Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 50-71-HPA Axis
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-60
Alejandro L Arregger*1, Estela ML Cardoso2, Alfredo Zucchini3, Elvira C Aguirre3, Alicia Elbet4 and Liliana N Contreras5
1University of Buenos Aires, Buenos Aires CF, Argentina, 2CONICET, 3University of Buenos Aires, 4CEREHA, 5University of Buenos Aires-CONICET, Buenos Aires, Argentina
Hypotension is a major complication of dialysis. Different etiopathogenic mechanisms have been proposed but cortisol deficiency has been poorly investigated. Our aim was to assess adrenal function in fifty chronic hypotensive patients with end stage renal disease  (ESRDH)  and evaluate their outcome along 24 months. They had systolic blood pressure (BP) ≤ 100 mmHg for more than 3 months unresponsive to conventional treatments. They were on dialysis replacement therapy ,off glucocorticoids and drugs that affect steroidogenesis. At 8.0 a.m. blood was drawn for ACTH, cortisol, renin and aldosterone and   whole saliva was obtained. Then, 25 µg of synthetic ACTH was injected intramuscularly as previously described (1). At 30 minutes saliva was collected for salivary cortisol  (SAF30) and aldosterone ( SAL30). ACTH and renin were assessed by IRMA, serum cortisol, serum aldosterone and  salivary steroids by RIA as described (1). Reference values: ACTH:5.0-50.0 pg/ml; renin:0.7-3.0 pM,  aldosterone/renin ratio:9.0-28.6 , SAF30 ≥ 20.0 nM; SAL30 ≥ 100.0 pM. Results: patients had adequate salivary flow rate (0.66±18.0 ml/min). Basal cortisol and aldosterone in saliva and serum correlated positively and significantly in ESRDH(r= 0.923 and r= 0.90, respectively; p< 0.0001, for both).Fifteen patients (R) achieved SAF30: 37,0 ±19,0 nM and SAL30:178.0±177.0 pM.  Four patients (R1) had primary adrenal insufficiency: SAF30:7.0 ±4.0 nM , SAL30 :  27.0  ± 15.0 pM. and ACTH : 99.0± 17.0 pg/ml. Six patients (R2) had  secondary adrenal insufficiency: SAF30 :11.0 ± 5.0 nM, SAL30  163.0±22.0 pM and ACTH :11.0 ±3.8 pg/ml. Nine patients (R3) had  selective hypoaldosteroism : SAF 30 :40.0± 21.0 nM ,SAL 30 :16.0±6.0 pM and renin:    0.2±0.1 pM. Sixteen patients (R4) had secondary hyperaldosteronism: SAF30: 35.0±11.0 nM, basal SAL: 272.0±196.0 pM and SAL30: 497.0±305.0 pM; aldosterone/renin ratio: 22.0 ± 5.5. The duration of dialysis was not different among groups. Outcome: three out of 4  R1 received steroid therapy and normalized systolic BP (> 100.0 mmHg). Six R2 improved BP on hydrocortisone until adrenal recovery. Eight ESRDH died  (1 R, 1 R1; 1R2; 3 R3; 2 R4). After kidney transplantation, five patients (1 R,1R2,3 R4) recovered and maintained systolic blood pressure levels (≥110 mmHg) . Conclusion: cortisol deficiency was detected in 20% of ESRDH normalizing BP on steroid replacement. Successful kidney transplantation was associated with recovery of BP.

1. Arregger et al. Steroids 2008; 73:77-82.

Nothing to Disclose: ALA, EMC, AZ, ECA, AE, LNC

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