Renal system fluid volume

The primary function of the renal system is the elimination of waste products, derived either from endogenous metabolism or from the metabolism of xenobiotics. The latter function is discussed in detail in Chapter 10. The kidney also plays an important role in regulation of body homeostasis, regulating extracellular fluid volume, and electrolyte balance. 

Adverse effects Renal function may deteriorate with the decreased circulating fluid volume, especially after the addition of another diuretic drug acting on the RAAS system, and careful monitoring of serum creatinine is essential. Serum potassium should be monitored within one week of initiation and at least every four weeks for the first three months and every three months thereafter. It should also be monitored at any dose change in spironolactone or if there is a change in concomitant medications that affects the potassium balance. The spironolactone dose (standard 25 mg per day) should be reduced if potassium levels are <5.4 mEq/L, and treatment should be discontinued if painful gynecomastia or serious renal dysfunction or hyperkalemia result. 

Figure 33-3. Summary of the renin-angiotensin-aldosterone system. Aldosterone secretion is controlled by several factors, including increased K+,ACTH, or angiotensin II.A1-dosterone acts to increase Na+ retention by both the kidney and colon.Aldosterone also promotes renal K+ excretion, which contributes to maintenance of Na+/K+ balance. In the absence of aldosterone, Na+ is lost, K+ is enhanced, the extracellular fluid volume is reduced, and mean arterial pressure and renal perfusion pressure are decreased. As a result, renin secretion is increased, leading to increased formation of angiotensin II, which promotes vasoconstriction and aldosterone secretion.

Under conditions in which arterial pressure or body fluid volumes are sensed as subnormal, the renin-angiotensin system will be activated and plasma renin activity and angiotensin II levels will be elevated. These conditions include dietary sodium restriction or sodium depletion (such as during diuretic therapy), renal artery stenosis, and congestive heart failure. In each case, fluid and sodium will be retained until the pressure and volume are again sensed as normal. Note... 

Corticosteroids, CSA, TAC, and impaired kidney graft function may cause post-transplant hypertension. The primary mechanism of CI-associated hypertension in heart transplant recipients may be related to the Cl-induced stimulation of intact renal sympathetic nerves and the absence of reflex cardiac inhibition of the sympathetic nervous system, but a number of other mechanisms, including decreased prostacyclin and nitric oxide production, also have been proposed. " In addition to the propensity to cause peripheral vasoconstriction, CIs promote sodium retention, resulting in extracellular fluid volume expansion. TAC appears to have less potential to induce hypertension following transplantation than CSA. Most classes of antihypertensive medications effectively reduce blood pressure in transplant patients (see Chap. 13). ... 

Diuretics are drugs that increase the rate of urine flow clinically useful diuretics also increase the rate of excretion of Na+ (natiiuresis) and an accompanying anion, usually CD. Most clinical applications of diuretics aim to reduce extracellular fluid volume by decreasing total-body NaCl content. Although continued administration of a diuretic causes a sustained net deficit in total-body Na+, the time course of natriuresis is finite because renal compensatory mechanisms bring Na+ excretion in line with Na+ intake, a phenomenon known as diuretic braking. Compensatory mechanisms include activation of the sympathetic nervous system, activation of the renin-angiotensin-aldosterone axis, decreased arterial blood pressure (which reduces pressure natriuresis), hypertrophy of renal epithelial cells, increased expression of renal epithelial transporters, and perhaps alterations in natriuretic hormones such as atrial natriuretic peptide. 

The sodium ion concentrations in body fluids are listed in Table 1 [2]. From a physiological viewpoint, Na provides the bulk of osmotically active solutes in plasma with its associated anions, thus affecting the distribution of the body water significantly. An excess translocation of Na into cells or a loss of it from the body results in a decrease of extracellular fluid volume, affecting circulation, renal function, and nervous system function. 

Ruid volume regulation is necessary to maintain life. Decreased and inadequate fluid volume (i.e., hypovolemia) can result in decreased flow and perfusion to the tissues. Increased or excessive fluid volume (i.e., hypervolemia) can placed stress on the heart and cause dilutional electrolyte imbalance. It is clear that the renal system plays a vital role in fluid management. If the kidneys are not functioning fully, fluid excretion and retention will not occur appropriately in response to fluid adjustment needs. 2... 

From the point of view of potassium balance, there is increased renal excretion of potassium, loss of potassium in the vomitus and no potassium being delivered for absorption in the alimentary tract. All these factors contribute to a severe depletion of the body s total potassium content. Yet another factor contributes to potassium loss. A drop in volume of the circulating blood leads to aldosterone secretion via the renin-angiotensin mechanism which, in turn, promotes sodium reabsorption in the renal tubule this contributes further to excessive renal loss of potassium and hydrogen ions. The acidity of the urine is inappropriate as a response to metabolic alkalosis, but the preservation of electrolyte and fluid volume takes precedence over the acid-base disturbance. These various efiects all combine to yield a positive feedback system driving the metabolic alkalosis which, if not treated, reaches lethal levels in a few days. 

As previously discussed, increased portal pressure triggers the release of nitric oxide to directly vasodilate the splanchnic arterial bed and decrease portal pressure. Unfortunately, nitric oxide also dilates the systemic arterial system, causing a decrease in blood pressure and a decrease in renal perfusion by lowering the effective intravascular volume. The kidney reacts by activating the renin-angiotensin-aldosterone system, which increases plasma renin activity, aldosterone production, and sodium retention. This increase in intravascular volume furthers the imbalance of intravascular oncotic pressure, allowing even more fluid to escape to the extravascular spaces. 

In the early phase of serious intraabdominal infections, attention should be given to preserving major organ system function. With generalized peritonitis, large volumes of intravenous (IV) fluids are required to maintain intravascular volume, to improve cardiovascular function, and to ensure adequate tissue perfusion and oxygenation. Adequate urine output should be maintained to ensure appropriate fluid resuscitation and to preserve renal function. A common cause of early death is hypovolemic shock caused by inadequate intravascular volume expansion and tissue perfusion. 

Patients predicted to follow a severe course require treatment of any cardiovascular, respiratory, renal, and metabolic complications. Aggressive fluid resuscitation is essential to correct intravascular volume depletion and maintain blood pressure. IV colloids may be required because fluid losses are rich in protein. Drotrecogin alfa may benefit patients with pancreatitis and systemic inflammatory response syndrome. IV potassium, calcium, and magnesium are used to correct deficiency states. Insulin is used to treat hyperglycemia. Patients with necrotizing pancreatitis may require antibiotics and surgical intervention. 

Diuretics increase the formation and excretion of urine. These drugs are used as antihypertensive agents because of their ability to increase the renal excretion of water and sodium, thus decreasing the volume of fluid within the vascular system. This situation is somewhat analogous to the decrease in pressure that would occur inside a balloon if some of the air inside were allowed to leak out. Consequently, diuretics appear to have a rather direct effect on blood pressure... 

The papilla is the smallest anatomical portion of the kidney. Papillary tissue consists primarily of terminal portions of the collecting duct system and the vasa recta. Papillary blood flow is low relative to cortex and medulla less than 1% of total renal blood flow reaches the papilla. However, tubular fluid is maximally concentrated and the volume of luminal fluid is maximally reduced within the papilla. Potential toxicants trapped in tubular lumens may attain extremely high concentrations within the papilla during the process of urinary concentration. High intraluminal concentrations of potential toxicants may result in diffusion of these chemicals into papillary tubular epithelial and/or interstitial cells, leading to cellular injury. 

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