The kidneys are bilateral, bean shaped organs that are situated retroperitoneally. The organs lie along the posterior abdominal wall, where they filter blood, maintain ionic homeostasis and produce urine. The body of the liver displaces the right kidney inferiorly, resulting in the left kidney being slightly superior to the right.
Along the medial surface, there is a concavity known as the hilum. At this point, the renal arteries enter, and the renal veins and pelvis (beginning of the ureters) leave the kidney. The neural supply from both divisions from the autonomic nervous system also enters the kidney at the hilum. Lymphatic drainage from both the renal cortex (outer layer of kidney) and renal medulla (inner layer of kidney) go to the same group of nodes.
Subsequent to branching from the aorta, the renal artery enters the kidney at the hilum, where it divides into anterior and posterior branches. The posterior division goes on to supply the posterior region of the kidney, while the anterior branch divides further to produce apical, anterior superior, anterior inferior and inferior segmental arteries; each supplying their respective segments.
Finally, the arteries enter the nephrons (functional units of the kidneys) as the interlobular arteries, where afferent arterioles bring blood to the glomerulus to be filtered. It should be noted that these arteries neither anastomose nor have accompanying veins.
Both the sympathetic and parasympathetic divisions of the autonomic nervous system are responsible for innervating the kidneys. Thoracolumbar outflow from T10 to L1 provide vasomotor supply via the thoracolumbar splanchnic nerve, after synapsing at the renal and coeliac ganglia.
Renal infarction subsequent to occlusion of any of the arterial branches supplying the kidneys is of concern considering that there are no communicating arterial branches. Additionally, the segmental branches of the renal artery are terminal arteries. Furthermore, the medulla is also susceptible to ischemic necrosis because its arterial supply is derived from the efferent arterioles exiting the glomerulus. Therefore, any form of vasculitis can further reduce the already, remarkably low oxygen content of the medulla.
Clinicians should take into account the possibility that some cases of hypertension could be resultant of renal artery stenosis. The narrowing of the renal arteries results in ischemia. The kidneys attempt to correct this by producing excess renin, which causes an elevation in blood pressure. This pathology can be corrected surgically.
Because the kidney filters blood, its network of blood vessels is an important component of its structure and function. The arteries, veins, and nerves that supply the kidney enter and exit at the renal hilum.
The renal arteries branch off of the abdominal aorta and supply the kidneys with blood. The arterial supply of the kidneys is variable from person to person, and there may be one or more renal arteries supplying each kidney.
Renal blood supply starts with the branching of the aorta into the renal arteries (which are each named based on the region of the kidney they pass through) and ends with the exiting of the renal veins to join the inferior vena cava. The renal arteries split into several segmental arteries upon entering the kidneys, which then split into several arterioles.
The renal veins are the veins that drain the kidneys and connect them to the inferior vena cava. The renal vein drains blood from venules that arise from the interlobular capillaries inside the parenchyma of the kidney.
The renal plexus are the source of nervous tissue innervation within the kidney, which surround and primarily alter the size of the arterioles within the renal cortex. Input from the sympathetic nervous system triggers vasoconstriction of the arterioles in the kidney, thereby reducing renal blood flow into the glomerulus.
The kidney also receives input from the parasympathetic nervous system, by way of the renal branches of the vagus nerve (cranial nerve X), which causes vasodilation and increased blood flow of the afferent arterioles. Due to this mechanism, sympathetic nervous stimulation will decrease urine production, while parasympathetic nervous stimulation will increase urine production.
The gonadal artery is an important collateral pathway of blood flow to the kidney. Collateral routes may be from the gonadal artery to the inferior capsular artery (gonadal-renal capsular artery) or to the periureteric arteries. These pathways develop in cases of renal artery stenosis, or when a vascular renal tumor increases the kidneys need for blood. We present five cases in which the gonadal artery served as a source of blood supply to the kidney.
Planned second look techniques are required after restoration of SMA flow, with or without resection of ischemic bowel (and no anastomosis or stoma) following resuscitation in intensive care unit [64, 65]. Given frequent uncertainty with regard to bowel viability, the stapled off bowel ends should be left in discontinuity and re-inspected after a period of continued ICU resuscitation to restore physiological balance. Often, bowel which is borderline ischemic at the initial exploration will improve after restoration of blood supply and physiologic stabilization. Of note, however, multiple adjuncts have been suggested to assess intestinal viability, but none have proven to be uniformly reliable [66, 67].
Incremental dialysis is entirely consistent with the concepts of adequate dialysis dose established in the NCDS and HEMO studies as discussed in Section 1, but incorporates the contribution of residual function, so that dialysis and residual function are seen as both contributing to overall clearance. There are a number of different methods for quantifying combined kidney and dialysis urea clearance (summarised in Appendix 2) which can help with schedule and dose selection. These should be interpreted in clinical context, with due observation of indirect measures of dialysis adequacy such as control of symptoms, blood pressure, fluid gains and electrolytes, so that dialysis dose can be appropriately escalated if treatment appears clinically inadequate.
These studies are non-interventional, therefore associations are with observed (rather than prescribed) ultrafiltration rate, and there is also a close interaction with session length (since rate is obviously the volume over the time) but these data provide a convincing argument for avoidance of excessive rates. This should not however be at the expense of non-achievement of target weight and acceptance of over-hydration (though staged achievement over a number of sessions is frequently appropriate) but rather should focus clinicians on session length or addressing fluid gains between dialysis sessions. The ultrafiltration required during dialysis depends on the degree of over-hydration present at the start of the session, so restricting fluid intake reduces ultrafiltration rate, and is part of standard advice for the majority of patients. Consideration must be given to the cause of increased fluid intake such as habitual drinking or thirst associated with either dietary sodium intake or raised blood glucose. Advice on managing fluid intake is therefore best delivered on an individualised basis, as part of a dietary management plan to support adherence and patient experience. This topic is covered in guidelines for the nutritional management of kidney disease.
Diagrammatic representation of the embryological development of the PV. a The vitelline venous system arrives at the primitive liver as two paired veins (right and left), branches into the hepatic sinusoids, and then coalesce, pierce the septum tranversum (primitive diaphragm) and drain into the sinus venosus (primitive heart). These two vitelline veins communicate through three pre-hepatic anastomoses around the developing duodenum (cranial-ventral, dorsal, and caudal-ventral). b Over time, a selective involution occurs, involving the caudal part of the right vitelline vein, the cranial part of the left vitelline vein, and the caudal-ventral anastomosis. The dorsal and cranial-ventral anastomoses persist and give rise to the main PV and to the left PV, respectively. Initially, the paired umbilical veins lie more lateral than the vitelline ones, and also pierce the septum tranversum and drain into the sinus venosus. With the development of the liver, the umbilical veins fragment and connect to the hepatic sinusoids. Over time, a selective involution of the right umbilical vein and cranial portion of the left umbilical vein also occurs. c The remnant left umbilical vein cranially bifurcates, forming two new communications: one with the IVC through the ductus venosus, carrying oxygenated blood from the placenta directly to the fetus; and another with the left PV, supplying directly the liver. After birth, the ductus venosus and the left umbilical vein involute and become the ligamentum venosum and ligamentum teres, respectively
THED is the end result of the decreased portal venous flow to a liver segment or region and subsequent buffer response of the arterial counterpart via the opening of the physiological distal arterioportal shunts. Thus, the arterial flow takes the role and is responsible for keeping the blood supply to that segment/region, in contrast to the remaining liver, that continues to receive the vast majority of its blood supply from PVS. The net difference results in arterial hyper-enhancement of the involved segment/region, in contrast to the low-attenuating remaining parenchyma. The perfusion abnormality is no longer recognized in the portal venous and/or equilibrium phases of the dynamic study (Fig. 16). 2b1af7f3a8