Yetişkinlerde Akut Böbrek Hasarı
Özet
Akut böbrek hasarı (ABH), glomerüler filtrasyon hızında (GFR) ani ve çoğunlukla düzelebilen bir düşüştür. Klinik durum böbrek- lerin sıvı elektrolit dengesini sağlayamaması sonucu böbrek tara- fından atılan serum kan üre nitrojeni (BUN: Blood urea nitrogen), kreatinin ve diğer metabolik atık ürünlerin kandaki değerlerinin yükelmesiyle karakterizedir. Yazımızda Acil Servislerde hastalara yaklaşımı içermektedir.
Referanslar
Khwaja, A., KDIGO clinical practice guidelines for acute kidney injury. Nephron Clinical Practice, 2012. 120(4): p. c179-c184.
Bellomo, R., et al., Acute renal failure–definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Critical care, 2004. 8(4): p. 1-9.
Levin, A., et al., Improving outcomes from acute kidney injury: report of an initiative. American Journal of Kidney Diseases, 2007. 50(1): p. 1-4.
Mehta, R.L., et al., Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Critical care, 2007. 11(2): p. 1-8.
Molitoris, B.A., et al., Improving outcomes of acute kidney injury: report of an initiative. Nature clinical practice Nephrology, 2007. 3(8): p. 439-442.
Kellum, J.A., et al., Kidney disease: improving global outcomes (KDIGO) acute kidney injury work group. KDIGO clinical practice guideline for acute kidney injury. Kidney international supplements, 2012. 2(1): p. 1-138.
Koyner, J.L., et al., Furosemide stress test and biomarkers for the prediction of AKI severity. Journal of the American Society of Nephrology, 2015. 26(8): p. 2023-2031.
Matsuura, R., et al., Response to different furosemide doses predicts AKI progression in ICU patients with elevated plasma NGAL levels. Annals of Intensive Care, 2018. 8(1): p. 1-10.
Pon, A.G., et al., Clinical significance of frusemide stress test in predicting the severity of acute kidney injury. Brazilian Journal of Nephrology, 2021. 43: p. 470-477.
van der Voort, P.H., E.C. Boerma, and P. Pickkers, The furosemide stress test to predict renal function after continuous renal replacement therapy. Critical Care, 2014. 18(3): p. 1-2.
Cooper, M.S. and N.J. Gittoes, Diagnosis and management of hypocalcaemia. Bmj, 2008. 336(7656): p. 1298-1302.
Schilling, T. and R. Ziegler, Current therapy of hypoparathyroidism—a survey of German endocrinology centers. Experimental and clinical endocrinology & diabetes, 1997. 105(04): p. 237-241.
Thakker, R.V., Hypocalcemia: Pathogenesis, differential diagnosis, and management. American Society for Bone and Mineral Research, 2006: p. 213-215.
Tohme, J.F. and J.P. Bilezikian, Diagnosis and treatment of hypocalcemic emergencies. The Endocrinologist, 1996. 6(1): p. 10-18.
Agus, Z. and M. Morad, Modulation of cardiac ion channels by magnesium. Annual review of physiology, 1991. 53(1): p. 299-307.
Krendel, D.A. Hypermagnesemia and neuromuscular transmission. in Seminars in neurology. 1990. © 1990 by Thieme Medical Publishers, Inc.
Neumar, R.W., et al., Part 8: adult advanced cardiovascular life support: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation, 2010. 122(18_suppl_3): p. S729-S767.
MORDES, J.P., R. SWARTZ, and R.A. ARKY, Extreme hypermagnesemia as a cause of refractory hypotension. Annals of Internal Medicine, 1975. 83(5): p. 657-658.
JOURNA, T.A. and O.C. NUTRITION, N THS M8SUE. Nutrition, 1993. 58.
Glaser, N., et al., Kuppermann Nthe Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med, 2001. 344: p. 264-269.
Kraut, J.A. and I. Kurtz, Use of base in the treatment of severe acidemic states. American Journal of Kidney Diseases, 2001. 38(4): p. 703-727.
Kraut, J.A. and N.E. Madias, Treatment of acute metabolic acidosis: a pathophysiologic approach. Nature Reviews Nephrology, 2012. 8(10): p. 589-601.
Marsh, J.D., T.I. Margolis, and D. Kim, Mechanism of diminished contractile response to catecholamines during acidosis. American Journal of Physiology-Heart and Circulatory Physiology, 1988. 254(1): p. H20-H27.
MATHIEU, D., et al., Effects of bicarbonate therapy on hemodynamics and tissue oxygenation in patients with lactic acidosis: a prospective, controlled clinical study. Critical care medicine, 1991. 19(11): p. 1352-1356.
Mitchell, J.H., K. Wildenthal, and R.L. Johnson Jr, The effects of acid-base disturbances on cardiovascular and pulmonary function. Kidney international, 1972. 1(5): p. 375-389.
Orchard, C. and J.C. Kentish, Effects of changes of pH on the contractile function of cardiac muscle. American Journal of Physiology-Cell Physiology, 1990. 258(6): p. C967-C981.
Orchard, C.H. and H.E. Cingolani, Acidosis and arrhythmias in cardiac muscle. Cardiovascular research, 1994. 28(9): p. 1312-1319.
Teplinsky, K., et al., Effect of lactic acidosis on canine hemodynamics and left ventricular function. American Journal of Physiology-Heart and Circulatory Physiology, 1990. 258(4): p. H1193-H1199.
Huber, L. and F.J. Gennari, Severe metabolic alkalosis in a hemodialysis patient. American journal of kidney diseases, 2011. 58(1): p. 144-149.
Lisawat, P. and F.J. Gennari, Approach to the hemodialysis patient with an abnormal serum bicarbonate concentration. American journal of kidney diseases, 2014. 64(1): p. 151-155.
Fiaccadori, E. and E. Cremaschi, Nutritional assessment and support in acute kidney injury. Current opinion in critical care, 2009. 15(6): p. 474-480.
Bellomo, R., et al., A prospective comparative study of moderate versus high protein intake for critically ill patients with acute renal failure. Renal failure, 1997. 19(1): p. 111-120.
Krishnan, J.A., et al., Caloric intake in medical ICU patients: consistency of care with guidelines and relationship to clinical outcomes. Chest, 2003. 124(1): p. 297-305.
Fouque, D., et al., A proposed nomenclature and diagnostic criteria for protein–energy wasting in acute and chronic kidney disease. Kidney international, 2008. 73(4): p. 391-398.
McClave, S.A., R.G. Martindale, and L. Kiraly, The use of indirect calorimetry in the intensive care unit. Current Opinion in Clinical Nutrition & Metabolic Care, 2013. 16(2): p. 202-208.
Fiaccadori, E., E. Parenti, and U. Maggiore, Nutritional support in acute kidney injury. JN journal of nephrology, 2008. 21(5): p. 645.
Li, Y., et al., Nutritional support for acute kidney injury. Cochrane Database of Systematic Reviews, 2010(1).
Benigni, A., et al., Reversible activation defect of the platelet glycoprotein IIb-IIIa complex in patients with uremia. American journal of kidney diseases, 1993. 22(5): p. 668-676.
Escolar, G., et al., Uremic platelets have a functional defect affecting the interaction of von Willebrand factor with glycoprotein Ilb-IIIa. Blood, 1990. 76(7): p. 1336-1340.
Gawaz, M.P., et al., Impaired function of platelet membrane glycoprotein IIb-IIIa in end-stage renal disease. Journal of the American Society of Nephrology, 1994. 5(1): p. 36-46.
Referanslar
Khwaja, A., KDIGO clinical practice guidelines for acute kidney injury. Nephron Clinical Practice, 2012. 120(4): p. c179-c184.
Bellomo, R., et al., Acute renal failure–definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Critical care, 2004. 8(4): p. 1-9.
Levin, A., et al., Improving outcomes from acute kidney injury: report of an initiative. American Journal of Kidney Diseases, 2007. 50(1): p. 1-4.
Mehta, R.L., et al., Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Critical care, 2007. 11(2): p. 1-8.
Molitoris, B.A., et al., Improving outcomes of acute kidney injury: report of an initiative. Nature clinical practice Nephrology, 2007. 3(8): p. 439-442.
Kellum, J.A., et al., Kidney disease: improving global outcomes (KDIGO) acute kidney injury work group. KDIGO clinical practice guideline for acute kidney injury. Kidney international supplements, 2012. 2(1): p. 1-138.
Koyner, J.L., et al., Furosemide stress test and biomarkers for the prediction of AKI severity. Journal of the American Society of Nephrology, 2015. 26(8): p. 2023-2031.
Matsuura, R., et al., Response to different furosemide doses predicts AKI progression in ICU patients with elevated plasma NGAL levels. Annals of Intensive Care, 2018. 8(1): p. 1-10.
Pon, A.G., et al., Clinical significance of frusemide stress test in predicting the severity of acute kidney injury. Brazilian Journal of Nephrology, 2021. 43: p. 470-477.
van der Voort, P.H., E.C. Boerma, and P. Pickkers, The furosemide stress test to predict renal function after continuous renal replacement therapy. Critical Care, 2014. 18(3): p. 1-2.
Cooper, M.S. and N.J. Gittoes, Diagnosis and management of hypocalcaemia. Bmj, 2008. 336(7656): p. 1298-1302.
Schilling, T. and R. Ziegler, Current therapy of hypoparathyroidism—a survey of German endocrinology centers. Experimental and clinical endocrinology & diabetes, 1997. 105(04): p. 237-241.
Thakker, R.V., Hypocalcemia: Pathogenesis, differential diagnosis, and management. American Society for Bone and Mineral Research, 2006: p. 213-215.
Tohme, J.F. and J.P. Bilezikian, Diagnosis and treatment of hypocalcemic emergencies. The Endocrinologist, 1996. 6(1): p. 10-18.
Agus, Z. and M. Morad, Modulation of cardiac ion channels by magnesium. Annual review of physiology, 1991. 53(1): p. 299-307.
Krendel, D.A. Hypermagnesemia and neuromuscular transmission. in Seminars in neurology. 1990. © 1990 by Thieme Medical Publishers, Inc.
Neumar, R.W., et al., Part 8: adult advanced cardiovascular life support: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation, 2010. 122(18_suppl_3): p. S729-S767.
MORDES, J.P., R. SWARTZ, and R.A. ARKY, Extreme hypermagnesemia as a cause of refractory hypotension. Annals of Internal Medicine, 1975. 83(5): p. 657-658.
JOURNA, T.A. and O.C. NUTRITION, N THS M8SUE. Nutrition, 1993. 58.
Glaser, N., et al., Kuppermann Nthe Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med, 2001. 344: p. 264-269.
Kraut, J.A. and I. Kurtz, Use of base in the treatment of severe acidemic states. American Journal of Kidney Diseases, 2001. 38(4): p. 703-727.
Kraut, J.A. and N.E. Madias, Treatment of acute metabolic acidosis: a pathophysiologic approach. Nature Reviews Nephrology, 2012. 8(10): p. 589-601.
Marsh, J.D., T.I. Margolis, and D. Kim, Mechanism of diminished contractile response to catecholamines during acidosis. American Journal of Physiology-Heart and Circulatory Physiology, 1988. 254(1): p. H20-H27.
MATHIEU, D., et al., Effects of bicarbonate therapy on hemodynamics and tissue oxygenation in patients with lactic acidosis: a prospective, controlled clinical study. Critical care medicine, 1991. 19(11): p. 1352-1356.
Mitchell, J.H., K. Wildenthal, and R.L. Johnson Jr, The effects of acid-base disturbances on cardiovascular and pulmonary function. Kidney international, 1972. 1(5): p. 375-389.
Orchard, C. and J.C. Kentish, Effects of changes of pH on the contractile function of cardiac muscle. American Journal of Physiology-Cell Physiology, 1990. 258(6): p. C967-C981.
Orchard, C.H. and H.E. Cingolani, Acidosis and arrhythmias in cardiac muscle. Cardiovascular research, 1994. 28(9): p. 1312-1319.
Teplinsky, K., et al., Effect of lactic acidosis on canine hemodynamics and left ventricular function. American Journal of Physiology-Heart and Circulatory Physiology, 1990. 258(4): p. H1193-H1199.
Huber, L. and F.J. Gennari, Severe metabolic alkalosis in a hemodialysis patient. American journal of kidney diseases, 2011. 58(1): p. 144-149.
Lisawat, P. and F.J. Gennari, Approach to the hemodialysis patient with an abnormal serum bicarbonate concentration. American journal of kidney diseases, 2014. 64(1): p. 151-155.
Fiaccadori, E. and E. Cremaschi, Nutritional assessment and support in acute kidney injury. Current opinion in critical care, 2009. 15(6): p. 474-480.
Bellomo, R., et al., A prospective comparative study of moderate versus high protein intake for critically ill patients with acute renal failure. Renal failure, 1997. 19(1): p. 111-120.
Krishnan, J.A., et al., Caloric intake in medical ICU patients: consistency of care with guidelines and relationship to clinical outcomes. Chest, 2003. 124(1): p. 297-305.
Fouque, D., et al., A proposed nomenclature and diagnostic criteria for protein–energy wasting in acute and chronic kidney disease. Kidney international, 2008. 73(4): p. 391-398.
McClave, S.A., R.G. Martindale, and L. Kiraly, The use of indirect calorimetry in the intensive care unit. Current Opinion in Clinical Nutrition & Metabolic Care, 2013. 16(2): p. 202-208.
Fiaccadori, E., E. Parenti, and U. Maggiore, Nutritional support in acute kidney injury. JN journal of nephrology, 2008. 21(5): p. 645.
Li, Y., et al., Nutritional support for acute kidney injury. Cochrane Database of Systematic Reviews, 2010(1).
Benigni, A., et al., Reversible activation defect of the platelet glycoprotein IIb-IIIa complex in patients with uremia. American journal of kidney diseases, 1993. 22(5): p. 668-676.
Escolar, G., et al., Uremic platelets have a functional defect affecting the interaction of von Willebrand factor with glycoprotein Ilb-IIIa. Blood, 1990. 76(7): p. 1336-1340.
Gawaz, M.P., et al., Impaired function of platelet membrane glycoprotein IIb-IIIa in end-stage renal disease. Journal of the American Society of Nephrology, 1994. 5(1): p. 36-46.
