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Verminderung der Progression einer chronischen Niereninsuffizienz

Strategien

Reduction the progression of chronic kidney disease

Strategies

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Zusammenfassung

Chronische Nierenerkrankungen (CKD) sind ein weltweit zunehmendes Problem, so dass diese auch eine rasch zunehmende Bedeutung als Mortalitätsursache erlangen. Wesentlich für die Progressionsverlangsamung einer CKD ist die optimale Einstellung des Blutdrucks wobei die Zielblutdruckwerte bei Patienten mit CKD keine klare Evidenz für die jeweiligen Zielwerte besteht. Diese hängen zudem auch von der Grundkrankheit, wie z. B. einer ADPKD, ab. Ein wesentlicher Mechanismus zur Kontrolle des arteriellen Blutdrucks beseht in der Blockade des Renin-Angiotensin-Aldosteronsystems (RAAS) mittels ACE-Inhibitoren (ACEI) bzw. Angiotensinrezeptorblockern (ARB). Aufgrund der zusätzlichen blutdruckunabhängigen Reduktion von Proliferations- und Entzündungsprozessen sind diese Substanzen sehr gut für eine Progressionsverminderung einer CKD geeignet. Des weiteren sollte eine Dyslipidämie bei Patienten mit einer CKD behandelt werden, wobei die Effekte im Hinblick auf eine Reduktion des kardiovaskulären Risikos bei Patienten mit CKD geringer sind als in der Allgemeinbevölkerung. Die Behandlung sollte mit Statinen erfolgen; zu den Wirkungen der neuen PCSK 9 Inhibitoren fehlen bisher Daten zu Patienten mit CKD. Bei Patienten mit Diabetes mellitus und CKD sollte der Blutzucker sollte so behandelt werden, dass das HbA1c unter 7 % liegt. Metformin kann dabei bei Patienten mit einer mäßigen GFR-Einschränkung gegeben werden. Allerdings sollte die Nierenfunktion kontrolliert werden und bei einer weiteren Verschlechterung das Medikament abgesetzt/pausiert werden. Auch Faktoren des sog. Lifestyles, darunter vor allem die Ernährung, sind von wesentlicher Bedeutung für die Progression einer CKD. In diesem Zusammenhang sollte vor allem die Natriumzufuhr, die Harnsäureproduktion und der Säure-Basenhaushalt behandelt werden. Insgesamt kann auf diese Weise die Progression einer CKD vermindert werden, wobei zukünftige Studien helfen müssen, Zielwerte besser zu definieren und neue Therapeutika vor allem bei Patienten mit CKD zu untersuchen.

Abstract

Chronic kidney diseases (CKD) are a worldwide increasing problem that is also reflected by the fact that CKD is an increasing reason for overall mortality. Blood pressure control is a key factor to delay the progression of CKD. However, little evidence exists for the correct target levels in patients with CKD. Such targets depend also from the underlying disease, i.e. ADPKD. A central mechanism to control the blood pressure in CKD patients is blockade of the renin angiotensin aldosterone (RAAS) system by ACEI or ARB. Due to their additional effects regarding the reduction of proliferation and inflammation independent of their blood pressure lowering effects, these compounds are well suitable for delaying the progression of CKD. Furthermore, a dyslipidemia should be treated in patients with CKD, although such effects in reducing cardiovascular risk are lower in CKD patients as compared to the general population. The treatment should be started with statins. Regarding the effects of the new PCSK 9 inhibitors data in patients with CKD are not yet available. Blood glucose should be managed in order to reach HbA1c levels below 7 %. Metformin can be administered in patients with a moderate CKD. However the renal function should be monitored and in case of further declining renal function metformin should be stopped or paused. Life style factors, among them particularly the diet, are of special importance for the progression of CKD. Here, especially the sodium intake, the production of uric acid as well as the control of the acid base metabolism. Altogether the progression of CKD can be delayed by a control of these factors, while it is necessary to better define target values as well as to analyze new therapeutics particularly in patients with CKD.

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Literatur

  1. Evenepoel, P. (2016) Darm-Nieren-Achse. Einfluss der Darmmikrobiota auf die Progression einer chronischen Nierenerkrankung. Nephrologe doi:10.1007/s11560-016-0067-0

  2. Leehey DJ, Zhang JH, Emanuele NV, Whaley-Connell A, Palevsky PM, Reilly RF, Guarino P, Fried LF, Group VN-DS (2015) BP and renal outcomes in diabetic kidney disease: the veterans affairs Nephropathy in diabetes trial. Clin J Am Soc Nephrol 10:2159–2169

    Article  PubMed  Google Scholar 

  3. Group SR, Wright JT Jr., Williamson JD, Whelton PK, Snyder JK, Sink KM, Rocco MV, Reboussin DM, Rahman M, Oparil S et al (2015) A randomized trial of intensive versus standard blood-pressure control. N Engl J Med 373:2103–2116

    Article  Google Scholar 

  4. Haller H, Ito S, Izzo JL Jr, Januszewicz A, Katayama S, Menne J, Mimran A, Rabelink TJ, Ritz E, Ruilope LM et al (2011) Olmesartan for the delay or prevention of microalbuminuria in type 2 diabetes. N Engl J Med 364:907–917

    Article  CAS  PubMed  Google Scholar 

  5. Ruggenenti P, Fassi A, Ilieva AP, Bruno S, Iliev IP, Brusegan V, Rubis N, Gherardi G, Arnoldi F, Ganeva M et al (2004) Preventing microalbuminuria in type 2 diabetes. N Engl J Med 351:1941–1951

    Article  CAS  PubMed  Google Scholar 

  6. Lv J, Perkovic V, Foote CV, Craig ME, Craig JC, Strippoli GF (2012) Antihypertensive agents for preventing diabetic kidney disease. Cochrane Database Syst Rev 12:CD004136

    PubMed  Google Scholar 

  7. Investigators O, Yusuf S, Teo KK, Pogue J, Dyal L, Copland I, Schumacher H, Dagenais G, Sleight P, Anderson C (2008) Telmisartan, ramipril, or both in patients at high risk for vascular events. N Engl J Med 358:1547–1559

    Article  Google Scholar 

  8. Tylicki L, Jakubowska A, Lizakowski S, Swietlik D, Rutkowski B (2015) Management of renin-angiotensin system blockade in patients with chronic kidney disease under specialist care. Retrospective cross-sectional study. J Renin Angiotensin Aldosterone Syst 16:145–152

    Article  CAS  PubMed  Google Scholar 

  9. Susantitaphong P, Sewaralthahab K, Balk EM, Eiam-ong S, Madias NE, Jaber BL (2013) Efficacy and safety of combined vs. single renin-angiotensin-aldosterone system blockade in chronic kidney disease: a meta-analysis. Am J Hypertens 26:424–441

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Heerspink HJ, Persson F, Brenner BM, Chaturvedi N, Brunel P, McMurray JJ, Desai AS, Solomon SD, Pfeffer MA, Parving HH et al (2016) Renal outcomes with aliskiren in patients with type 2 diabetes: a prespecified secondary analysis of the ALTITUDE randomised controlled trial. Lancet Diabetes Endocrinol Apr;4(4):309–317

  11. Parving HH, Brenner BM, McMurray JJ, Zeeuw D de, Haffner SM, Solomon SD, Chaturvedi N, Persson F, Desai AS, Nicolaides M et al (2012) Cardiorenal end points in a trial of aliskiren for type 2 diabetes. N Engl J Med 367:2204–2213

    Article  CAS  PubMed  Google Scholar 

  12. Remuzzi A, Gagliardini E, Sangalli F, Bonomelli M, Piccinelli M, Benigni A, Remuzzi G (2006) ACE inhibition reduces glomerulosclerosis and regenerates glomerular tissue in a model of progressive renal disease. Kidney Int 69:1124–1130

    Article  CAS  PubMed  Google Scholar 

  13. Remuzzi A, Sangalli F, Macconi D, Tomasoni S, Cattaneo I, Rizzo P, Bonandrini B, Bresciani E, Longaretti L, Gagliardini E et al (2015) Regression of renal disease by Angiotensin II antagonism is caused by regeneration of kidney Vasculature. J Am Soc Nephrol 27:699–705

    Article  PubMed  Google Scholar 

  14. Abe M, Okada K, Soma M (2013) T‑type Ca channel blockers in patients with chronic kidney disease in clinical practice. Curr Hypertens Rev 9:202–209

    Article  CAS  PubMed  Google Scholar 

  15. Bianchi S, Bigazzi R, Campese VM (2006) Long-term effects of spironolactone on proteinuria and kidney function in patients with chronic kidney disease. Kidney Int 70:2116–2123

    Article  CAS  PubMed  Google Scholar 

  16. Attman PO, Samuelsson OG, Moberly J, Johansson AC, Ljungman S, Weiss LG, Knight-Gibson C, Alaupovic P (1999) Apolipoprotein B‑containing lipoproteins in renal failure: the relation to mode of dialysis. Kidney Int 55:1536–1542

    Article  CAS  PubMed  Google Scholar 

  17. Samuelsson O, Attman PO, Knight-Gibson C, Larsson R, Mulec H, Weiss L, Alaupovic P (1998) Complex apolipoprotein B‑containing lipoprotein particles are associated with a higher rate of progression of human chronic renal insufficiency. J Am Soc Nephrol 9:1482–1488

    CAS  PubMed  Google Scholar 

  18. Goeij MC de, Rotmans JI, Matthijssen X, Jager DJ de, Dekker FW, Halbesma N, Group P‑S (2015) Lipid levels and renal function decline in pre-dialysis patients. Nephron Extra 5:19–29

    Article  PubMed  PubMed Central  Google Scholar 

  19. Fried LF, Orchard TJ, Kasiske BL (2001) Effect of lipid reduction on the progression of renal disease: a meta-analysis. Kidney Int 59:260–269

    Article  CAS  PubMed  Google Scholar 

  20. Baigent C, Landray MJ, Reith C, Emberson J, Wheeler DC, Tomson C, Wanner C, Krane V, Cass A, Craig J et al (2011) The effects of lowering LDL cholesterol with simvastatin plus ezetimibe in patients with chronic kidney disease (Study of Heart and Renal Protection): a randomised placebo-controlled trial. Lancet 377:2181–2192

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Rahman M, Baimbridge C, Davis BR, Barzilay J, Basile JN, Henriquez MA, Huml A, Kopyt N, Louis GT, Pressel SL et al (2008) Progression of kidney disease in moderately hypercholesterolemic, hypertensive patients randomized to pravastatin versus usual care: a report from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). Am J Kidney Dis 52:412–424

    Article  PubMed  PubMed Central  Google Scholar 

  22. Fellstrom B, Holdaas H, Jardine AG, Holme I, Nyberg G, Fauchald P, Gronhagen-Riska C, Madsen S, Neumayer HH, Cole E et al (2004) Effect of fluvastatin on renal end points in the Assessment of Lescol in Renal Transplant (ALERT) trial. Kidney Int 66:1549–1555

    Article  PubMed  Google Scholar 

  23. Huskey J, Lindenfeld J, Cook T, Targher G, Kendrick J, Kjekshus J, Pedersen T, Chonchol M (2009) Effect of simvastatin on kidney function loss in patients with coronary heart disease: findings from the Scandinavian Simvastatin Survival Study (4S). Atherosclerosis 205:202–206

    Article  CAS  PubMed  Google Scholar 

  24. Zhang Z, Wu P, Zhang J, Wang S, Zhang G (2016) The effect of statins on microalbuminuria, proteinuria, progression of kidney function, and all-cause mortality in patients with non-end stage chronic kidney disease: A meta-analysis. Pharmacol Res 105:74–83

    Article  CAS  PubMed  Google Scholar 

  25. Jun M, Zhu B, Tonelli M, Jardine MJ, Patel A, Neal B, Liyanage T, Keech A, Cass A, Perkovic V (2012) Effects of fibrates in kidney disease: a systematic review and meta-analysis. J Am Coll Cardiol 60:2061–2071

    Article  CAS  PubMed  Google Scholar 

  26. Tonelli M, Collins D, Robins S, Bloomfield H, Curhan GC, Veterans’ Affairs High-Density Lipoprotein Intervention Trial, I. (2004) Gemfibrozil for secondary prevention of cardiovascular events in mild to moderate chronic renal insufficiency. Kidney Int 66:1123–1130

    Article  CAS  PubMed  Google Scholar 

  27. Morita T, Morimoto S, Nakano C, Kubo R, Okuno Y, Seo M, Someya K, Nakahigashi M, Ueda H, Toyoda N et al (2014) Renal and vascular protective effects of ezetimibe in chronic kidney disease. Intern Med 53:307–314

    Article  PubMed  Google Scholar 

  28. Cho KH, Kim HJ, Kamanna VS, Vaziri ND (2010) Niacin improves renal lipid metabolism and slows progression in chronic kidney disease. Biochim Biophys Acta 1800:6–15

    Article  CAS  PubMed  Google Scholar 

  29. Jin Kang H, Kim do K, Mi Lee S, Han Kim K, Hee Han S, Hyun Kim K, Eun Kim S, Ki Son Y, An WS (2013) Effects of low-dose niacin on dyslipidemia and serum phosphorus in patients with chronic kidney disease. Kidney Res Clin Pract 32:21–26

    Article  PubMed  Google Scholar 

  30. Wang PH, Lau J, Chalmers TC (1993) Meta-analysis of effects of intensive blood-glucose control on late complications of type I diabetes. Lancet 341:1306–1309

    Article  CAS  PubMed  Google Scholar 

  31. Shichiri M, Kishikawa H, Ohkubo Y, Wake N (2000) Long-term results of the Kumamoto Study on optimal diabetes control in type 2 diabetic patients. Diabetes Care 23(Suppl 2):B21–29

    PubMed  Google Scholar 

  32. UK Prospective Diabetes Study (UKPDS) Group (1998) Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet 352:854–865.

  33. UK Prospective Diabetes Study (UKPDS) Group (1998) Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 352:837–853.

  34. Group AC, Patel A, MacMahon S, Chalmers J, Neal B, Billot L, Woodward M, Marre M, Cooper M, Glasziou P et al (2008) Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes. N Engl J Med 358:2560–2572

    Article  Google Scholar 

  35. Zinman B, Wanner C, Lachin JM, Fitchett D, Bluhmki E, Hantel S, Mattheus M, Devins T, Johansen OE, Woerle HJ et al (2015) Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. N Engl J Med 373:2117–2128

    Article  CAS  PubMed  Google Scholar 

  36. Vegter S, Perna A, Postma MJ, Navis G, Remuzzi G, Ruggenenti P (2012) Sodium intake, ACE inhibition, and progression to ESRD. J Am Soc Nephrol 23:165–173

    Article  CAS  PubMed  Google Scholar 

  37. He J, Mills KT, Appel LJ, Yang W, Chen J, Lee BT, Rosas SE, Porter A, Makos G, Weir MR et al (2015) Urinary sodium and potassium excretion and CKD progression. J Am Soc Nephrol 27(4):1202–1212

    Article  PubMed  Google Scholar 

  38. Talbott JH, Terplan KL (1960) The kidney in gout. Medicine (Baltimore) 39:405–467

    Article  CAS  Google Scholar 

  39. Kanji T, Gandhi M, Clase CM, Yang R (2015) Urate lowering therapy to improve renal outcomes in patients with chronic kidney disease: systematic review and meta-analysis. BMC Nephrol 16:58

    Article  PubMed  PubMed Central  Google Scholar 

  40. Sircar D, Chatterjee S, Waikhom R, Golay V, Raychaudhury A, Chatterjee S, Pandey R (2015) Efficacy of Febuxostat for slowing the GFR decline in patients with CKD and asymptomatic Hyperuricemia: A 6‑month, double-blind, randomized, placebo-controlled trial. Am J Kidney Dis 66:945–950

    Article  CAS  PubMed  Google Scholar 

  41. Phisitkul S, Khanna A, Simoni J, Broglio K, Sheather S, Rajab MH, Wesson DE (2010) Amelioration of metabolic acidosis in patients with low GFR reduced kidney endothelin production and kidney injury, and better preserved GFR. Kidney Int 77:617–623

    Article  CAS  PubMed  Google Scholar 

  42. acks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E, Conlin PR, Miller ER 3rd, Simons-Morton DG (2001) Effects on blood pressure of reduced dietary sodium and the dietary approaches to stop hypertension (DASH) diet. DASH-sodium collaborative research group. N Engl J Med 344:3–10

    Article  Google Scholar 

  43. Goraya N, Simoni J, Jo C, Wesson DE (2012) Dietary acid reduction with fruits and vegetables or bicarbonate attenuates kidney injury in patients with a moderately reduced glomerular filtration rate due to hypertensive nephropathy. Kidney Int 81:86–93

    Article  CAS  PubMed  Google Scholar 

  44. Goraya N, Simoni J, Jo CH, Wesson DE (2014) Treatment of metabolic acidosis in patients with stage 3 chronic kidney disease with fruits and vegetables or oral bicarbonate reduces urine angiotensinogen and preserves glomerular filtration rate. Kidney Int 86:1031–1038

    Article  CAS  PubMed  Google Scholar 

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Sollinger, D., Schamberger, B., Weinmann-Menke, J. et al. Verminderung der Progression einer chronischen Niereninsuffizienz. Nephrologe 11, 260–267 (2016). https://doi.org/10.1007/s11560-016-0076-z

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  • DOI: https://doi.org/10.1007/s11560-016-0076-z

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