Books on the topic 'Renal blood flow'
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1
Jia, Zhi-Qiang. Temperature homogeneity and blood flow in renal hyperthermia. Ottawa: National Library of Canada, 1994.
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2
Young, Leonie S. Measurement and mechanisms of alterations in intrarenal blood flow in the rat. Dublin: University College Dublin, 1997.
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3
Miller, Judith Anne. Determinants of glomerular filtration rate and renal blood flow in human insulin dependent diabetes mellitus. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.
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4
Sharkey, Rose A. Renal blood flow in respiratory failure. 1997.
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5
Endlich, Karlhans, and Rodger Loutzenhiser. Tubuloglomerular feedback, renal autoregulation, and renal protection. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0209.
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Vascular tone of glomerular blood vessels is controlled dynamically in response to a number of stimuli of which tubuloglomerular feedback and blood flow (and glomerular filtration rate) autoregulation are the most prominent. Both tubuloglomerular feedback- and myogenic-mediated pre-glomerular vasoconstriction are important in the response to reduced pressure. The renal myogenic mechanism, which has the potential to adjust steady-state tone in response to the oscillating systolic pressure signal, additionally plays an essential role in protecting the kidney from the damaging effects of hypertension.
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Bramham, Kate, and Catherine Nelson-Piercy. Pregnancy and renal physiology. Edited by Norbert Lameire and Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0294_update_001.
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Pregnancy is characterized by unique physiological changes within the kidney, resulting in a marked increase in renal blood flow and glomerular filtration, which are associated with successful pregnancy outcomes. Early in normal pregnancy there are increases in plasma volume and cardiac output, but a lowered peripheral resistance leads to average blood pressures being lower. A pregnancy-associated respiratory alkalosis occurs. Protein excretion tends to increase slightly in women without kidney disease. Kidney size is increased, and pelvicalyceal system dilatation is noticeable in most women in the third trimester, right greater than left.
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Cupples, William Angus. Effect of changes in renal medullary blood flow on function of the inner medullary collecting duct. 1985.
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8
Mehta, Nikhil, and Bulent Arslan. Techniques for Treating Visceral Aneurysms and High-Flow Arteriovenous Malformations of the Renal and Visceral Vasculature. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0028.
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Techniques for treating visceral aneurysms are based on location and anatomic region and also on whether an aneurysm is a true aneurysm or a pseudoaneurysm. Visceral artery aneurysms typically require treatment if they are greater than 2 cm. Aneurysms that are favorable for endovascular therapy include saccular aneurysms preferably with a narrow neck and/or aneurysms that have good collateral blood flow to the target organ. Endovascular techniques for treating arteriovenous malformations (AVMs) are multifaceted and require appropriate identification of the AVM using multiple imaging modalities in addition to angiography. AVMs can be defined as slow flow, intermediate flow, and high flow.
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Stewart, Douglas, Gaurav Shah, Jeremiah R. Brown, and Peter A. McCullough. Contrast-induced acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0246.
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Contrast-induced acute kidney injury (CI-AKI) occurs because all forms of intravascular contrast contain iodine and their biochemical structures induce immediate changes in systemic and renal vasoreactivity. In the kidneys, contrast induces a transient decrease in renal blood flow. This is more pronounced in patients with chronic kidney disease and diabetes mellitus. The reduction in blood flow allows slowed transit of contrast and reabsorption by the proximal tubular cells where contrast is directly toxic resulting in tubular cell dysfunction and death. When there is considerable damage, a transient rise in serum creatinine and reduction in urine output will be observed in the hours to days after contrast exposure. Principles to reduce CI-AKI include limiting the amount of contrast used, intravascular volume expansion to maximize renal blood flow and speed transit of contrast, and possibly agents to reduce the oxidative damage caused by the contrast agents themselves.
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Ramrakha, Punit, and Jonathan Hill, eds. Eponymous syndromes. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199643219.003.0016.
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698–699700–704706–708A clinical triad of congenital anaemia, triphalangeal thumbs, and VSD. The aetiology is unknown.See Stokes–Adams syndrome ( p. 706).Hypertension resulting from occlusion of the coeliac axis, leading to diversion of collateral blood flow from the right renal artery. Originally described as renal-splanchnic steal syndrome....
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Dussaule, Jean-Claude, Martin Flamant, and Christos Chatziantoniou. Function of the normal glomerulus. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0044_update_001.
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Glomerular filtration, the first step leading to the formation of primitive urine, is a passive phenomenon. The composition of this primitive urine is the consequence of the ultrafiltration of plasma depending on renal blood flow, on hydrostatic pressure of glomerular capillary, and on glomerular coefficient of ultrafiltration. Glomerular filtration rate (GFR) can be precisely measured by the calculation of the clearance of freely filtrated exogenous substances that are neither metabolized nor reabsorbed nor secreted by tubules: its mean value is 125 mL/min/1.73 m² in men and 110 mL/min/1.73 m² in women, which represents 20% of renal blood flow. In clinical practice, estimates of GFR are obtained by the measurement of creatininaemia followed by the application of various equations (MDRD or CKD-EPI) and more recently by the measurement of plasmatic C-cystatin. Under physiological conditions, GFR is a stable parameter that is regulated by the intrinsic vascular and tubular autoregulation, by the balance between paracrine and endocrine agents acting as vasoconstrictors and vasodilators, and by the effects of renal sympathetic nerves. The mechanisms controlling GFR regulation are complex. This is due to the variety of vasoactive agents and their targets, and multiple interactions between them. Nevertheless, the relative stability of GFR during important variations of systemic haemodynamics and volaemia is due to three major operating mechanisms: autoregulation of the afferent arteriolar resistance, local synthesis and action of angiotensin II, and the sensitivity of renal resistance vessels to respond to NO release.
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Fervenza, Fernando C. Evaluation of Kidney Function, Glomerular Disease, and Tubulointerstitial Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0472.
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Several measures are used to evaluate kidney function: serum creatinine, urinalysis, renal clearance, and renal imaging. Creatinine is an end product of muscle catabolism and is commonly used as a filtration marker. Dysmorphic erythrocytes in the urinary sediment indicate bleeding in the upper urinary tract. A urine pH less than 5.5 excludes type 1 renal tubular acidosis. A pH greater than 7 suggests infection. Acidic urine is indicative of a high-protein diet, acidosis, and potassium depletion. Alkaline urine is associated with a vegetarian diet, alkalosis and urease-producing bacteria. Clearance of p-aminohippurate is a measure of renal blood flow. Kidney function is evaluated to determine disease states such as glomeruluar disease or tubulointerstitial disease. Clinical manifestations of glomerular injury can vary from the finding of isolated hematuria or proteinuria, or both. In addition, some patients who present with advanced renal insufficiency, hypertension, and shrunken, smooth kidneys are presumed to have chronic glomerulonephritis. Acute and chronic interstitial disease preferentially involves renal tubules.
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Kellum, John A. Diagnosis of oliguria and acute kidney injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0212.
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Diagnosis and classification of acute pathology in the kidney is major clinical problem. Azotemia and oliguria represent not only disease, but also normal responses of the kidney to extracellular volume depletion or a decreased renal blood flow. Clinicians routinely make inferences about both the presence of renal dysfunction and its cause. Pure prerenal physiology is unusual in hospitalized patients and its effects are not necessary benign. Sepsismay alter renal function without the characteristic changes in urine indices. The clinical syndrome known as acute tubular necrosis does not actually manifest the histological changes that the name implies. Acute kidney injury (AKI) is a term proposed to encompass the entire spectrum of the syndrome from minor changes in renal function to a requirement for renal replacement therapy. Criteria based on both changes in serum creatinine and urine output represent a broad international consensus for diagnosing and staging AKI.
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Kahn, S. Lowell. Catheter Modification Techniques for Venous Sampling. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0062.
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Venous sampling is critically important in the diagnosis and localization of pituitary, parathyroid, renal, adrenal, and ovarian endocrine tumors and conditions. Catheterization of smaller veins can present a challenge and may be responsible for technical failures, particularly with adrenal vein, parathyroid, and inferior petrosal sinus venous sampling. Beyond the inherent challenges of catheterization posed by small veins, obtaining adequate blood samples can be difficult because the return of blood from a small vein may be exceedingly slow. This chapter discusses techniques to enhance the return of venous blood flow from a diagnostic catheter in a small vein. These techniques are applicable to all venous sampling, but they are particularly beneficial when sampling small-caliber veins.
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Erickson, Stephen B., Hatem Amer, and Timothy S. Larson. Urolithiasis, Kidney Transplantation, and Pregnancy and Kidney Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0475.
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It was previously assumed that all kidney stones crystallized as urine passed through the renal tubules and were retained by means of crystal-tubular cell interactions. Recently uroscopy with papillary biopsies has shown 2 different pathways for stone formation, both mediated by calcium phosphate crystals. Kidney transplant has become the preferred treatment for patients with end-stage renal disease. Those benefiting from transplant included patients who would be deemed "high risk," such as those with diabetes mellitus and those older than 70 years. Anatomical changes associated with pregnancy are renal enlargement and dilatation of the calyces, renal pelvis, and ureters. Physiologic changes include a 30% to 50% increase in glomerular filtration rate and renal blood flow; a mean decrease of 0.5 mg/dL in the creatinine level and a mean decrease of 18 mg/dL in the serum urea nitrogen level; intermittent glycosuria independent of plasma glucose; proteinuria; aminoaciduria; increased uric acid excretion; increased total body water, with osmostat resetting; 50% increase in plasma volume and cardiac output; and increased ureteral peristalsis.
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Ho, Kwok M. Kidney and acid–base physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0005.
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Anatomically the kidney consists of the cortex, medulla, and renal pelvis. The kidneys have approximately 2 million nephrons and receive 20% of the resting cardiac output making the kidneys the richest blood flow per gram of tissue in the body. A high blood and plasma flow to the kidneys is essential for the generation of a large amount of glomerular filtrate, up to 125 ml min−1, to regulate the fluid and electrolyte balance of the body. The kidneys also have many other important physiological functions, including excretion of metabolic wastes or toxins, regulation of blood volume and pressure, and also production and metabolism of many hormones. Although plasma creatinine concentration has been frequently used to estimate glomerular filtration rate by the Modification of Diet in Renal Disease (MDRD) equation in stable chronic kidney diseases, the MDRD equation has limitations and does not reflect glomerular filtration rate accurately in healthy individuals or patients with acute kidney injury. An optimal acid–base environment is essential for many body functions, including haemoglobin–oxygen dissociation, transcellular shift of electrolytes, membrane excitability, function of many enzymes, and energy production. Based on the concepts of electrochemical neutrality, law of conservation of mass, and law of mass action, according to Stewart’s approach, hydrogen ion concentration is determined by three independent variables: (1) carbon dioxide tension, (2) total concentrations of weak acids such as albumin and phosphate, and (3) strong ion difference, also known as SID. It is important to understand that the main advantage of Stewart over the bicarbonate-centred approach is in the interpretation of metabolic acidosis.
17
Lewington, Andrew, and Michael Weston. Imaging the urinary tract in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0210.
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Imaging the urinary tract of patients in the intensive care unit (ICU) may assist identifying the cause of acute kidney injury (AKI). By the nature of their illness patients on ICU will often be clinically unstable and this will restrict the choice of imaging. Ultrasound is the most commonly used non-invasive imaging technique used, and is essential for assessing renal anatomy, determining kidney size and the presence of obstruction. New developments hold much promise and there are a number of centres now using this technology. Doppler ultrasonography has become increasingly popular to assess intrarenal blood flow. CT scanning can be used with or without contrast when ultrasonography is non-diagnostic and is very useful in identifying calcification within the renal tract. However, the patient must be stable enough for transfer to the radiology department. It is important to consider the risk of iodinated contrast-induced AKI (CI-AKI) in critically-ill patients and minimize potential renal injury. Magnetic resonance imaging may be preferred where there is risk of CI-AKI, but the logistics may prove even more demanding. Renal arteriography is rarely performed, but may be required for diagnostic and interventional procedures for renal artery stenosis or sites of active haemorrhage.
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Neligan, Patrick J., and Clifford S. Deutschman. Management of metabolic acidosis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0256.
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Metabolic acidosis (MA) commonly complicates critical illness, usually manifesting as a fall in arterial pH (<7.4) accompanied by a concomitant fall in serum bicarbonate concentration. Acidosis caused by unmeasured anions (UMA), can be distinguished from Hyperchloraemic acidosis by demonstrating a widening of the anion gap (AG). AG should be corrected for albumin and lactate. The base deficit (BD) calculates degree of metabolic acidosis and represents the amount of strong cation required to restore the pH to 7.4. Neither the AG nor the BD specify the cause of acidosis, and are unhelpful in the setting of mixed disorders. The base deficit gap (BDG) is used to calculate the effect of free water, sodium, chloride and albumin on the BD. It is the difference between BDcalc and BDmeasured (on a blood gas) and represents UMA. The strong ion gap more robustly calculates the amount of UMA than AG or BDG, and may be more accurate at predicting outcomes in the emergency room. Lactic acidosis is due to hypovolaemia until otherwise proven. In the majority of cases aggressive fluid resuscitation is warranted. In the presence of normal tissue blood flow regional hypoperfusion, poisoning or exogenous catecholamines should be considered. Ketoacidosis is due to intracellular glucose deficiency, caused by hypoinsulinaemia or starvation. The former is treated with isotonic crystalloid and insulin. Renal acidosis is treated with renal replacement therapy or recovery of renal function.
19
Ronco, Pierre M. Kidney involvement in plasma cell dyscrasias. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0150.
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Monoclonal proliferations of the B-cell lineage are characterized by abnormal and uncontrolled expansion of a single clone of B cells at different maturation stages, with a variable degree of differentiation to immunoglobulin-secreting plasma cells. Therefore, they are usually associated with the production and secretion in blood of a monoclonal immunoglobulin and/or a fragment thereof which may become deposited in tissues. These deposits can take the form of casts (in myeloma cast nephropathy), crystals (in myeloma-associated Fanconi syndrome), fibrils (in light-chain and exceptional heavy-chain amyloidosis), or granular precipitates (in monoclonal immunoglobulin deposition disease). They may disrupt organ structure and function, inducing life-threatening complications. All of the pathologic entities related to immunoglobulin deposition principally involve the kidney, which is not only explained by the high levels of renal plasma flow and glomerular filtration rate, but also by the sieving properties of the glomerular capillary wall and by the prominent role of the renal tubule in LC handling and catabolism.The different renal (and other) manifestations are related to the unique physicochemical characteristics of each paraprotein or immunoglobulin fragment, and the rate of their production.
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Coleman, John Kevin Michael. Changes in renal blood flow due to infusions of angiotensin II (3-8) [ANG IV] and its peptide analogs lysine℗£, ANG IV and norleucine℗£, ANG IV; ANG IV relation to nitric oxide and distribution of ANG IV binding in the rat and guinea pig kidney. 1993.
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21
Beydon, Laurent, and Flavie Duc. Inhalational anaesthetic agents in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0046.
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Inhalational anaesthetic agents have limited applications in the intensive care unit (ICU), as their delivery requires specific equipment, which are not routinely available. Sevoflurane and isoflurane are the two agents eligible for this purpose. They both show good clinical tolerance and versatility, but may raise cerebral blood flow above 1 minimum alveolar concentration. This property makes them unsuitable for sedation in patients suffering from acute brain injury. Sevoflurane is known to be partly metabolized via the cytochrome pathway in inorganic fluoride. This latter accumulates in a dose- and time-dependent manner, especially in a closed circuit with soda lime. However, no clinical renal injury has been proven, despite several studies reporting on sevoflurane in ICUs. A fresh gas flow above 2 L/min is required to limit inorganic fluoride build-up. Halogenates have been proven to allow efficient sedation in ICU patients for up to several days. They may be considered as therapeutic agents especially in refractory status asthmaticus. Insufficient data exist to recommend halogenates to treat status epilepticus. Nitrous oxide, in 50% oxygen, may serve to allow sedation/analgesia for short and moderately procedures. Xenon, an inert gas that discloses anaesthetic properties with extremely fast onset and recovery, and also has no haemodynamic side effects remains confined to the operating theatre. It requires specific anaesthetic machines and is, at present, too expensive to represent a routine inhalational anaesthetic agent.
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Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.
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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, accompanied by changes in the microcirculation. Although all renal resident cells participate in AKI, the brunt falls on the epithelial and endothelial cells, the fact that underlies the development of tubular epithelial and vascular compromise.This chapter further summarizes the involvement of several cell organelles in AKI: mitochondrial involvement in perturbed energy metabolism, lysosomal involvement in degradation of misfolded proteins and damaged organelles, and peroxisomal involvement in the regulation of oxidative stress and metabolism, all of which become defective. Common molecular pathways are engaged in cellular stress response and their roles in cell death or survival. The diverse families of nephrotoxic medications and the respective mechanisms they induce AKI are discussed. The mechanisms of action of some nephrotoxins are analysed, and also of the preventive therapies of ischaemic or pharmacologic pre-conditioning.An emerging concept of the systemic inflammatory response triggered by AKI, which can potentially aggravate the local injury or tend to facilitate the repair of the kidney, is presented. Rational therapeutic strategies should be based on these well-established pathophysiological hallmarks of AKI.
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Shirali, Anushree, and Mark A. Perazella. Drug-induced nephropathies. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0362.
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Pharmacological therapy with prescription medications and other drugs is the mainstay of modern medical practice. In addition, an increasing number of people use over-the-counter and complementary treatments for management of acute and chronic disease. The kidney faces constant exposure to some of these medications and drugs since it receives significant blood flow from the systemic circulation and importantly participates in excretion of many of these substances. Some of these agents have the innate potential for nephrotoxicity, which is modified by patient- as well as drug-related factors. As a result, drug-induced nephropathies can complicate patient management and require diligent investigation and management by the consulting nephrologist. This chapter highlights those agents commonly associated with drug-induced nephropathies affecting various segments of the nephron. It reviews the drug- and patient-specific factors that increase susceptibility to kidney injury. In addition, it discusses the commonly encountered patterns of kidney injury with a particular drug, recognizing that some agents can cause injury via multiple pathways, and provides an overview of the mechanisms by which kidney disease occurs. Finally, the features that dictate renal recovery, including prophylactic and treatment measures, are reviewed.
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Bushi, Simon Subhakar. Real time analysis of skin capillary blood flow on a motorola MC68008 based system. Bradford, 1986.
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