Haemodynamic consequences of changing potassium concentrations in haemodialysis fluids

Luca Gabutti, Igor Salvadé, Barbara Lucchini, Davide Soldini, Michel Burnier, Luca Gabutti, Igor Salvadé, Barbara Lucchini, Davide Soldini, Michel Burnier

Abstract

Background: A rapid decrease of serum potassium concentrations during haemodialysis produces a significant increase in blood pressure parameters at the end of the session, even if effects on intra-dialysis pressure are not seen. Paradoxically, in animal models potassium is a vasodilator and decreases myocardial contractility. The purpose of this trial is to study the precise haemodynamic consequences induced by acute changes in potassium concentration during haemodialysis.

Methods: In 24 patients, 288 dialysis sessions, using a randomised single blind crossover design, we compared six dialysate sequences with different potassium profiles. The dialysis sessions were divided into 3 tertiles, casually modulating potassium concentration in the dialysate between the value normally used K and the two cut-off points K+1 and K-1 mmol/l. Haemodynamics were evaluated in a non-invasive manner using a finger beat-to-beat monitor.

Results: Comparing K-1 and K+1, differences were found within the tertiles regarding systolic (+5.3, +6.6, +2.3 mmHg, p < 0.05, < 0.05, ns) and mean blood pressure (+4.3, +6.4, -0.5 mmHg, p < 0.01, < 0.01, ns), as well as peripheral resistance (+212, +253, -4 dyne.sec.cm-5, p < 0.05, < 0.05, ns). The stroke volume showed a non-statistically-significant inverse trend (-3.1, -5.2, -0.2 ml). 18 hypotension episodes were recorded during the course of the study. 72% with K-1, 11% with K and 17% with K+1 (p < 0.01 for comparison K-1 vs. K and K-1 vs. K+1).

Conclusions: A rapid decrease in the concentration of serum potassium during the initial stage of the dialysis-obtained by reducing the concentration of potassium in the dialysate-translated into a decrease of systolic and mean blood pressure mediated by a decrease in peripheral resistance. The risk of intra-dialysis hypotension inversely correlates to the potassium concentration in the dialysate.

Trial registration number: NCT01224314.

Figures

Figure 1
Figure 1
Systolic blood pressure. Systolic blood pressure as a function of the dialysis tertiles in the 6 dialysate sequences (1 to 6).
Figure 2
Figure 2
Mean blood pressure. Mean blood pressure as a function of the dialysis tertiles in the 6 dialysate sequences (1 to 6).
Figure 3
Figure 3
Peripheral resistance. Total peripheral resistance as a function of the dialysis tertiles in the 6 dialysate sequences (1 to 6).
Figure 4
Figure 4
Stroke volume. Stroke volume as a function of the dialysis tertiles in the 6 dialysate sequences (1 to 6).
Figure 5
Figure 5
Systolic blood pressure. Systolic blood pressure as a function of dialysis tertiles comparing treatments with the two potassium (K) concentration cut-off points in the dialysate (high = K+1 and low = K-1). P for the 1st, 2nd and 3rd tertiles: < 0.05, < 0.05 and ns respectively.
Figure 6
Figure 6
Mean blood pressure. Mean blood pressure as a function of dialysis tertiles comparing treatments with the two potassium (K) concentration cut-off points in the dialysate (high = K+1 and low = K-1). P for the 1st, 2nd and 3rd tertiles: < 0.01, < 0.01 and ns respectively.
Figure 7
Figure 7
Total peripheral resistance. Total peripheral resistance as a function of dialysis tertiles comparing treatments with the two potassium (K) concentration cut-off points in the dialysate (high = K+1 and low = K-1). P for the 1st, 2nd and 3rd tertiles: < 0.05, < 0.05 and ns respectively.
Figure 8
Figure 8
Stroke volume. Stroke volume as a function of dialysis tertiles comparing treatments with the two potassium (K) concentration cut-off points in the dialysate (high = K+1 and low = K-1). P for the 1st, 2nd and 3rd tertiles: ns.
Figure 9
Figure 9
Incidence of hypotension episodes. Incidence of hypotension episodes as a function of the dialysate potassium (K) concentration. P for the differences between both K-1 and K and K-1 and K+1 < 0.01; n = 18.

References

    1. Rastegar A, Soleimani M. Hypokalaemia and hyperkalaemia. Postgrad Med J. 2001;77:759–764. doi: 10.1136/pmj.77.914.759. PMID: 11723313.
    1. Bia MJ, DeFrontzo RA. Extrarenal potassium homeostasis. Am J Physiol. 1981;240:257–268. PMID: 6111930.
    1. Fernandez J, Oster JR, Perez GO. Impaired extrarenal disposal of an acute oral potassium load in patients with end-stage renal disease on chronic hemodialysis. Miner Electrolyte Metab. 1986;12:125–129. PMID: 3960016.
    1. Perez GO, Pelleya R, Oster JR, Kem DC, Vaamonde CA. Blunted kaliuresis after an acute potassium load in patients with chronic renal failure. Kidney Int. 1983;24:656–662. doi: 10.1038/ki.1983.208. PMID: 6663988.
    1. Musso CG. Potassium metabolism in patients with chronic kidney disease. Part II: patients on dialysis (stage 5) Int Urol Nephrol. 2004;36:469–472. doi: 10.1007/s11255-004-6194-y. PMID: 15783126.
    1. Dolson GM, Ellis KJ, Bernardo MV, Prakash R, Adrogué HJ. Acute decreases in serum potassium augment blood pressure. Am J Kidney Dis. 1995;26:321–326. doi: 10.1016/0272-6386(95)90652-5. PMID: 7645536.
    1. Locatelli F, Covic A, Chazot C, Leunissen K, Luño J, Yaqoob M. Optimal composition of the dialysate, with emphasis on its influence on blood pressure. Nephrol Dial Transplant. 2004;19:785–796. doi: 10.1093/ndt/gfh102. PMID: 15031331.
    1. Morris RC Jr, Sebastian A, Forman A, Tanaka M, Schmidlin O. Normotensive salt sensitivity: effects of race and dietary potassium. Hypertension. 1999;33:18–23. PMID: 9931076.
    1. Stamler J, Rose G, Elliott P, Dyer A, Marmot M, Kesteloot H, Stamler R. Findings of the International Cooperative INTERSALT Study. Hypertension. 1991;17:I9–15. PMID: 1987018.
    1. Whelton PK, He J, Cutler JA. et al.Effects of oral potassium on blood pressure: meta-analysis of randomized controlled clinical trials. JAMA. 1997;277:1624–1632. doi: 10.1001/jama.277.20.1624. PMID: 9168293.
    1. Amberg GC, Bonev AD, Rossow CF, Nelson MT, Santana LF. Modulation of the molecular composition of large conductance, Ca2+ activated K+ channels in vascular smooth muscle during hypertension. J Clin Invest. 2003;112:717–724. PMID: 12952920.
    1. Haddy FJ, Vanhoutte PM, Feletou M. Role of potassium in regulating blood flow and blood pressure. Am J Physiol Regul Integr Comp Physiol. 2006;290:546–552. doi: 10.1152/ajpregu.00491.2005. PMID: 16467502.
    1. Prasad K, Koob R. Cardiovascular function in dogs with acute hypokalemia. Angiology. 1978;29:589–600. doi: 10.1177/000331977802900803. PMID: 686495.
    1. Rodrigo F, Shideman J, McHugh R, Buselmeier T, Kjellstrand C. Osmolality changes during hemodialysis. Natural history, clinical correlations, and influence of dialysate glucose and intravenous mannitol. Ann Intern Med. 1977;86:554–561. PMID: 851303.
    1. Van der Sande FM, Kooman JP, Leunissen KM. Intradialytic hypotension--new concepts on an old problem. Nephrol Dial Transplant. 2000;15:1746–1748. doi: 10.1093/ndt/15.11.1746. PMID: 11071958.
    1. Gabutti L, Bianchi G, Soldini D, Marone C, Burnier M. Haemodynamic consequences of changing bicarbonate and calcium concentrations in haemodialysis fluids. Nephrol Dial Transplant. 2009;24:973–981. doi: 10.1093/ndt/gfn541. PMID: 18842671.
    1. Gabutti L, Ferrari N, Giudici G, Mombelli G, Marone C. Unexpected haemodynamic instability associated with standard bicarbonate haemodialysis. Nephrol Dial Transplant. 2003;18:2369–2376. doi: 10.1093/ndt/gfg383. PMID: 14551368.
    1. Sułowicz W, Radziszewski A. Dialysis induced hypotension--a serious clinical problem in renal replacement therapy. Med Pregl. 2007;60:14–20. PMID: 18928150.
    1. Leunissen KM, Kooman JP, van Kuijk W, van der Sande F, Luik AJ, van Hooff JP. Preventing haemodynamic instability in patients at risk for intra-dialytic hypotension. Nephrol Dial Transplant. 1996;11:11–15. PMID: 8803987.
    1. Kyriazis J, Kalogeropoulou K, Bilirakis L, Smirnioudis N, Pikounis V, Stamatiadis D, Liolia E. Dialysate magnesium level and bood pressure. Kidney Int. 2004;66:1221–1231. doi: 10.1111/j.1523-1755.2004.00875.x. PMID:15327421.
    1. Selby NM, McIntyre CW. A systematic review of the clinical effects of reducing dialysate fluid temperature. Nephrol Dial Transplant. 2006;21:1883–1898. doi: 10.1093/ndt/gfl126. PMID: 16601075.
    1. Van Kuijk WH, Wirtz JJ, Grave W, de Heer F, Menheere PP, van Hooff JP, Leunissen KM. Vascular reactivity during combined ultrafiltration-haemodialysis: influence of dialysate sodium. Nephrol Dial Transplant. 1996;11:323–328. PMID: 8671787.
    1. Kim MJ, Song J, Kim G, Lim H, Lee S. Optimization of dialysate sodium in sodium profiling haemodialysis. Nephrology (Carlton) 2003;8:S16–22. doi: 10.1046/j.1440-1797.8.s.2.x. PMID: 15012686.
    1. Stefanidis I, Stiller S, Ikonomov V, Mann H. Sodium and body fluid homeostasis in profiling hemodialysis treatment. Int J Artif Organs. 2002;25:421–428. PMID: 12074340.
    1. Stiller S, Bonnie-Schorn E, Grassmann A, Uhlenbusch-Körwer I, Mann H. A critical review of sodium profiling for hemodialysis. Semin Dial. 2001;14:337–347. doi: 10.1046/j.1525-139X.2001.00086.x. PMID: 11679103.
    1. shapiro JI, Banerjee A, Reiss OK, Elkins N. Acute and chronic hypokalemia sensitize the isolated heart to hypoxic injury. Am J Physiol. 1998;274:1598–1604. PMID:9612369.
    1. Knoll GA, Sahgal A, Nair RC, Graham J, Van Walraven C, Burns KD. Renin-angiotensin system blockade and the risk of hyperkalemia in chronic hemodialysis patients. Am J Med. 2002;112:110–114. doi: 10.1016/S0002-9343(01)01068-3. PMID:11835948.
    1. Furuya R, Kumagai H, Sakao T, Maruyama Y, Hishida A. Potassium-lowering effect of mineralocorticoid therapy in patients undergoing hemodialysis. Nephron. 2002;92:576–581. doi: 10.1159/000064116. PMID:12372940.

Source: PubMed

3
Předplatit