IntroductionOne of the most severe complications of repair surgery for abdominal aortic aneurysms (AAA) is acute kidney injury (AKI). Acute kidney injury is an inflammatory process whose pathogenesis involves endothelial cells (EC). The aim of this study was to assess the dynamics of endothelium injury markers measured during elective AAA surgery which might confirm the inflammatory character of AKI.Material and methodsThe study group consisted of 14 patients with AAA. We measured plasma soluble forms of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, P-selectin as well as the levels of von Willebrand factor (vWF) before, during (including intra-abdominal vein levels before and after aortic clamp removal) and within 2 days after surgery.ResultsWe have found a biphasic response of ICAM-1, VCAM-1 and P-selectin with an initial fall and subsequent rise. However, only VCAM-1 changes were significant compared to its baseline value. The maximum decrease of VCAM-1 was observed in the renal vein 5 min after aortic clamp removal (335.42 ±129.63 ng/ml vs. 488.90 ±169.80 ng/ml baseline value, p < 0.05), and the highest rise 48 h after aortic clamp removal (721.46 ±333.99 vs. baseline, p < 0.05).ConclusionsVascular cell adhesion molecule-1 turned out to be the most sensitive indicator of EC injury and inflammatory status after AAA surgery. During AAA surgery, soluble forms of P-selectin, ICAM-1 and VCAM-1 demonstrate a biphasic response with an initial fall and subsequent rise. These soluble forms could have a modulatory effect on the development of inflammation.

Tamm-Horsfall protein (THP) is a glycoprotein that is

INTROduCTION One of the most severe complications of repair surgery for abdominal aortic aneurysms (AAA) is acute kidney injury (AKI). Even small rises in serum creatinine after surgery are associated with increased mortality. ObjECTIvEs The aim of the study was to assess the dynamics of AKI after elective AAA surgery using novel markers. PATIENTs ANd mEThOds The study group consisted of 14 patients with AAA. We measured serum neutrophil gelatinase-associated lipocalin (NGAL) before, during (including intra-abdominal vein levels before and after removal of aortic clamp), and within 2 days after surgery. Moreover, we assessed urinary NGAL, interleukin 18 (IL-18), and liver-type fatty acid-binding protein (L-FABP) before, during, and within 3 days after surgery. REsuLTs We observed a marked but nonsignificant increase in serum NGAL directly after clamp removal (75.21 ±55.83 vs. 46.37 ±21.60 ng/ml baseline value, P >0.05) and significantly elevated plasma NGAL at 2 hours (91.54 ±76.54 vs. baseline, P <0.05), 12 hours (100.78 ±44.92 vs. baseline, P <0.05) and 24 hours (89.46 ±94.18 vs. baseline, P <0.05) after clamp release. There was also significant elevation of urinary IL-18 at 2 hours (51.60 [12.12-527.16] vs. 25.99 [9.34-187.80] pg/ml at baseline, P <0.05); L-FABP at 2 hours (47.10 [5.40-500.00] vs. 5.50 (2.20-27.20) ng/ml at baseline, P <0.05) and 12 hours (39.00 [5.20-500.00] vs. baseline, P <0.05); NGAL at 12 hours (20.75 [5.00-176.10] vs. 5.85 [1.40-16.00] ng/ml at baseline, P <0.05) and 24 hours (13.95 [3.90-163.30] vs. baseline, P <0.05) after clamp release. CONCLusIONs Elective AAA surgery may induce AKI. Novel markers can facilitate early detection of AKI, thus allowing to start therapy at an appropriate time point.

Recent data indicated the importance of urinary losses of erythropoietin (Epo) in the pathogenesis of anaemia in patients with nephrotic syndrome. In the present study we aimed to investigate plasma and urinary Epo levels and their renal handling in relation to beta 2-microglobulin (beta 2m), sodium metabolism and the renin-angiotensin-aldosterone system (RAAS), respectively, in patients with sub-nephrotic range proteinuria (SNP), microalbuminuric diabetics and hypertensives, and in healthy subjects studied on a standardized diet containing 120 mmol sodium and 70 g protein per day. We found that patients with SNP were characterized by lower plasma levels of Epo than healthy subjects but no differences were found in urinary excretion of Epo, endogenous Epo clearance and its fractional excretion (FEEpo). There were no differences between groups in FE beta 2m and FENa and plasma aldosterone levels but plasma renin activity was higher in patients with SNP than in the controls. No relationships were found between Epo levels and activity of the RAAS and sodium metabolism, respectively. Our data suggest that lower levels of plasma Epo in patients with SNP and normal renal excretory function are not due to urinary losses of Epo but rather to the decreased production/degradation ratio.

We assessed the influence of hyperoxemia on erythropoietin secretion in patients with various etiological forms of arterial hypertension (essential, n=15; renoparenchymal, n=16; renovascular, n=15) and in 15 healthy subjects. On the first day of the study, blood was withdrawn at 1-hour intervals for the estimation of erythropoietin during a total of 6 hours and at 2-hour intervals for the assessment of PO2. Three days later the same parameters were assessed again at identical time intervals, but the subjects were breathing pure oxygen during the first 2 hours. Breathing with pure oxygen resulted in a significant increase of blood (EPO) was introduced in the treatment of anemia caused by renal failure, the most important side effect of the therapy was an increase of blood pressure or worsening of preexisting hypertension. 12 The proposed mechanisms of hypertension during EPO treatment were increased blood viscosity, loss of hypoxic vasodilation, and inappropriately reduced cardiac output after correction of anemia.24 Furthermore, recent studies suggested that EPO could induce a direct or hormonally mediated vasopressor effect. 36The main stimulus for EPO secretion seems to be a decrease of oxygen supply to the renal tissue.7 As shown by Kurtz et al,7 EPO secretion is determined by the ratio of oxygen supply to oxygen demand in the kidney. The parameter that adequately reflects this ratio is Po 2 in small postcapillary peritubular veins. This local P02 is detected by a putative oxygen sensor regulating EPO secretion. -8 Limited information is currently available on the influence of hyperoxia on the regulation of EPO secretion.9 -" Changes in renal hemodynamics and tubular function are well described in hypertension. © 1994 American Heart Association, Inc.sive patients. In patients with essential hypertension, unlike in healthy subjects and patients with other etiological forms of arterial hypertension, only a very short-term suppression of erythropoietin levels was observed during hyperoxemia. No significant changes in blood pressure during breathing with pure oxygen were found in any of the studied groups. We conclude the following: (1) Isobaric hyperoxia exerts a significant suppressive effect on plasma erythropoietin levels both in patients with different etiological forms of arterial hypertension and in healthy subjects. (2) Patients with essential hypertension are characterized by a quantitatively different response of plasma erythropoietin to isobaric hyperoxia compared with healthy subjects and patients with renoparenchymal or renovascular hypertension. (3) Oxygen physically dissolved in blood plasma seems to be an important determinant of erythropoietin secretion independent of hemoglobin concentration and oxygen saturation. (Hypertension. 1994;24:486-490.) Key Words • erythropoietin • hypertension, essential • erythropoiesis • oxygen regulation of EPO production, both of these factors might influence EPO secretion. Limited available information on endogenous EPO in arterial hypertension did no...