Failed Renal Allograft: Not So Fast

NKF 2016 Spring Clinical Meetings Abstracts

Case Report 69

71

ASSOCIATION OF NADIR INTRADIALYTIC BLOOD PRESSURE AND MORTALITY IN HEMODIALYSIS PATIENTS. Jason Chou1; Yoshitsugu Obi1; Tae Hee Kim1; Elani Streja1; Connie M. Rhee1; Melissa Soohoo1; John Sim2 Kamyar Kalantar-Zadeh1. 1Harold Simmons Center, UC Irvine, Orange, CA. 2Kaiser Permanente Southern California, Pasadena, CA Intradialytic hypotension (IDH) is a well-known complication in maintenance hemodialysis (HD) patients that is still without a consensus definition. Recent publications with varying definitions of IDH have shown that IDH is associated with higher mortality risk. We hypothesize that lower nadir intradialytic (NI) SBP is inversely associated with all-cause mortality and aim to find the optimal NI-SBP goals for HD patients with varying pre-HD SBP. We examined the association of NI-SBP and all-cause mortality in a study cohort of incident adult HD patients during 2007–2011. Baseline (first 91 days of dialysis) NI-SBP-mortality associations were examined using Cox regression models with restricted cubic splines and adjustment for case-mix, comorbidities, and lab covariates. Associations were also examined according to pre-HD SBP strata. Over 5 years, in a cohort of 112,013 HD patients, incrementally lower NI-SBP less than 115 mmHg was consistently and linearly associated with higher death risk across all pre-dialysis BP strata, while higher NI-SBP>140 was associated with a slightly higher mortality risk, and these associations remain robust to adjustment 6

120-130 mmHg

140-150 mmHg

130-140 mmHg

Casemix Casemix+Comorbidities

150-160 mmHg 160-170 mmHg

Mean Nadir Intradialytic SBP Q1

Percent 70 80

90 10 0 11 0 12 0 13 0 14 0 15 0 16 0 17 0 18 0 19 0 20 0 21 0

0

.25 50 60

21 0

20 0

19 0

18 0

17 0

16 0

15 0

14 0

13 0

12 0

80

11 0

90 10 0

70

60

50

0

.25

.5

.5

2

2

1

Percent

2 1

>170 mmHg

2

4

4

Casemix+Comorbidities+Labs

4

6 8

<120 mmHg

6

8

Percent

6

Unadjusted

4

Percent

Mean Nadir Intradialytic SBP Q1 Casemix+Comorbidities+Labs Adjusted

for demographics, laboratory values and comorbidities. In conclusion lower NI-SBP tends to be associated with higher all-cause mortality risk in incident HD patients. Further studies are needed to identify optimal NI-SBP goals in HD patients according to pre-HD SBP.

70 ASSOCIATION OF PARATHORMONE (PTH) WITH COLON ADENOMAS (CA) IN DIABETICS WITH CHRONIC KIDNEY DISEASE (CKD): D. Nag Chowdhury, VA DeBari, W Baddoura and C. Chandran`, St. Joseph’s Regional Med. Ctr. Paterson, NJ USA Malignancy and pre-malignant conditions are more common in patients with CKD. The purpose of this study was to investigate the epidemiology of CA as it occurs in diabetics with CKD. This is a retrospective cohort study of adult (≥18 years) patients with DM (n=565) who had undergone colonoscopy during the period 2000-2010 inclusive in a 650-bed, tertiary care, teaching hospital. The cohort was bifurcated into those with CKD (GFR< 60 ml/min; n= 296 and those with normal renal function (n=269). The outcome for CKD as an exposure for the cohort was the presence or absence of colon adenomas (CA). Concentration of serum PTH, Ca+2, and phosphorous (P), measured within 6 months of the colonoscopy, were recorded for the CKD group. The levels of those with adenomas (n=171) were compared with the levels from those without adenomas (n=175). Continuous data were tested for normality (D’AgostinoPearson test) without transformation; parametric and nonparametric methods were used based on the results of normality tests. Statistical significance was based on a two-sided p-value <0.05. The presence of CKD in this cohort demonstrated a significant association with colon adenomas (OR: 2.96; 95% CI: 2.02 to 4.34; p<0.0001. Gender and race, as potential confounders, were included as covariates in a logistic regression model and found to not significantly alter the univariate OR (adjusted OR, black race: 3.10 (CI: 2.11 to 4.55, p<0.0001, p for interaction=0.740; male gender: 3.01 (CI: 2.05 to 4.40, p<0.0001, p for interaction = 0.786). We did not detect statistical significance in P nor Ca+2 between the groups (Ca+2 in CA group: 8.5 ± 0.7 vs 8.5 ± 0.7 mg/dl in group without CA, p= 0.383; P in CA group: 4.0 ± 1.1 vs 4.2 ± 1.17 mg/dl in group without CA, p= 0.113). There was, however, a statistically significant difference in PTH; for the group with CA, PTH: 387.7 ± 351.3 ng/L vs. 172.2 ± 196.7 ng/L; p<0.0001). These data suggest that CKD is associated with CA in subjects with DM. Diabetics with CKD and CA exhibit PTH levels significantly and substantially (~2-fold) higher than those without CA, while neither P nor Ca+2 differ significantly in these two groups. While we caution against attempting to assign causality to highly elevated PTH in DM patients with CKD and CA, our data suggest that a strong association may exist between PTH levels and CA in these subjects and that PTH may put diabetics with CKD at risk for CA.

A36

FAILED RENAL ALLOGRAFT: NOT SO FAST Pregnancy in a Patient Wit Raad B. Chowdhury, Tsering Dhondup, Thomas R. and Circulating Anti-P Schwab, Hatem Amer The William J von Liebig Transplant Center, Mayo Clinic, Rochester, MN USA. Laith Al-Rabadi, MBBS,1,* Rivka A 52-year-old female patient presents seeking a thirdE. Ballard, MD,2,y Alan Jennifer kidney transplant. She had developed renal failure from David J. Salant, MD,1 lupus nephritis and received her first kidney transplant 21 years previously. That living donor transplant failed almost immediately for unknown reasons and then after 7 years of There is little information about pregnancy o dialysis, received her second transplant. Her especially immunosuppression consisted of mycophenolate those mofetilwith circulating autoantibod in primary MN. We present what and prednisone. Her creatinine was inautoantigen the low 1 range for a 39-year-old woman with PLA2R-associate 14 years. Following an upper respiratory tract infection anasarca, hypoalbuminemia (albumin, 1.3-2. creatinine increased and did not recover. She contacted the opsytwo revealed MN with staining for PLA2R, a transplant center that performed her prior transplants She did not respond and was informed that her deceased donor allograft was to conservative therapy a Several weeks after presentation, she was fou failing and that she should undergo a transplant evaluation. immunosuppressive treatment. Protei At presentation to our center for thefurther evaluation, the treating physician elected to investigate the cause anti-PLA of her 2R levels declined but w Circulating allograft dysfunction. Testing revealedwithout mild hydronephrosis proteinuria at birth or at her subseque and BK viremia. A renal biopsy showed nephropathy. hadBK detectable circulating anti-PLA2R of imm Reduction of immunosuppression andlow repair of a distal titers. Only trace amounts of IgG4 ant ureteral stricture resulted in improvingdiscrepancy renal function. This anti-PLA2R levels in th between allograft continues to function 4 yearsAm afterJ presenting for67(5):775-778. a Kidney Dis. ª 2016 by transplant evaluation. This case highlights the importance of fully investigating INDEX WORDS: Membranous nephropathy ( late renal allograft dysfunction even ifreceptor grafts are(PLA considered 2R); autoantibody; placenta; ritu to have passed the expected life expectancy. It also highlights that BK nephropathy can occur many years after the transplant.

P

regnant patients with autoimmune disease deliver newborns with a spectrum of cl manifestations due to the transplacental passa 72 circulating autoantibodies. Pregnant patients A CASE OF REFRACTORY HYPOKALEMIA FROM lupus or myasthenia gravis can deliver babies BARBITUATE COMA THERAPY: Hisham Ibrahim, Rajyalakshmi Cheng Chu, Omar Mudallal, corresponding diseaseGadi,in the neonate.1,2 Neo Saint Louis University School of Medicine, St Louis, MO, USA membranous Introduction: Barbituate Coma Therapy(BCT) nephropathy is used for refractory(MN) not associated intracranial hypertension andcongenital has shown to reduce cerebral blood infection was flow first described in 199 and metabolic activity. However, one of the rare consequences is attributed to the passive transfer of maternal refractory hypokalemia, which can lead to life threatening arrhythmias. 3 Case Report: A 35 year oldbodies male, alleged fall from height, wasantigens. found to putative renal More than a d disoriented by EMS with a GCS of 9. CT of head showed 4 multiple later, Debiec et al identified the first antigen inv hemorrhagic contusions, hematomas, and diffuse sulci effacement consistent with intracranial hypertension. the ICU,as patient was in such Incases neutral endopeptidase (NE started on hypertonic saline, however, mental status worsened and ICP present on the surface of the pod remained above goal despite metalloprotease a targeted serum Na 160-165. Decision was made to start pentobarbital at 2involved mg/kg/hr within q2hr electrolyte and the proteolytic regulation of va monitoring. After 24 hrs of BCT infusion, K decreased from 3.9 tive peptides. Debiec et alanddescribed a mother w mmol/L to 1.3 mmol/L despite aggressive potassium replacement infusion at 10 meq/hr. EKG mutation showed diffuse ST depressionsNEP in leadsexpression II, preventing who had fo III, V3-V6. Decision was made to initiate a concentrated solution of anti-NEP antibodies due to fetomaternal alloi potassium and infuse at 40 meq/hr via a central line. Within next 16 nization from aIn previous miscarriage; these antib hrs, K increase from 1.3 mmol/L to 4.0 mmol/L. the interim, patient developed acute kidney injury(ATN) from hypotension induced by were to cross the placenta and cause subepit BCT therapy despite aggressive fluid and pressor support. In spite of in continued the fetal kidney of a subsequent stopping potassium infusion,deposits serum potassium to increase and peaked at 7.2 mmol/L 24nancy. hrs later. In essence, patient’s potassium M-type phospholipase A2 receptor (PL level fluctuated wildly within 48 hrs, and fortunately, without any was later identified as the major autoantigen fo arrhythmias on cardiac monitoring. Discussion: BCT leads to inhibition of neuronal mary MN in voltage-dependence adults.5 Little literature exists on potassium current and inhibition of phosphofructokinase. outcomes in patients with nephrotic Hypokalemia is explained bypregnancy an increase in intracellular pH and promote a shift of K into the drome cell. Increase also provoke an with no data ava duein ICP to can primary MN, intense release of endogenous catecholamine and induce β2 stimulation about pregnancy in PLA 2R-associated disease of Na-K pump. In our experience, potassium infusion should be started no more than 20 meq/hr to prevent overshooting the target and causing present what we believe to be the first known ca iatrogenic hyperkalemia and to take in to consideration rapid change in pregnancy in athepatient with PLA2R-associated hemodynamics induced by BCT that directly affect kidneys ability to excrete potassium. who was seropositive for anti-PLA2R autoantib throughout the course of her pregnancy. Am J Kidney Dis. 2016;67(5):A1-A118