The kidneys are a pair of bean shaped organs that sit to each side of the vertebral column, with the left kidney situated slightly lower than the right. Remarkably, the pair of organs are able to process in the region of 1700 L of blood a day whilst only weighing approximately 113 – 170g (Porth, 2005). The blood is supplied to each kidney via a renal artery branching off from either side of the aorta (Martini, 2006), the renal artery then divides into segmental arteries that sub-divide into interlobular arteries as shown in figure 1 (Openstax College, 2013). The interlobular arteries go through a series of further branching until they form the afferent arterioles (Openstax College, 2013).
Figure 1: Blood flow in the kidney (Openstax …show more content…
HF is defined as a disorder that can either be structural or functional that inhibits the hearts ability to pump efficiently and effectively (Hunt, et al., 2009, cited in Shiba & Shimokawa, 2011). Chronic kidney disease (CKD) affects approximately 9-13% of the global population (Shiba & Shimokawa, 2011), and is defined as kidney damage or a GFR of less than 60ml/min/1.73m2 lasting for a period of more than 3 months regardless of the cause of the disease (Levey , et al., 2005). CKD and HF are progressive diseases, therefore treatment of each of these conditions can be targeted to the specific stage of disease and to prevent progression from one stage to the next. However, in cases of CRS the outcomes for these patients are very poor due to one disease process exacerbating the progression of the other (Shiba & Shimokawa, 2011). Renin-angiotensin-aldosterone system (RAAS) amplification resulting in the initiation of oxidases by angiotensin II (AT-II) in either the kidneys or the heart, aggravates inflammation in the other (Bock & Gottlieb, …show more content…
(2008) divided CRS into 5 subtypes in order to define each of the varying effects HF and CKD have on each other, however the beneficial value of this system should be established in prospective studies (Shiba & Shimokawa, 2011). CRS type 1, or acute CRS, is described as acute HF initiating acute kidney injury (AKI) and CRS type 2, or chronic CRS, is described as chronic HF resulting in progressive CKD. The pathophysiology of impaired renal function in HF patients is not very well understood (Nohria, et al., 2007, cited in Ronco, et al., 2008), but early hypotheses stated that insufficient renal blood flow due to a decrease in cardiac output causes renin release and activation of the renin-angiotensin-aldosterone system (RAAS) which in turn results in increased sodium reabsorption and water retention subsequently worsening cardiac function and the GFR. Nevertheless, recent studies suggest that this is not the whole story and treating patients based purely on this concept does not lead to an improvement of the outcome for the patient (Bock & Gottlieb,
Figure 1: Blood flow in the kidney (Openstax …show more content…
HF is defined as a disorder that can either be structural or functional that inhibits the hearts ability to pump efficiently and effectively (Hunt, et al., 2009, cited in Shiba & Shimokawa, 2011). Chronic kidney disease (CKD) affects approximately 9-13% of the global population (Shiba & Shimokawa, 2011), and is defined as kidney damage or a GFR of less than 60ml/min/1.73m2 lasting for a period of more than 3 months regardless of the cause of the disease (Levey , et al., 2005). CKD and HF are progressive diseases, therefore treatment of each of these conditions can be targeted to the specific stage of disease and to prevent progression from one stage to the next. However, in cases of CRS the outcomes for these patients are very poor due to one disease process exacerbating the progression of the other (Shiba & Shimokawa, 2011). Renin-angiotensin-aldosterone system (RAAS) amplification resulting in the initiation of oxidases by angiotensin II (AT-II) in either the kidneys or the heart, aggravates inflammation in the other (Bock & Gottlieb, …show more content…
(2008) divided CRS into 5 subtypes in order to define each of the varying effects HF and CKD have on each other, however the beneficial value of this system should be established in prospective studies (Shiba & Shimokawa, 2011). CRS type 1, or acute CRS, is described as acute HF initiating acute kidney injury (AKI) and CRS type 2, or chronic CRS, is described as chronic HF resulting in progressive CKD. The pathophysiology of impaired renal function in HF patients is not very well understood (Nohria, et al., 2007, cited in Ronco, et al., 2008), but early hypotheses stated that insufficient renal blood flow due to a decrease in cardiac output causes renin release and activation of the renin-angiotensin-aldosterone system (RAAS) which in turn results in increased sodium reabsorption and water retention subsequently worsening cardiac function and the GFR. Nevertheless, recent studies suggest that this is not the whole story and treating patients based purely on this concept does not lead to an improvement of the outcome for the patient (Bock & Gottlieb,