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• W2009187810 abstract "Related Article, p. 510 Patients receiving erythropoietin therapy show enormous variability in their responsiveness to the drug, many factors have been recognized as contributing to this phenomenon.1Macdougall IC Poor response to erythropoietin: Practical guidelines on investigation and management.Nephrol Dial Transplant. 1995; 10: 607-614Google Scholar Some of these (eg, iron deficiency, acute infections, blood loss, and underdialysis) are well-established, whereas others, such as the role of angiotensin-converting enzyme (ACE) inhibitors, are more controversial.2Macdougall IC The role of ACE inhibitors and angiotensin II receptor blockers in the response to epoetin.Nephrol Dial Transplant. 1999; 14: 1836-1841Google Scholar Indeed, the evidence that this group of widely used drugs affects the response to erythropoietin is conflicting.3Walter J Does captopril decrease the effect of human recombinant erythropoietin in haemodialysis patients?.Nephrol Dial Transplant. 1993; 8 (letter): 1428Google Scholar, 4Hess E Sperschneider H Stein G Do ACE inhibitors influence the dose of human recombinant erythropoietin in dialysis patients?.Nephrol Dial Transplant. 1996; 11 (letter): 749-751Google Scholar, 5Erturk S Ates K Duman N Karatan O Erbay B Ertug E Unresponsiveness to recombinant human erythropoietin in haemodialysis patients: Possible implications of angiotensin converting enzyme inhibitors.Nephrol Dial Transplant. 1996; 11 (letter): 396-397Google Scholar, 6Matsumura M Nomura H Koni I Mabuchi H Angiotensin-converting enzyme inhibitors are associated with the need for increased recombinant human erythropoietin maintenance doses in hemodialysis patients.Nephron. 1997; 77: 164-168Google Scholar, 7Albitar S Genin R Fen-Chong M Serveaux M-O Bourgeon B High dose enalapril impairs the response to erythropoietin treatment in haemodialysis patients.Nephrol Dial Transplant. 1998; 13: 1206-1210Google Scholar, 8Erturk S Nergizoglu G Ates K Duman N Erbay B Karatan O Ertug AE The impact of withdrawing ACE inhibitors on erythropoietin responsiveness and left ventricular hypertrophy in haemodialysis patients.Nephrol Dial Transplant. 1999; 14: 1912-1916Google Scholar, 9Conlon PJ Albers F Butterly D Schwab SJ ACE inhibitors do not affect erythropoietin efficacy in haemodialysis patients.Nephrol Dial Transplant. 1994; 9 (letter): 1358Google Scholar, 10Sánchez JA ACE inhibitors do not decrease rHuEpo response in patients with end-stage renal failure.Nephrol Dial Transplant. 1995; 10 (letter): 1476-1477Google Scholar, 11Cruz DN Perazella MA Abu-Alfa AK Mahnensmith RL Angiotensin-converting enzyme inhibitor therapy in chronic hemodialysis patients: Any evidence of erythropoietin resistance?.Am J Kidney Dis. 1996; 28: 535-540Google Scholar, 12Chew CG Weise MD Disney APS The effect of angiotensin II receptor antagonist on the exogenous erythropoietin requirement of haemodialysis patients.Nephrol Dial Transplant. 1999; 14 (letter): 2047-2049Google Scholar Various mechanisms have been offered to explain why ACE inhibitors might affect the response to erythropoietin. First, it has been shown that angiotensin II directly increases the proliferation of erythroid progenitor cells in vitro.13Mrug M Stopka T Julian BA Prchal JF Prchal JT Angiotensin II stimulates proliferation of normal early erythroid progenitors.J Clin Invest. 1997; 100: 2310-2314Google Scholar Thus, any agent decreasing angiotensin II levels could potentially have a negative effect on erythropoiesis. Second, a natural stem cell regulator called N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) has been identified as inhibiting the recruitment of pluripotent hemopoietic stem cells and normal early progenitors into the S-phase.14Azizi M Rousseau A Ezan E Guyene TT Michelet S Grognet JM Lenfant M Corvol P Menard J Acute angiotensin-converting enzyme inhibition increases the plasma level of the natural stem cell regulator N-acetyl-seryl-aspartyl-lysyl-proline.J Clin Invest. 1996; 97: 839-844Google Scholar ACE inhibitors have been found to increase plasma levels of AcSDKP markedly and, hence, inhibit erythroid growth. Third, ACE inhibitors may act by reducing serum insulin-like growth factor-1 (IGF-1) levels. IGF-1 is known to enhance erythropoiesis. A recent study suggested that this growth factor might play a role in the ACE inhibitor-related decrease in hematocrit in patients with transplant polycythemia.15Morrone LF Di Paolo S Logoluso F Schena A Stallone G Giorgino F Schena FP Interference of angiotensin-converting enzyme inhibitors on erythropoiesis in kidney transplant recipients: Role of growth factors and cytokines.Transplantation. 1997; 64: 913-918Google Scholar Serum erythropoietin and IGF-1 levels were significantly higher in patients with this condition than in a control group without transplant polycythemia. ACE inhibitors significantly reduced hematocrit, IGF-1, and erythropoietin levels. A direct relationship was found between hematocrit and serum IGF-1 levels but not between hematocrit and serum erythropoietin levels.15Morrone LF Di Paolo S Logoluso F Schena A Stallone G Giorgino F Schena FP Interference of angiotensin-converting enzyme inhibitors on erythropoiesis in kidney transplant recipients: Role of growth factors and cytokines.Transplantation. 1997; 64: 913-918Google Scholar Finally, ACE inhibitors have been shown to reduce the production of interleukin-12, a cytokine known to stimulate erythropoiesis.16Constantinescu CS Goodman DB Ventura ES Captopril and lisinopril suppress production of interleukin-12 by human peripheral blood mononuclear cells.Immunol Lett. 1998; 62: 25-31Google Scholar Thus, it is apparent that several means exist by which ACE inhibitors could inhibit erythropoietic activity. In this issue of the Journal, Le Meur et al17Le Meur Y Lorgeot V Comte L Szelag J-C Aldigier J-C Leroux-Robert C Praloran V Plasma levels and metabolism of AcSDKP in patients with chronic renal failure: Relationship with erythropoietin requirements.Am J Kidney Dis. 2001; 38: 510-517Abstract Full Text Full Text PDF Scopus (66) Google Scholar have extended the earlier work by Azizi et al14Azizi M Rousseau A Ezan E Guyene TT Michelet S Grognet JM Lenfant M Corvol P Menard J Acute angiotensin-converting enzyme inhibition increases the plasma level of the natural stem cell regulator N-acetyl-seryl-aspartyl-lysyl-proline.J Clin Invest. 1996; 97: 839-844Google Scholar on the role of AcSDKP levels in mediating the suppression of erythropoiesis caused by ACE inhibitors. This interesting tetrapeptide, which has a molecular weight of 487 daltons, is normally degraded by angiotensin-converting enzyme, and it is partially excreted in the urine. Levels of this small peptide in plasma are therefore influenced by how much is synthesized, how effectively it is degraded by angiotensin-converting enzyme, and how efficiently it is cleared via the kidneys. In normal healthy individuals, plasma levels of this physiological inhibitor of erythropoiesis are maintained at fairly constant levels, but plasma concentrations can increase dramatically in patients treated with ACE inhibitors.14Azizi M Rousseau A Ezan E Guyene TT Michelet S Grognet JM Lenfant M Corvol P Menard J Acute angiotensin-converting enzyme inhibition increases the plasma level of the natural stem cell regulator N-acetyl-seryl-aspartyl-lysyl-proline.J Clin Invest. 1996; 97: 839-844Google Scholar Le Meur et al17Le Meur Y Lorgeot V Comte L Szelag J-C Aldigier J-C Leroux-Robert C Praloran V Plasma levels and metabolism of AcSDKP in patients with chronic renal failure: Relationship with erythropoietin requirements.Am J Kidney Dis. 2001; 38: 510-517Abstract Full Text Full Text PDF Scopus (66) Google Scholar have measured the plasma AcS-DKP concentrations in 176 patients with chronic renal failure, including 120 hemodialysis and 56 nondialyzed patients. Thirty-nine of these patients were receiving ACE inhibitors. The authors studied the relationships between AcSDKP levels, various hematological parameters, and erythropoietin dose requirements. Compared with those in controls, AcSDKP levels were significantly higher in both dialysis and nondialyzed patients who were not receiving ACE inhibitors. This difference was caused by the reduced renal elimination of this peptide. Treatment with ACE inhibitors significantly increased these levels by a factor of 4, although the levels could be partly reduced after a session of hemodialysis. Hemodialysis patients treated with ACE inhibitors had the highest AcSDKP levels, and in this group of patients the weekly doses of erythropoietin correlated with the plasma levels of the peptide. Thus, the results of this study contribute further evidence that AcSDKP in high levels can cause some resistance to erythropoietin by directly suppressing erythropoiesis. This provides a strong scientific rationale for how ACE inhibitor therapy could indeed affect responsiveness to erythropoietin. The question remains, however, as to how important this effect is clinically. There are many other factors present in uremic serum that have long been known to inhibit erythropoiesis, such as spermine, spermidine, putrescine, and parathyroid hormone.18Kushner DS Beckman BS Fisher JW Do polyamines play a role in the pathogenesis of the anemia of end-stage renal disease?.Kidney Int. 1989; 36: 171-174Google Scholar The effect of these inhibitory substances, however, can be easily overcome by exogenous erythropoietin, and one has to turn to clinical trial data to ascertain whether this is a clinically relevant phenomenon or simply an interesting piece of laboratory research. There are studies both supporting and refuting the hypothesis that ACE inhibitors inhibit the action of erythropoietin.3Walter J Does captopril decrease the effect of human recombinant erythropoietin in haemodialysis patients?.Nephrol Dial Transplant. 1993; 8 (letter): 1428Google Scholar, 4Hess E Sperschneider H Stein G Do ACE inhibitors influence the dose of human recombinant erythropoietin in dialysis patients?.Nephrol Dial Transplant. 1996; 11 (letter): 749-751Google Scholar, 5Erturk S Ates K Duman N Karatan O Erbay B Ertug E Unresponsiveness to recombinant human erythropoietin in haemodialysis patients: Possible implications of angiotensin converting enzyme inhibitors.Nephrol Dial Transplant. 1996; 11 (letter): 396-397Google Scholar, 6Matsumura M Nomura H Koni I Mabuchi H Angiotensin-converting enzyme inhibitors are associated with the need for increased recombinant human erythropoietin maintenance doses in hemodialysis patients.Nephron. 1997; 77: 164-168Google Scholar, 7Albitar S Genin R Fen-Chong M Serveaux M-O Bourgeon B High dose enalapril impairs the response to erythropoietin treatment in haemodialysis patients.Nephrol Dial Transplant. 1998; 13: 1206-1210Google Scholar, 8Erturk S Nergizoglu G Ates K Duman N Erbay B Karatan O Ertug AE The impact of withdrawing ACE inhibitors on erythropoietin responsiveness and left ventricular hypertrophy in haemodialysis patients.Nephrol Dial Transplant. 1999; 14: 1912-1916Google Scholar, 9Conlon PJ Albers F Butterly D Schwab SJ ACE inhibitors do not affect erythropoietin efficacy in haemodialysis patients.Nephrol Dial Transplant. 1994; 9 (letter): 1358Google Scholar, 10Sánchez JA ACE inhibitors do not decrease rHuEpo response in patients with end-stage renal failure.Nephrol Dial Transplant. 1995; 10 (letter): 1476-1477Google Scholar, 11Cruz DN Perazella MA Abu-Alfa AK Mahnensmith RL Angiotensin-converting enzyme inhibitor therapy in chronic hemodialysis patients: Any evidence of erythropoietin resistance?.Am J Kidney Dis. 1996; 28: 535-540Google Scholar, 12Chew CG Weise MD Disney APS The effect of angiotensin II receptor antagonist on the exogenous erythropoietin requirement of haemodialysis patients.Nephrol Dial Transplant. 1999; 14 (letter): 2047-2049Google Scholar Some of these are small and uncontrolled studies, and many are retrospective. Albitar et al,7Albitar S Genin R Fen-Chong M Serveaux M-O Bourgeon B High dose enalapril impairs the response to erythropoietin treatment in haemodialysis patients.Nephrol Dial Transplant. 1998; 13: 1206-1210Google Scholar however, conducted a prospective nonrandomized controlled study of 60 patients with a follow-up period of 12 months. Twenty of the patients received enalapril (dose ranging from 5 to 20 mg/d) as antihypertensive therapy and 20 received nifedipine. There were 20 controls receiving no antihypertensive medication. The group of patients receiving enalapril required significantly higher doses of erythropoietin compared with the patients receiving nifedipine or no antihypertensive therapy. A further prospective study by Erturk et al8Erturk S Nergizoglu G Ates K Duman N Erbay B Karatan O Ertug AE The impact of withdrawing ACE inhibitors on erythropoietin responsiveness and left ventricular hypertrophy in haemodialysis patients.Nephrol Dial Transplant. 1999; 14: 1912-1916Google Scholar assessed the effects of stopping treatment with ACE inhibitors on the response to erythropoietin. Fifteen patients in whom ACE inhibitors were withdrawn showed an increase in hematocrit level and a decrease in erythropoietin dose requirements. Three retrospective studies over the last few years provided evidence that ACE inhibitors did not significantly affect the response to erythropoietin therapy.9Conlon PJ Albers F Butterly D Schwab SJ ACE inhibitors do not affect erythropoietin efficacy in haemodialysis patients.Nephrol Dial Transplant. 1994; 9 (letter): 1358Google Scholar, 10Sánchez JA ACE inhibitors do not decrease rHuEpo response in patients with end-stage renal failure.Nephrol Dial Transplant. 1995; 10 (letter): 1476-1477Google Scholar, 11Cruz DN Perazella MA Abu-Alfa AK Mahnensmith RL Angiotensin-converting enzyme inhibitor therapy in chronic hemodialysis patients: Any evidence of erythropoietin resistance?.Am J Kidney Dis. 1996; 28: 535-540Google Scholar Another interesting aspect of the AcSDKP story is that one would only expect levels of this peptide to be affected by ACE inhibitors and not by angiotensin II blockers. As with bradykinin levels, the latter group of drugs should not significantly affect the levels of AcSDKP. If this were really an important mechanism in affecting the response to erythropoietin, then one might expect to see differences between patients receiving ACE inhibitors and those receiving angiotensin II blockers. In contrast, if the effect were mainly mediated via angiotensin II, then both classes of drugs would be expected to show similar effects. What clinical evidence do we have, then, that angiotensin II blockers affect erythropoiesis or the response to erythropoietin therapy? There is good evidence that, like ACE inhibitors, the angiotensin II blockers can reduce hemoglobin levels in patients with transplant polycythemia.19Kupin W Venkat KK Goggins M Abouljoud M Escobar F Mozes M Benefit of angiotensin II receptor blockade in the treatment of posttransplant polycythemia in renal transplant recipients.Transplant Proc. 1997; 29: 207-208Google Scholar The mechanism for this effect, however, may not be mediated via AcSDKP, but rather via suppressing inappropriately higher levels of circulating erythropoietin. It is well known that the renin angiotensin system is intricately linked with the production of endogenous erythropoietin in the peritubular fibroblasts of the kidney. Activation of this system will enhance erythropoietin production,20Vlahakos DV Balodimos C Papachristopoulos V Vassilakos P Hinari E Vlachojannis JG Renin-angiotensin system stimulates erythropoietin secretion in chronic hemodialysis patients.Clin Nephrol. 1995; 43: 53-59Google Scholar which is thought to explain why some patients with renal artery stenosis become polycythemic. Similarly, suppression of angiotensin II production may inhibit erythropoietin synthesis, reducing circulating levels of the hormone and thereby causing a decrease in hemoglobin.19Kupin W Venkat KK Goggins M Abouljoud M Escobar F Mozes M Benefit of angiotensin II receptor blockade in the treatment of posttransplant polycythemia in renal transplant recipients.Transplant Proc. 1997; 29: 207-208Google Scholar Because this effect is mediated by angiotensin II, one would expect both ACE inhibitors and angiotensin II blockers to be effective in transplant polycythemia. The situation in patients on erythropoietin therapy may be very different, however. Suppressing endogenous erythropoietin production is irrelevant here, given the high doses of exogenous erythropoietin administered, and if the data reported in this issue of the Journal by Le Meur et al17Le Meur Y Lorgeot V Comte L Szelag J-C Aldigier J-C Leroux-Robert C Praloran V Plasma levels and metabolism of AcSDKP in patients with chronic renal failure: Relationship with erythropoietin requirements.Am J Kidney Dis. 2001; 38: 510-517Abstract Full Text Full Text PDF Scopus (66) Google Scholar are clinically relevant, then one should see a different effect between the 2 classes of drugs in affecting responsiveness to erythropoietin. There is indeed some supporting clinical evidence for this. There are much more limited data on the effect of angiotensin II blockers on erythropoietin responsiveness than there are for ACE inhibitors. Chew et al,12Chew CG Weise MD Disney APS The effect of angiotensin II receptor antagonist on the exogenous erythropoietin requirement of haemodialysis patients.Nephrol Dial Transplant. 1999; 14 (letter): 2047-2049Google Scholar however, conducted a prospective double-blind, placebo-controlled, crossover study examining the effect of losartan on the action of erythropoietin in 14 patients. At a dose of 25 mg/d, there was no difference between the group of patients receiving the angiotensin II blocker and the placebo group. Part of the explanation for this, however, could be the low doses of angiotensin II blocker used in the study. Schiffl and Lang21Schiffl H Lang SM Angiotensin-converting enzyme inhibitors but not angiotensin II AT 1 receptor antagonists affect erythropoiesis in patients with anemia of end-stage renal disease.Nephron. 1999; 81 (letter): 106-108Google Scholar compared the effects of captopril and losartan in 2 groups of 12 dialysis patients using a prospective randomized study design. The group of patients treated with captopril required higher doses of erythropoietin to maintain the same target hematocrit level, compared with the group receiving losartan (mean erythropoietin dose, 2,413 ± 157 v 1,685 ± 212). It is tempting to speculate that the reason for this difference is that captopril increased AcSDKP levels, causing some resistance to erythropoietin, whereas losartan had no effect on this. In summary, therefore, the paper by Le Meur et al17Le Meur Y Lorgeot V Comte L Szelag J-C Aldigier J-C Leroux-Robert C Praloran V Plasma levels and metabolism of AcSDKP in patients with chronic renal failure: Relationship with erythropoietin requirements.Am J Kidney Dis. 2001; 38: 510-517Abstract Full Text Full Text PDF Scopus (66) Google Scholar has not only provided interesting data to suggest why some patients receiving ACE inhibitors might be less responsive to erythropoietin, but it also provides a putative mechanism whereby ACE inhibitors but not angiotensin II blockers could cause this effect. Further supportive clinical evidence is required to confirm or refute this hypothesis. In the meantime, if one is faced with a patient who seems somewhat resistant to erythropoietin on an ACE inhibitor but in whom it is difficult to stop treatment with the drug, then it might be reasonable to try switching them to an angiotensin II blocker in the hope that it might have less effect on erythropoiesis. Plasma levels and metabolism of AcSDKP in patients with chronic renal failure: Relationship with erythropoietin requirementsAmerican Journal of Kidney DiseasesVol. 38Issue 3PreviewN-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) is a physiological inhibitor of hematopoiesis that is maintained at stable levels in normal plasma. Its degradation in vivo and in vitro by angiotensin-converting enzyme (ACE) accounts for the high plasma concentrations of AcSDKP in patients treated with ACE inhibitors. Because ACE inhibitors can induce anemia in some patients, we measured plasma AcSDKP concentrations in 176 patients with chronic renal failure: 120 hemodialysis (HD) and 56 nondialysis (nD) patients, 39 of whom were administered ACE inhibitors. Full-Text PDF" @default.
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