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A TWIST IN THE TALE: AN UNCOMMON CAUSE OF TRANSPLANT FAILURE
NKF 2015 Spring Clinical Meetings Abstracts
229 UNUSUAL PRESENTATION OF POST-TRANSPLANT LYMPHOPROLIFERATIVE DISEASE (PTLD) IN THE NATIVE KIDNEY Snigdha Reddy, Jerry Yee, Anita Patel, Henry Ford Hospital, Detroit, MI, USA. PTLD is a known complication following solid-organ transplantation. This is most commonly linked to Ebstein-Barr virus (EBV) transformation of B lymphocytes. Given the nature of the transformed cell, PTLD typically involves lymphoid tissues in proximity to the transplanted allograft. We report a case of a 68 year-old male twelve years post-deceased donor kidney transplantation maintained on tacrolimus and sirolimus. He presented with weight loss of 18 kg over 3 months and vague abdominal pain. His baseline serum creatinine was ~1.5 m/dL. Computed tomography of the abdomen revealed an interval increase in his left renal cyst sizes, some with hemorrhage. A follow-up magnetic resonance imaging of his abdomen failed to characterize the nature of these cystic lesions, and urine cytology was negative for malignant cells. A positron emission tomography from his skull base to mid-thigh revealed intense radiotracer activity in an anterior cystic lesion in the native left kidney with variable degrees of avidity compatible with renal cell carcinoma. The EBV PCR was 12,000 copies/ml. A robotic left radical nephrectomy was done and histopathology revealed PTLD, monomorphic type, with classification as high-grade diffuse large Bcell lymphoma (DLBCL) with plasmacytoid features, partial CD20 expression, lack of CD138 expression, and strong CD30 expression. Oncologic evaluation was Stage IV DLBCL. The patient developed a left calf mass with needle-biopsy findings of DLBCL. Immunosuppression was changed to prednisone monotherapy and followed by 6 cycles of cyclophosphamide, doxorubicin, vincristine and prednisone, combined with rituxan (R-CHOP). The patient subsequently developed a complete remission of his lymphoma. In summary, this report highlights the importance of remaining vigilant and continued surveillance for masses in the native kidney as a presenting feature for PTLD.
230 PRE-DIALYSIS SERUM SODIUM AND MORTALITY IN A NATIONAL INCIDENT HEMODIALYSIS COHORT. Connie M. Rhee1, Vanessa Ravel1, Juan Carlos Ayus2, Elani Streja1, Rajnish Mehrotra3, Alpesh N. Amin1, Steven M. Brunelli4, Csaba P. Kovesdy5, Kamyar Kalantar-Zadeh1. 1UC Irvine, Irvine, CA; 2 Renal Consultants of Houston, Houston, TX, 3Univ. Washington, Seattle, WA, 4DaVita Clinical Research, Minn., MN, 5Univ. of Tennessee Health Sciences Center, Memphis, TN. A consistent association between low serum sodium measured at a single-point-in-time (i.e., baseline sodium, as a proxy of long-term exposure) and higher mortality has been observed in hemodialysis (HD) patients. In a recent study examining time-dependent sodium (i.e., sodium levels updated at quarterly intervals, as a proxy of short-term exposure) in non-dialysis dependent CKD patients, both hypo- and hypernatremia were associated with higher mortality. We hypothesized that both low and high time-dependent sodium levels are independently associated with higher death risk in HD patients. Among 27,180 adult incident HD patients from a large national dialysis organization during 2007-2011, we examined the association of time-dependent sodium with all-cause mortality using Cox models with 5 levels of adjustment: Models 1 (unadjusted), 2 (case-mix), 2A (case-mix+interdialytic weight gain [IDWG]), 3 (casemix+laboratory tests), 4 (model 3+IDWG), and 5 (model 4+BUN+glucose). Across all models, sodium levels <138 and ≥144mEq/L were associated with higher mortality (ref.: 138140mEq/L): HRs (95%CI): 2.24 (1.93-2.59), 1.71 (1.50-1.94), 1.50 (1.36-1.65), 1.31 (1.21-1.41), 1.11 (1.04-1.19), 0.97 (0.90-1.04), 1.09 (0.99-1.21), and 1.47 (1.26-1.71) for sodium levels <130, 130-<132, 132-<134, 134-<136, 136-<138, 140-<142, 142-<144, ≥144mEq/L, respectively, adjusted for covariates in Model 5. In conclusion, there is a U-shaped sodium-mortality association in HD patients, suggesting both hypo- and hypernatremia carry short-term risk in this population.
A72
231 RELATIONSHIP BETWEEN THYROTROPIN AND FREE THYROXINE MEASURED BY TANDEM MASS SPECTROMETRY AND IMMUNOASSAY IN HEMODIALYSIS PATIENTS. Connie Rhee1, Gregory Brent2, Danh Nguyen1, Jennie Jing1, Tracy Nakata1, Elani Streja1, Angela Leung2, Csaba Kovesdy3, Steven Brunelli4, Kam Kalantar-Zadeh1. 1UC Irvine, Irvine, CA; 2 UCLA, Los Angeles, CA; 3Univ. Tennessee Health Science Center, Memphis, TN; 4DaVita Clinical Research, Minn., MN. Hypothyroidism (HT), defined by elevated thyrotropin (TSH) and normal (subclinical HT) or low free thyroxine (FT4) (overt HT), is common in hemodialysis (HD) patients. Yet accurate diagnosis of HT in HD is limited by inaccuracy of routinely-used indirect FT4 (iFT4) assays which are protein-hormone binding dependent (uremic toxins impair protein-hormone binding). Direct FT4 (dFT4) assays more exactly represent the inverse log-linear TSH—FT4 relationship in populations with altered protein-hormone binding (pregnancy, nonthyroidal illness). We hypothesized that TSH has stronger correlation with dFT4 vs. iFT4 in HD patients, and that these associations differ across race. We conducted cross-sectional analyses in 144 HD patients from the MADRAD study. TSH and iFT4 were measured by immunoassay, and dFT4 was ascertained by equilibrium dialysis+ tandem mass spectrometry. We estimated unadjusted and case-mix adjusted Pearson correlations (R) of TSH with dFT4 vs. iFT4 in the overall cohort and within racial subgroups (non-black vs. black). While dFT4 and iFT4 were closely correlated (Fig.), TSH had stronger inverse correlation with dFT4 (adjusted R=-0.12, p=0.1) vs. iFT4 (adjusted R=0.07, p=0.4) in the overall cohort, although not statistically significant. In non-blacks, TSH had an even stronger inverse correlation with dFT4 vs. iFT4 in unadjusted (R=-0.19, p=0.06 vs. R=0.15, p=0.1, respectively) and adjusted (R=-0.22, p=0.03 vs. R=-0.19, p=0.07, respectively) analyses. In HD patients, TSH has stronger inverse correlation with dFT4 vs. iFT4, particularly in non-blacks.
232 A TWIST IN THE TALE: AN UNCOMMON CAUSE OF TRANSPLANT FAILURE Mahrukh Rizvi, Richard Wing, Karandeep Shergill, Fatima Khalid, Strong Memorial Hospital, Rochester, NY, USA. Torsion of renal transplant allograft is a serious and potentially under recognised condition. Diagnosis is challenging due to lack of specific clinical features and misleading radiographic findings mimicking other more common etiologies of acute kidney injury (AKI). A 56 year old female with Alport’s syndrome had undergone an intra peritoneal renal transplant 15 months ago. Four months ago, she had presented with abrupt onset of anuria and AKI and was found to have renal allograft hydronephrosis which resolved with emergent nephrostomy tube placement. She now presented with an 11 hour history of anuria, nausea and chills after intense hiking and pilates. She denied any pain over the allograft, medication non-compliance or dehydration. On examination, she was hypertensive with no tenderness over the allograft. Work up revealed AKI with renal ultrasound reveling an enlarged renal allograft with no hydronephrosis, a patent renal vein but no identifiable renal arterial blood flow. Emergent computed tomography angiography revealed an edematous allograft with good renal artery flow but a non-visualizated renal vein. Her worsening clinical status and confounding imaging findings were concerning for vascular compromise. Emergent surgical exploration revealed a free floating renal allograft that had been volvulized in the mesentero-axial direction. Detorsion of the allograft restored vascular flow and the patient subsequently had an uneventful recovery. As demonstrated in our case, kidney torsion may decievingly simulate a variety of radiologic presentations ranging from ureteral obstruction, arterial thrombosis, venous thrombosis, and acute rejection. From the cases in literature, however, the most suggestive imaging finding is change in axis of the allograft. Retrospectively, this was present on imaging in our patient. Through this case, we hope to bring awareness of this potential complication and stress a high index of suspicion on both the nephrologist and the radiologist. The proximity to vigorous exercise also raises the question of aggressive physical activity as a possible inciting factor and once again brings into question the role of prophylactic nephropexy.
Am J Kidney Dis. 2015;65(4):A1-A93
229 UNUSUAL PRESENTATION OF POST-TRANSPLANT LYMPHOPROLIFERATIVE DISEASE (PTLD) IN THE NATIVE KIDNEY Snigdha Reddy, Jerry Yee, Anita Patel, Henry Ford Hospital, Detroit, MI, USA. PTLD is a known complication following solid-organ transplantation. This is most commonly linked to Ebstein-Barr virus (EBV) transformation of B lymphocytes. Given the nature of the transformed cell, PTLD typically involves lymphoid tissues in proximity to the transplanted allograft. We report a case of a 68 year-old male twelve years post-deceased donor kidney transplantation maintained on tacrolimus and sirolimus. He presented with weight loss of 18 kg over 3 months and vague abdominal pain. His baseline serum creatinine was ~1.5 m/dL. Computed tomography of the abdomen revealed an interval increase in his left renal cyst sizes, some with hemorrhage. A follow-up magnetic resonance imaging of his abdomen failed to characterize the nature of these cystic lesions, and urine cytology was negative for malignant cells. A positron emission tomography from his skull base to mid-thigh revealed intense radiotracer activity in an anterior cystic lesion in the native left kidney with variable degrees of avidity compatible with renal cell carcinoma. The EBV PCR was 12,000 copies/ml. A robotic left radical nephrectomy was done and histopathology revealed PTLD, monomorphic type, with classification as high-grade diffuse large Bcell lymphoma (DLBCL) with plasmacytoid features, partial CD20 expression, lack of CD138 expression, and strong CD30 expression. Oncologic evaluation was Stage IV DLBCL. The patient developed a left calf mass with needle-biopsy findings of DLBCL. Immunosuppression was changed to prednisone monotherapy and followed by 6 cycles of cyclophosphamide, doxorubicin, vincristine and prednisone, combined with rituxan (R-CHOP). The patient subsequently developed a complete remission of his lymphoma. In summary, this report highlights the importance of remaining vigilant and continued surveillance for masses in the native kidney as a presenting feature for PTLD.
230 PRE-DIALYSIS SERUM SODIUM AND MORTALITY IN A NATIONAL INCIDENT HEMODIALYSIS COHORT. Connie M. Rhee1, Vanessa Ravel1, Juan Carlos Ayus2, Elani Streja1, Rajnish Mehrotra3, Alpesh N. Amin1, Steven M. Brunelli4, Csaba P. Kovesdy5, Kamyar Kalantar-Zadeh1. 1UC Irvine, Irvine, CA; 2 Renal Consultants of Houston, Houston, TX, 3Univ. Washington, Seattle, WA, 4DaVita Clinical Research, Minn., MN, 5Univ. of Tennessee Health Sciences Center, Memphis, TN. A consistent association between low serum sodium measured at a single-point-in-time (i.e., baseline sodium, as a proxy of long-term exposure) and higher mortality has been observed in hemodialysis (HD) patients. In a recent study examining time-dependent sodium (i.e., sodium levels updated at quarterly intervals, as a proxy of short-term exposure) in non-dialysis dependent CKD patients, both hypo- and hypernatremia were associated with higher mortality. We hypothesized that both low and high time-dependent sodium levels are independently associated with higher death risk in HD patients. Among 27,180 adult incident HD patients from a large national dialysis organization during 2007-2011, we examined the association of time-dependent sodium with all-cause mortality using Cox models with 5 levels of adjustment: Models 1 (unadjusted), 2 (case-mix), 2A (case-mix+interdialytic weight gain [IDWG]), 3 (casemix+laboratory tests), 4 (model 3+IDWG), and 5 (model 4+BUN+glucose). Across all models, sodium levels <138 and ≥144mEq/L were associated with higher mortality (ref.: 138140mEq/L): HRs (95%CI): 2.24 (1.93-2.59), 1.71 (1.50-1.94), 1.50 (1.36-1.65), 1.31 (1.21-1.41), 1.11 (1.04-1.19), 0.97 (0.90-1.04), 1.09 (0.99-1.21), and 1.47 (1.26-1.71) for sodium levels <130, 130-<132, 132-<134, 134-<136, 136-<138, 140-<142, 142-<144, ≥144mEq/L, respectively, adjusted for covariates in Model 5. In conclusion, there is a U-shaped sodium-mortality association in HD patients, suggesting both hypo- and hypernatremia carry short-term risk in this population.
A72
231 RELATIONSHIP BETWEEN THYROTROPIN AND FREE THYROXINE MEASURED BY TANDEM MASS SPECTROMETRY AND IMMUNOASSAY IN HEMODIALYSIS PATIENTS. Connie Rhee1, Gregory Brent2, Danh Nguyen1, Jennie Jing1, Tracy Nakata1, Elani Streja1, Angela Leung2, Csaba Kovesdy3, Steven Brunelli4, Kam Kalantar-Zadeh1. 1UC Irvine, Irvine, CA; 2 UCLA, Los Angeles, CA; 3Univ. Tennessee Health Science Center, Memphis, TN; 4DaVita Clinical Research, Minn., MN. Hypothyroidism (HT), defined by elevated thyrotropin (TSH) and normal (subclinical HT) or low free thyroxine (FT4) (overt HT), is common in hemodialysis (HD) patients. Yet accurate diagnosis of HT in HD is limited by inaccuracy of routinely-used indirect FT4 (iFT4) assays which are protein-hormone binding dependent (uremic toxins impair protein-hormone binding). Direct FT4 (dFT4) assays more exactly represent the inverse log-linear TSH—FT4 relationship in populations with altered protein-hormone binding (pregnancy, nonthyroidal illness). We hypothesized that TSH has stronger correlation with dFT4 vs. iFT4 in HD patients, and that these associations differ across race. We conducted cross-sectional analyses in 144 HD patients from the MADRAD study. TSH and iFT4 were measured by immunoassay, and dFT4 was ascertained by equilibrium dialysis+ tandem mass spectrometry. We estimated unadjusted and case-mix adjusted Pearson correlations (R) of TSH with dFT4 vs. iFT4 in the overall cohort and within racial subgroups (non-black vs. black). While dFT4 and iFT4 were closely correlated (Fig.), TSH had stronger inverse correlation with dFT4 (adjusted R=-0.12, p=0.1) vs. iFT4 (adjusted R=0.07, p=0.4) in the overall cohort, although not statistically significant. In non-blacks, TSH had an even stronger inverse correlation with dFT4 vs. iFT4 in unadjusted (R=-0.19, p=0.06 vs. R=0.15, p=0.1, respectively) and adjusted (R=-0.22, p=0.03 vs. R=-0.19, p=0.07, respectively) analyses. In HD patients, TSH has stronger inverse correlation with dFT4 vs. iFT4, particularly in non-blacks.
232 A TWIST IN THE TALE: AN UNCOMMON CAUSE OF TRANSPLANT FAILURE Mahrukh Rizvi, Richard Wing, Karandeep Shergill, Fatima Khalid, Strong Memorial Hospital, Rochester, NY, USA. Torsion of renal transplant allograft is a serious and potentially under recognised condition. Diagnosis is challenging due to lack of specific clinical features and misleading radiographic findings mimicking other more common etiologies of acute kidney injury (AKI). A 56 year old female with Alport’s syndrome had undergone an intra peritoneal renal transplant 15 months ago. Four months ago, she had presented with abrupt onset of anuria and AKI and was found to have renal allograft hydronephrosis which resolved with emergent nephrostomy tube placement. She now presented with an 11 hour history of anuria, nausea and chills after intense hiking and pilates. She denied any pain over the allograft, medication non-compliance or dehydration. On examination, she was hypertensive with no tenderness over the allograft. Work up revealed AKI with renal ultrasound reveling an enlarged renal allograft with no hydronephrosis, a patent renal vein but no identifiable renal arterial blood flow. Emergent computed tomography angiography revealed an edematous allograft with good renal artery flow but a non-visualizated renal vein. Her worsening clinical status and confounding imaging findings were concerning for vascular compromise. Emergent surgical exploration revealed a free floating renal allograft that had been volvulized in the mesentero-axial direction. Detorsion of the allograft restored vascular flow and the patient subsequently had an uneventful recovery. As demonstrated in our case, kidney torsion may decievingly simulate a variety of radiologic presentations ranging from ureteral obstruction, arterial thrombosis, venous thrombosis, and acute rejection. From the cases in literature, however, the most suggestive imaging finding is change in axis of the allograft. Retrospectively, this was present on imaging in our patient. Through this case, we hope to bring awareness of this potential complication and stress a high index of suspicion on both the nephrologist and the radiologist. The proximity to vigorous exercise also raises the question of aggressive physical activity as a possible inciting factor and once again brings into question the role of prophylactic nephropexy.
Am J Kidney Dis. 2015;65(4):A1-A93