全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...
PLOS ONE  2013 

Hypokalemia, Its Contributing Factors and Renal Outcomes in Patients with Chronic Kidney Disease

DOI: 10.1371/journal.pone.0067140

Full-Text   Cite this paper   Add to My Lib

Abstract:

Background In the chronic kidney disease (CKD) population, the impact of serum potassium (sK) on renal outcomes has been controversial. Moreover, the reasons for the potential prognostic value of hypokalemia have not been elucidated. Design, Participants & Measurements 2500 participants with CKD stage 1–4 in the Integrated CKD care program Kaohsiung for delaying Dialysis (ICKD) prospective observational study were analyzed and followed up for 2.7 years. Generalized additive model was fitted to determine the cutpoints and the U-shape association between sK and end-stage renal disease (ESRD). sK was classified into five groups with the cutpoints of 3.5, 4, 4.5 and 5 mEq/L. Cox proportional hazard regression models predicting the outcomes were used. Results The mean age was 62.4 years, mean sK level was 4.2±0.5 mEq/L and average eGFR was 40.6 ml/min per 1.73 m2. Female vs male, diuretic use vs. non-use, hypertension, higher eGFR, bicarbonate, CRP and hemoglobin levels significantly correlated with hypokalemia. In patients with lower sK, nephrotic range proteinuria, and hypoalbuminemia were more prevalent but the use of RAS (renin-angiotensin system) inhibitors was less frequent. Hypokalemia was significantly associated with ESRD with hazard ratios (HRs) of 1.82 (95% CI, 1.03–3.22) in sK <3.5mEq/L and 1.67 (95% CI,1.19–2.35) in sK = 3.5–4 mEq/L, respectively, compared with sK = 4.5–5 mEq/L. Hyperkalemia defined as sK >5 mEq/L conferred 1.6-fold (95% CI,1.09–2.34) increased risk of ESRD compared with sK = 4.5–5 mEq/L. Hypokalemia was also associated with rapid decline of renal function defined as eGFR slope below 20% of the distribution range. Conclusion In conclusion, both hypokalemia and hyperkalemia are associated with increased risk of ESRD in CKD population. Hypokalemia is related to increased use of diuretics, decreased use of RAS blockade and malnutrition, all of which may impose additive deleterious effects on renal outcomes.

References

[1]  Giebisch G, Hebert SC, Wang WH (2003) New aspects of renal potassium transport. Pflugers Arch 446: 289–297.
[2]  Einhorn LM, Zhan M, Hsu VD, Walker LD, Moen MF, et al. (2009) The frequency of hyperkalemia and its significance in chronic kidney disease. Arch Intern Med 169: 1156–1162.
[3]  Moranne O, Froissart M, Rossert J, Gauci C, Boffa JJ, et al. (2009) Timing of onset of CKD-related metabolic complications. J Am Soc Nephrol 20: 164–171.
[4]  Korgaonkar S, Tilea A, Gillespie BW, Kiser M, Eisele G, et al. (2010) Serum potassium and outcomes in CKD: insights from the RRI-CKD cohort study. Clin J Am Soc Nephrol 5: 762–769.
[5]  Hayes J, Kalantar-Zadeh K, Lu JL, Turban S, Anderson JE, et al. (2011) Association of Hypo- and Hyperkalemia with Disease Progression and Mortality in Males with Chronic Kidney Disease: The Role of Race. Nephron Clin Pract 120: 8–16.
[6]  Torres VE, Young WF Jr, Offord KP, Hattery RR (1990) Association of hypokalemia, aldosteronism, and renal cysts. N Engl J Med 322: 345–351.
[7]  Menahem SA, Perry GJ, Dowling J, Thomson NM (1999) Hypokalaemia-induced acute renal failure. Nephrol Dial Transplant 14: 2216–2218.
[8]  Bowling CB, Pitt B, Ahmed MI, Aban IB, Sanders PW, et al. (2010) Hypokalemia and outcomes in patients with chronic heart failure and chronic kidney disease: findings from propensity-matched studies. Circ Heart Fail 3: 253–260.
[9]  Acker CG, Johnson JP, Palevsky PM, Greenberg A (1998) Hyperkalemia in hospitalized patients: causes, adequacy of treatment, and results of an attempt to improve physician compliance with published therapy guidelines. Arch Intern Med 158: 917–924.
[10]  Takaichi K, Takemoto F, Ubara Y, Mori Y (2007) Analysis of factors causing hyperkalemia. Intern Med 46: 823–829.
[11]  Maddirala S, Khan A, Vincent A, Lau K (2008) Effect of angiotensin converting enzyme inhibitors and angiotensin receptor blockers on serum potassium levels and renal function in ambulatory outpatients: risk factors analysis. Am J Med Sci 336: 330–335.
[12]  Sarafidis PA, Blacklock R, Wood E, Rumjon A, Simmonds S, et al. (2012) Prevalence and factors associated with hyperkalemia in predialysis patients followed in a low-clearance clinic. Clin J Am Soc Nephrol 7: 1234–1241.
[13]  Tannen RL (1985) Diuretic-induced hypokalemia. Kidney Int 28: 988–1000.
[14]  Greenberg A (2000) Diuretic complications. Am J Med Sci 319: 10–24.
[15]  Weiner ID, Wingo CS (1997) Hypokalemia–consequences, causes, and correction. J Am Soc Nephrol 8: 1179–1188.
[16]  Yee TW (2012) VGAM: Vector generalized linear and additive models. R package, version 0.9–0 (URL: http://CRAN.R-project.org/package=VGAM. Accessed 2013 April 27.).
[17]  Yee TW, Wild CJ (1996) Vector generalized additive models. J R Stat Soc Ser C 58: 481–493.
[18]  Ahmed A, Husain A, Love TE, Gambassi G, Dell'Italia LJ, et al. (2006) Heart failure, chronic diuretic use, and increase in mortality and hospitalization: an observational study using propensity score methods. Eur Heart J 27: 1431–1439.
[19]  Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T (2008) Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens 17: 470–476.
[20]  Reungjui S, Hu H, Mu W, Roncal CA, Croker BP, et al. (2007) Thiazide-induced subtle renal injury not observed in states of equivalent hypokalemia. Kidney Int 72: 1483–1492.
[21]  Strippoli GF, Bonifati C, Craig M, Navaneethan SD, Craig JC (2006) Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists for preventing the progression of diabetic kidney disease. Cochrane Database Syst Rev: CD006257.
[22]  Chiurchiu C, Remuzzi G, Ruggenenti P (2005) Angiotensin-converting enzyme inhibition and renal protection in nondiabetic patients: the data of the meta-analyses. J Am Soc Nephrol 16 Suppl 1S58–63.
[23]  Baudin B (2000) Angiotensin I-converting enzyme gene polymorphism and drug response. Clin Chem Lab Med 38: 853–856.
[24]  Parving HH, de Zeeuw D, Cooper ME, Remuzzi G, Liu N, et al. (2008) ACE gene polymorphism and losartan treatment in type 2 diabetic patients with nephropathy. J Am Soc Nephrol 19: 771–779.
[25]  Ruggenenti P, Bettinaglio P, Pinares F, Remuzzi G (2008) Angiotensin converting enzyme insertion/deletion polymorphism and renoprotection in diabetic and nondiabetic nephropathies. Clin J Am Soc Nephrol 3: 1511–1525.
[26]  Alderman MH, Piller LB, Ford CE, Probstfield JL, Oparil S, et al. (2012) Clinical significance of incident hypokalemia and hyperkalemia in treated hypertensive patients in the antihypertensive and lipid-lowering treatment to prevent heart attack trial. Hypertension 59: 926–933.
[27]  Foley RN, Parfrey PS, Harnett JD, Kent GM, Murray DC, et al. (1996) Hypoalbuminemia, cardiac morbidity, and mortality in end-stage renal disease. J Am Soc Nephrol 7: 728–736.
[28]  Taal MW, Brenner BM (2006) Predicting initiation and progression of chronic kidney disease: Developing renal risk scores. Kidney Int 70: 1694–1705.
[29]  Menon V, Greene T, Wang X, Pereira AA, Marcovina SM, et al. (2005) C-reactive protein and albumin as predictors of all-cause and cardiovascular mortality in chronic kidney disease. Kidney Int 68: 766–772.
[30]  Erlinger TP, Tarver-Carr ME, Powe NR, Appel LJ, Coresh J, et al. (2003) Leukocytosis, hypoalbuminemia, and the risk for chronic kidney disease in US adults. Am J Kidney Dis 42: 256–263.
[31]  Kovesdy CP, Regidor DL, Mehrotra R, Jing J, McAllister CJ, et al. (2007) Serum and dialysate potassium concentrations and survival in hemodialysis patients. Clin J Am Soc Nephrol 2: 999–1007.
[32]  Soriano S, Gonzalez L, Martin-Malo A, Rodriguez M, Aljama P (2007) C-reactive protein and low albumin are predictors of morbidity and cardiovascular events in chronic kidney disease (CKD) 3–5 patients. Clin Nephrol 67: 352–357.
[33]  Tolins JP, Hostetter MK, Hostetter TH (1987) Hypokalemic nephropathy in the rat. Role of ammonia in chronic tubular injury. J Clin Invest 79: 1447–1458.
[34]  Ray PE, Suga S, Liu XH, Huang X, Johnson RJ (2001) Chronic potassium depletion induces renal injury, salt sensitivity, and hypertension in young rats. Kidney Int 59: 1850–1858.
[35]  Suga SI, Phillips MI, Ray PE, Raleigh JA, Vio CP, et al. (2001) Hypokalemia induces renal injury and alterations in vasoactive mediators that favor salt sensitivity. Am J Physiol Renal Physiol 281: F620–629.
[36]  Adrogue HJ, Madias NE (2007) Sodium and potassium in the pathogenesis of hypertension. N Engl J Med 356: 1966–1978.
[37]  Suga S, Mazzali M, Ray PE, Kang DH, Johnson RJ (2002) Angiotensin II type 1 receptor blockade ameliorates tubulointerstitial injury induced by chronic potassium deficiency. Kidney Int 61: 951–958.
[38]  Wang W, Soltero L, Zhang P, Huang XR, Lan HY, et al. (2007) Renal inflammation is modulated by potassium in chronic kidney disease: possible role of Smad7. Am J Physiol Renal Physiol 293: F1123–1130.
[39]  Reungjui S, Roncal CA, Sato W, Glushakova OY, Croker BP, et al. (2008) Hypokalemic nephropathy is associated with impaired angiogenesis. J Am Soc Nephrol 19: 125–134.
[40]  Novello M, Catena C, Nadalini E, Colussi GL, Baroselli S, et al. (2007) Renal cysts and hypokalemia in primary aldosteronism: results of long-term follow-up after treatment. J Hypertens 25: 1443–1450.
[41]  Miao Y, Dobre D, Heerspink HJ, Brenner BM, Cooper ME, et al. (2011) Increased serum potassium affects renal outcomes: a post hoc analysis of the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial. Diabetologia 54: 44–50.
[42]  Struthers AD, MacDonald TM (2004) Review of aldosterone- and angiotensin II-induced target organ damage and prevention. Cardiovasc Res 61: 663–670.
[43]  Epstein M (2001) Aldosterone and the hypertensive kidney: its emerging role as a mediator of progressive renal dysfunction: a paradigm shift. J Hypertens 19: 829–842.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133