Correspondence
Chronic kidney disease and stroke We appreciate the idea of cerebrorenal interaction, as proposed by Toyoda and colleagues in their recent Review,1 because it raises an important clinical issue with respect to chronic kidney disease in patients with stroke and cerebrovascular disease. The authors describe the mechanisms by which kidney disease might increase the risk of stroke and subclinical cerebral abnormalities, and affect cognitive function. However, the effect of stroke or cerebrovascular disease on renal function has scarcely been explored, which makes the comprehensive description of this two-way interaction more challenging than that of its cardiology counterpart, cardiorenal syndrome.2 Reports3,4 on hospital admissions show that 14·5–26·7% of patients with acute stroke develop acute kidney injury, which is itself an independent predictor of short-term and long-term outcomes after stroke. Kidney damage due to dehydration and electrolyte imbalance as a result of dysphagia and reactive hypertension after stroke, and the use of nephrotoxic drugs such as mannitol in the treatment of stroke might lead to acute kidney injury. Contrast medium for the diagnosis or endovascular treatment of stroke might lead to acute kidney injury in patients with acute stroke. Future research might be warranted on the question of whether the prevention of acute kidney injury improves outcomes in patients with acute stroke. More than a third of patients with acute stroke have an estimated glomerular filtration rate of less than 60 mL/min per 1·73 m² when admitted, but this might relate to a transient increase in serum creatinine concentration resulting either from the stroke or treatments.1 According to the National Kidney Foundation Kidney Disease Outcomes Quality Initiative,5 chronic kidney disease should be defined as persistently decreased
estimated glomerular filtration rate and proteinuria for at least 3 months. The prevalence of chronic kidney disease in patients with acute stroke therefore remains uncertain, because it is not clear whether renal changes persist beyond the acute phase. We declare no competing interests.
Cheng-Yang Hsieh, Huey-Juan Lin, Chih-Hung Chen, Edward Chia-Cheng Lai, *Yea-Huei Kao Yang [email protected] Department of Neurology, Tainan Sin Lau Hospital, Tainan, Taiwan (C-YH); and Department of Neurology, Chi Mei Medical Center (H-JL); and Department of Neurology, National Cheng Kung University Hospital and College of Medicine, National Cheng Kung University, Tainan, Taiwan (C-HC); and Institute of Clinical Pharmacy and Pharmaceutical Sciences (EC-CL, Y-HKY), College of Medicine, National Cheng Kung University, Tainan, Taiwan 1
2
3
4
5
Toyoda K, Ninomiya T. Stroke and cerebrovascular diseases in patients with chronic kidney disease. Lancet Neurol 2014; 13: 823–33. Ronco C, Haapio M, House AA, Anavekar N, Bellomo R. Cardiorenal syndrome. J Am Coll Cardiol 2008; 52: 1527–39. Covic A, Schiller A, Mardare NG, et al. The impact of acute kidney injury on short-term survival in an Eastern European population with stroke. Nephrol Dial Transplant 2008; 23: 2228–34. Tsagalis G, Akrivos T, Alevizaki M, et al. Renal dysfunction in acute stroke: an independent predictor of long-term all combined vascular events and overall mortality. Nephrol Dial Transplant 2009; 24: 194–200. National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis 2002; 39: S1–266.
Authors’ reply We thank Cheng-Yang Hsieh and colleagues for their interest in our Review.1 The effect of stroke on kidney function is an important point to consider in terms of cerebrorenal interactions. In 7 068 334 patients admitted to hospital with acute ischaemic stroke as part of the US Nationwide Inpatient Sample from 2002 to 2010, 2 372 223 patients had acute renal failure that was independently associated with moderate to severe disability (odds ratio [OR] 1·3, 95% CI 1·3–1·4), intracerebral haemorrhage (1·4, 1·3–1·6), and death (2·2, 2·0–2·2) after multivariable adjustment.
www.thelancet.com/neurology Vol 13 November 2014
In our Review, we showed that patients with intracerebral haemorrhage are more likely to receive intensive antihypertensive therapy than are those with ischaemic stroke in the emergency setting, and sometimes these patients have features of acute kidney injury. Our unpublished data show that excessive reduction of systolic blood pressure, hyperglycaemia, and decreased estimated glomerular filtration rate on admission are independently associated with acute kidney injury during the acute stage of intracerebral haemorrhage. Cheng-Yang Hsieh and colleagues list dehydration and electrolyte imbalance, reactive hypertension, and the use of nephrotoxic drugs in the treatment of stroke among the potential causes of acute kidney injury. Additionally, acute lowering of blood pressure, urinary tract infection (often a complication in critically ill patients), and cholesterol embolism due to antithrombotic therapy, thrombolysis and endovascular therapy are important causes of acute kidney injury during acute and chronic management of stroke. The brain tightly controls the balance of water and sodium throughout the body. Such regulation is another example of cerebrorenal interaction. A close liaison between neurologists and nephrologists would improve our understanding of cerebrorenal interactions and prevent acute kidney injury and chronic kidney damage in patients with stroke. I declare no competing interests.
Kazunori Toyoda, on behalf of all authors [email protected] Department of Cerebrovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan 1
2
Toyoda K, Ninomiya T. Stroke and cerebrovascular diseases in patients with chronic kidney disease. Lancet Neurol 2014; 13: 823–33. Saeed F, Adil MM, Khursheed F, et al. Acute renal failure is associated with higher death and disability in patients with acute ischemic stroke: analysis of nationwide inpatient sample. Stroke 2014; 45: 1478–80.
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Chronic kidney disease and stroke We appreciate the idea of cerebrorenal interaction, as proposed by Toyoda and colleagues in their recent Review,1 because it raises an important clinical issue with respect to chronic kidney disease in patients with stroke and cerebrovascular disease. The authors describe the mechanisms by which kidney disease might increase the risk of stroke and subclinical cerebral abnormalities, and affect cognitive function. However, the effect of stroke or cerebrovascular disease on renal function has scarcely been explored, which makes the comprehensive description of this two-way interaction more challenging than that of its cardiology counterpart, cardiorenal syndrome.2 Reports3,4 on hospital admissions show that 14·5–26·7% of patients with acute stroke develop acute kidney injury, which is itself an independent predictor of short-term and long-term outcomes after stroke. Kidney damage due to dehydration and electrolyte imbalance as a result of dysphagia and reactive hypertension after stroke, and the use of nephrotoxic drugs such as mannitol in the treatment of stroke might lead to acute kidney injury. Contrast medium for the diagnosis or endovascular treatment of stroke might lead to acute kidney injury in patients with acute stroke. Future research might be warranted on the question of whether the prevention of acute kidney injury improves outcomes in patients with acute stroke. More than a third of patients with acute stroke have an estimated glomerular filtration rate of less than 60 mL/min per 1·73 m² when admitted, but this might relate to a transient increase in serum creatinine concentration resulting either from the stroke or treatments.1 According to the National Kidney Foundation Kidney Disease Outcomes Quality Initiative,5 chronic kidney disease should be defined as persistently decreased
estimated glomerular filtration rate and proteinuria for at least 3 months. The prevalence of chronic kidney disease in patients with acute stroke therefore remains uncertain, because it is not clear whether renal changes persist beyond the acute phase. We declare no competing interests.
Cheng-Yang Hsieh, Huey-Juan Lin, Chih-Hung Chen, Edward Chia-Cheng Lai, *Yea-Huei Kao Yang [email protected] Department of Neurology, Tainan Sin Lau Hospital, Tainan, Taiwan (C-YH); and Department of Neurology, Chi Mei Medical Center (H-JL); and Department of Neurology, National Cheng Kung University Hospital and College of Medicine, National Cheng Kung University, Tainan, Taiwan (C-HC); and Institute of Clinical Pharmacy and Pharmaceutical Sciences (EC-CL, Y-HKY), College of Medicine, National Cheng Kung University, Tainan, Taiwan 1
2
3
4
5
Toyoda K, Ninomiya T. Stroke and cerebrovascular diseases in patients with chronic kidney disease. Lancet Neurol 2014; 13: 823–33. Ronco C, Haapio M, House AA, Anavekar N, Bellomo R. Cardiorenal syndrome. J Am Coll Cardiol 2008; 52: 1527–39. Covic A, Schiller A, Mardare NG, et al. The impact of acute kidney injury on short-term survival in an Eastern European population with stroke. Nephrol Dial Transplant 2008; 23: 2228–34. Tsagalis G, Akrivos T, Alevizaki M, et al. Renal dysfunction in acute stroke: an independent predictor of long-term all combined vascular events and overall mortality. Nephrol Dial Transplant 2009; 24: 194–200. National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis 2002; 39: S1–266.
Authors’ reply We thank Cheng-Yang Hsieh and colleagues for their interest in our Review.1 The effect of stroke on kidney function is an important point to consider in terms of cerebrorenal interactions. In 7 068 334 patients admitted to hospital with acute ischaemic stroke as part of the US Nationwide Inpatient Sample from 2002 to 2010, 2 372 223 patients had acute renal failure that was independently associated with moderate to severe disability (odds ratio [OR] 1·3, 95% CI 1·3–1·4), intracerebral haemorrhage (1·4, 1·3–1·6), and death (2·2, 2·0–2·2) after multivariable adjustment.
www.thelancet.com/neurology Vol 13 November 2014
In our Review, we showed that patients with intracerebral haemorrhage are more likely to receive intensive antihypertensive therapy than are those with ischaemic stroke in the emergency setting, and sometimes these patients have features of acute kidney injury. Our unpublished data show that excessive reduction of systolic blood pressure, hyperglycaemia, and decreased estimated glomerular filtration rate on admission are independently associated with acute kidney injury during the acute stage of intracerebral haemorrhage. Cheng-Yang Hsieh and colleagues list dehydration and electrolyte imbalance, reactive hypertension, and the use of nephrotoxic drugs in the treatment of stroke among the potential causes of acute kidney injury. Additionally, acute lowering of blood pressure, urinary tract infection (often a complication in critically ill patients), and cholesterol embolism due to antithrombotic therapy, thrombolysis and endovascular therapy are important causes of acute kidney injury during acute and chronic management of stroke. The brain tightly controls the balance of water and sodium throughout the body. Such regulation is another example of cerebrorenal interaction. A close liaison between neurologists and nephrologists would improve our understanding of cerebrorenal interactions and prevent acute kidney injury and chronic kidney damage in patients with stroke. I declare no competing interests.
Kazunori Toyoda, on behalf of all authors [email protected] Department of Cerebrovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan 1
2
Toyoda K, Ninomiya T. Stroke and cerebrovascular diseases in patients with chronic kidney disease. Lancet Neurol 2014; 13: 823–33. Saeed F, Adil MM, Khursheed F, et al. Acute renal failure is associated with higher death and disability in patients with acute ischemic stroke: analysis of nationwide inpatient sample. Stroke 2014; 45: 1478–80.
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