for 7 days to Sprague-Dawley rats did not affect ACVI abundance. However, infusion of a V2-selective vasopressin agonist, dDAVP ( ldesamino-8-D-arginine vasopressin) to Brattleboro rats (7d) dramatically decreased ACVI abundance in inner meduIlary homogenates. Mean band density for the specific 180 kDa band in dDAVP-infused rats was 46% of that for vehicle-treated animals. Nevertheless, cyclic AMP production capacity (in response to acute dDAVP, 5 minutes) in IMCD suspensions prepared from SD rats infused chronically with dDAVP (7d) was significantly greater (on average 75% higher, p=0.026) relative to vehicle-infused controls. These results suggest that despite apparent downregulation of the number of V2 receptor binding sites and the associated ACVI, vasopressin mediated signaling activity may actually be enhanced by chronic exposure to vasopressin.
22 MANAGEMENT OF HEMODIALYSIS PATIENTS WITH CENTRAL VENOUS STENOSES OR OCCLUSIONS. Abigail Falk, Jeffrey Gullet, Scott Nowakowski, Harold A. Mitty, Victoria Teodorsecu, Joseph Vassalotti, Jaime Uribarri. Mr. Sinai-NYU Med, Ctr., Depts of Radiology, Surgery & Medicine. N.Y., New York. Purpose: To prospectively evaluate the treatment and management of central venous (CV) stenoses and occlusions in hemodialysis patients with ipsilateral AVG/AVF so that access site patency may be preserved. Methods: From 10/98-9/00 27 patients with AVG/AVF had ipsilateral CV stenoses or occlusions manifested by upper extremity edema and/or thrombosed or failing access sites. All patients underwent angiographic evaluation with intent to treat the access site and/or CV stenoses/occ[usions (angioplasty for stenoses and stent placement for failed angioplasty or CV occlusion). These patients were routinely followed with angiography at 8 week intervals or sooner if the patient becmne symptomatic. Repeat intervention was performed when necessary. Prospective data collection included demographics, technical details of procedures, immediate outcomes, complications and patency rates. Results: Technical success, defined as complete CV recanalization with a functioning ipsiIateral upper extremity access site, was achieved in 20/27 patients. 4/27 patients failed CV recanalization and that side was abandoned for any future access. 3/27 patients received no treatment. 53 CV interventions (38 angioplasty and 15 stent placement) were performed in 20 patients (2.7 interventions/patient) to maintain CV patency. No procedural complications occurred. All treated patients maintained patent ipsilateral access sites for a cumulative assisted patency of 100% during the study period. Conclusions: Interventions performed to treat CV disease in hemodialysis patients are safe and effective. Close surveillance and routine foilow-up with repeat CV interventions are necessary to maintain CV patency so that ipsilateral access may be preserved.
23 NEW EMPIRIC EXPRESSIONS TO CALCULATE spKT/V AND eKTN. Alexander S~ Goldfarb-Rumyantzev, Samuel Liu, Michael Schwenk. KIN computations are somewhat cumbersome and require urea distribution volume (V) estimate. Calculating URR .is easier and does not require additional parameters, but it fails to account for ~e removal of urea when BUN does not change, e.g., during ultrafiltration (UF) or for residual renal function. URR potentially could be corrected for UF. The goal of this study ',yes to derive new expressions to calculate KIN based on URR. Following models were used in the study: 1) bivariate linear model (LM); nonli0ear models: 2) polynomial, 3) power, 4) exponential; multivariate LM: 5) URR corrected for UF, 6) URR corrected for UF and HD length (t); 7) bivadate LM based on URR adjusted for UF by simple theoretical expression: URRad?URR*PostWeight/(PostWeight+UF/0`6)~Models were based on the data from 602 dialysis (194 patients atithe NYHQ). ~,leanKtN was 1.6 (95% CI 1.57-1.63). Multivariate regression showed URRto be the best predictor of KtN. We derived following expression and calculated mean squared residuals and correlation with KIN calculated ' traditi0nalformula. Expression i MSR ,I R 1 spKtN=-1.466+0.O4203*URR 0.0053 0:96 eKW=-l.441 + 0:04217*URR 0.0056 0:96 2 spKW=1,35-0`03827*URR÷0.0005674*(URR)2 i 0.0044 0:97 eKW=1.386-0`03845*URR+0.0005697*URR2 0.0044 0.97 3 spKt/V=0.000376*URR~,~6 0`0047 0`97 eKW=0.0004539*URR19Q7 0.0048 '0:97 4 spKW=0.2061*e0,o2789.uaa 0.0044 0:97 eKW=0.2193*e o.o2z3"uRa 0.0044 0`97 5 spKI]V=-l.7026+0`0437*URR+0.0384*UF 0.17035 0:98 eKW=-1.6781+010438*URR+0.0384*UF ,0.0035 0;98 6 eKtN=-1.6445+0iO437*URR+0`0392*UF-0`000t*t 0`00~15 0.98 7 eKt/V=-1.167+0`041125*URRadl 0,0,171 ~188 The best bivariatemodNg for spKW and eKW are exponefltN and pdynomial. spKiN calculated from URR adjusted for UF (multivariate model) is th~ best model to compute spKW. The best formula for eKW is multivariate linear expression based 'on URR, UF; and :t. The second best expression was linear model based on URR and UF, both of these formulae can be used in clinical practice. TheoretiCal expression describing URR adjustment for UF is a poor parameter to calculate eKW. Using empiric formulae that we derived for spKt/V and eKW total body water/V can be calculated as well.
24 CYTOMEGALOVIRUS ASSOCIATED COLLAPSING GLOMERULOPATHY IN A NON IMMUNOCOMPROMISED HOST WITH NO RISK FACTORS. Induleldaa Gopal, Saba SiIe', Lillian Gaber, William Basmagel and Kunal Chaudhary. Depts. of Medicine and Pathology; Univ. of Termessee Health Sciences Ctr, Memphis, TN. Collapsing Glomerulonephritis has become an increasingly eommon cause of proteinuria and renal failgre in this country. Most of these cases have been associated with HIV infection or intravenous drug usage. There have been cases of this disease associated with other viral illnesses ie: Hepatitis C and HTLV-1. GlomerUlopathy associated with CMV has been described in renal allografts. We report a case of acute renal Faihire secondary to biopsy proven Collapsing Glomemlonephritis in a 19 yeaF old African American female with CMV septicemia who was HIV negative and had no other risk factors. She presented to the hospital with fever, chills, and acute renal failure. She had 4+ proteinuria with a telescopic urine, Renal biopsy showed moderate collapse of several glomemli. Initial treatment with pulse doses of intravenous methylpredinisolone showed no response. She was acutely dialyzed twice secondary to worsening renal function and uremia: Her workup Which included serological testing for HIV, Hepatitis B and C, RPR, ANN, ANCA, ASO titers, AntiGBM antibodies was negative. She had qlevated Liver Transaminases and Bilimbin. PCR for CMV was positive, urine cultures grew CMV and Serum IgM titers for CMV antigens were 1:256. She was placed on intravenous Gancyclovir and the serum creafinine which had risen m 9.0 mg/dI started to decrease. She recdived in~avenous Gancyclovir for a total of six weeks. Her serum creatinind at the time c~fdischarge was 1.8 mg/dI and the serum transaimnases had ~lso decreased. She was dischm'ged in good health and 6 months aRer th~ discharge her serum creatinine remains stable at 1.4 mg/dl. A repeat HIV +eatwas negative. Non HIV viral illnesses should be considered as a potential cause of Collapsing GN and acute renal failure. A timely diagnoses and appropriate treatment may arrest farther renal injury and prevent considerable morbidity and mortality as was illustrated in this case.
TENTH ANNUAL CLINICAL NEPHROLOGY MEETING ABSTRACTS
21 MODULATION OF VASOPRESSIN-V2 RECEPTOR SIGNALING AND ADENYLYL CYCLASE VI WITH CHRONIC VASOPRESSIN EXPOSURE 1N RAT KIDNEY. Carolyn'A. Ecelbar~er, Crystal A. Bickel, and Joseph G. Verbalis. Division of Endocrinology and Metabolism, Department of Medicine, Georgetown University, Washington, DC. Previous studies have shown that vasopressin V2 receptor mRNA and binding is down-regulated by chronically elevated circulating vasopressin. Nevertheless, these changes coincide with increased water reabsorptive capacity of the renal collecting duct, primarily as a result of increased relative abundance of aquaporins -2 and -3. Therefore, the aim of these studies was to examine the impact of high circulating vasopressin levels on cyclic AMP production in inner medullary collecting duct (1MCD) suspensions and on relative adenylyl cyclase VI (ACVI) abundance as assessed by semi-quantitative immunoblotting. Water restriction for 7 days to Sprague-Dawley rats did not affect ACVI abundance. However, infusion of a V2-selective vasopressin agonist, dDAVP ( ldesamino-8-D-arginine vasopressin) to Brattleboro rats (7d) dramatically decreased ACVI abundance in inner meduIlary homogenates. Mean band density for the specific 180 kDa band in dDAVP-infused rats was 46% of that for vehicle-treated animals. Nevertheless, cyclic AMP production capacity (in response to acute dDAVP, 5 minutes) in IMCD suspensions prepared from SD rats infused chronically with dDAVP (7d) was significantly greater (on average 75% higher, p=0.026) relative to vehicle-infused controls. These results suggest that despite apparent downregulation of the number of V2 receptor binding sites and the associated ACVI, vasopressin mediated signaling activity may actually be enhanced by chronic exposure to vasopressin.
22 MANAGEMENT OF HEMODIALYSIS PATIENTS WITH CENTRAL VENOUS STENOSES OR OCCLUSIONS. Abigail Falk, Jeffrey Gullet, Scott Nowakowski, Harold A. Mitty, Victoria Teodorsecu, Joseph Vassalotti, Jaime Uribarri. Mr. Sinai-NYU Med, Ctr., Depts of Radiology, Surgery & Medicine. N.Y., New York. Purpose: To prospectively evaluate the treatment and management of central venous (CV) stenoses and occlusions in hemodialysis patients with ipsilateral AVG/AVF so that access site patency may be preserved. Methods: From 10/98-9/00 27 patients with AVG/AVF had ipsilateral CV stenoses or occlusions manifested by upper extremity edema and/or thrombosed or failing access sites. All patients underwent angiographic evaluation with intent to treat the access site and/or CV stenoses/occ[usions (angioplasty for stenoses and stent placement for failed angioplasty or CV occlusion). These patients were routinely followed with angiography at 8 week intervals or sooner if the patient becmne symptomatic. Repeat intervention was performed when necessary. Prospective data collection included demographics, technical details of procedures, immediate outcomes, complications and patency rates. Results: Technical success, defined as complete CV recanalization with a functioning ipsiIateral upper extremity access site, was achieved in 20/27 patients. 4/27 patients failed CV recanalization and that side was abandoned for any future access. 3/27 patients received no treatment. 53 CV interventions (38 angioplasty and 15 stent placement) were performed in 20 patients (2.7 interventions/patient) to maintain CV patency. No procedural complications occurred. All treated patients maintained patent ipsilateral access sites for a cumulative assisted patency of 100% during the study period. Conclusions: Interventions performed to treat CV disease in hemodialysis patients are safe and effective. Close surveillance and routine foilow-up with repeat CV interventions are necessary to maintain CV patency so that ipsilateral access may be preserved.
23 NEW EMPIRIC EXPRESSIONS TO CALCULATE spKT/V AND eKTN. Alexander S~ Goldfarb-Rumyantzev, Samuel Liu, Michael Schwenk. KIN computations are somewhat cumbersome and require urea distribution volume (V) estimate. Calculating URR .is easier and does not require additional parameters, but it fails to account for ~e removal of urea when BUN does not change, e.g., during ultrafiltration (UF) or for residual renal function. URR potentially could be corrected for UF. The goal of this study ',yes to derive new expressions to calculate KIN based on URR. Following models were used in the study: 1) bivariate linear model (LM); nonli0ear models: 2) polynomial, 3) power, 4) exponential; multivariate LM: 5) URR corrected for UF, 6) URR corrected for UF and HD length (t); 7) bivadate LM based on URR adjusted for UF by simple theoretical expression: URRad?URR*PostWeight/(PostWeight+UF/0`6)~Models were based on the data from 602 dialysis (194 patients atithe NYHQ). ~,leanKtN was 1.6 (95% CI 1.57-1.63). Multivariate regression showed URRto be the best predictor of KtN. We derived following expression and calculated mean squared residuals and correlation with KIN calculated ' traditi0nalformula. Expression i MSR ,I R 1 spKtN=-1.466+0.O4203*URR 0.0053 0:96 eKW=-l.441 + 0:04217*URR 0.0056 0:96 2 spKW=1,35-0`03827*URR÷0.0005674*(URR)2 i 0.0044 0:97 eKW=1.386-0`03845*URR+0.0005697*URR2 0.0044 0.97 3 spKt/V=0.000376*URR~,~6 0`0047 0`97 eKW=0.0004539*URR19Q7 0.0048 '0:97 4 spKW=0.2061*e0,o2789.uaa 0.0044 0:97 eKW=0.2193*e o.o2z3"uRa 0.0044 0`97 5 spKI]V=-l.7026+0`0437*URR+0.0384*UF 0.17035 0:98 eKW=-1.6781+010438*URR+0.0384*UF ,0.0035 0;98 6 eKtN=-1.6445+0iO437*URR+0`0392*UF-0`000t*t 0`00~15 0.98 7 eKt/V=-1.167+0`041125*URRadl 0,0,171 ~188 The best bivariatemodNg for spKW and eKW are exponefltN and pdynomial. spKiN calculated from URR adjusted for UF (multivariate model) is th~ best model to compute spKW. The best formula for eKW is multivariate linear expression based 'on URR, UF; and :t. The second best expression was linear model based on URR and UF, both of these formulae can be used in clinical practice. TheoretiCal expression describing URR adjustment for UF is a poor parameter to calculate eKW. Using empiric formulae that we derived for spKt/V and eKW total body water/V can be calculated as well.
24 CYTOMEGALOVIRUS ASSOCIATED COLLAPSING GLOMERULOPATHY IN A NON IMMUNOCOMPROMISED HOST WITH NO RISK FACTORS. Induleldaa Gopal, Saba SiIe', Lillian Gaber, William Basmagel and Kunal Chaudhary. Depts. of Medicine and Pathology; Univ. of Termessee Health Sciences Ctr, Memphis, TN. Collapsing Glomerulonephritis has become an increasingly eommon cause of proteinuria and renal failgre in this country. Most of these cases have been associated with HIV infection or intravenous drug usage. There have been cases of this disease associated with other viral illnesses ie: Hepatitis C and HTLV-1. GlomerUlopathy associated with CMV has been described in renal allografts. We report a case of acute renal Faihire secondary to biopsy proven Collapsing Glomemlonephritis in a 19 yeaF old African American female with CMV septicemia who was HIV negative and had no other risk factors. She presented to the hospital with fever, chills, and acute renal failure. She had 4+ proteinuria with a telescopic urine, Renal biopsy showed moderate collapse of several glomemli. Initial treatment with pulse doses of intravenous methylpredinisolone showed no response. She was acutely dialyzed twice secondary to worsening renal function and uremia: Her workup Which included serological testing for HIV, Hepatitis B and C, RPR, ANN, ANCA, ASO titers, AntiGBM antibodies was negative. She had qlevated Liver Transaminases and Bilimbin. PCR for CMV was positive, urine cultures grew CMV and Serum IgM titers for CMV antigens were 1:256. She was placed on intravenous Gancyclovir and the serum creafinine which had risen m 9.0 mg/dI started to decrease. She recdived in~avenous Gancyclovir for a total of six weeks. Her serum creatinind at the time c~fdischarge was 1.8 mg/dI and the serum transaimnases had ~lso decreased. She was dischm'ged in good health and 6 months aRer th~ discharge her serum creatinine remains stable at 1.4 mg/dl. A repeat HIV +eatwas negative. Non HIV viral illnesses should be considered as a potential cause of Collapsing GN and acute renal failure. A timely diagnoses and appropriate treatment may arrest farther renal injury and prevent considerable morbidity and mortality as was illustrated in this case.