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Renal system balance

Along with the respiratory system, the renal system maintains acid-base balance by altering the excretion of hydrogen and bicarbonate ions in the urine. When the extracellular fluid becomes acidic and pH decreases, the... [Pg.308]

Sodium balance is achieved when salt intake is equal to salt output. The intake of salt in the average American diet (10 to 15 g/day) far exceeds what is required physiologically. Only about 0.5 g/day of salt is lost in sweat and feces. The remaining ingested salt must be excreted in the urine. The amount of sodium excreted by the renal system is determined by ... [Pg.336]

Lithium is an important element in many industries (Bach 1985). Lithium is used medically as a treatment for bipolar disorders (Schou 1988). Lithium toxicity, especially to the renal system, is problematical. Estimating systemic elemental mass balance, especially for patients receiving oral Li dosing, is important, and is one area in which Li isotope ratios are... [Pg.154]

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. [Pg.273]

The renal system is another major regulator of pH balance. The kidneys can control pH by secreting H+ from the body or retaining it to reverse an acidosis or alkalosis. The renal mechanism can correct an acidosis by reabsorbing CO, which then combines with water to form carbonic acid and bicarbonate, which is released into the bloodstream, and H+, as noted earlier in the carbonic acid-bicarbonate buffer system. The renal system can can correct alkalosis by excreting the CO, resulting in less bicarbonate formation. [Pg.45]

The renal system plays an important role in the regulation of fluids and electrolytes and is one of the two major systems involved in restoration of acid-base balance. In addition, the renal system has other vital roles, such as production of erythropoetin needed for red blood cells health, essential for oxygenation of tissues. The primary functions of the renal system are... [Pg.190]

AQP4 is the predominant water channel in the central nervous system (CNS), where it is involved in maintaining brain water balance and neural signal transduction. It is mainly expressed in astroglial cells, which support the neurons. Outside the CNS, AQP4 has been found in the basolateral membrane of renal principal cells as well as in various glandular epithelia, airways, skeletal muscle, stomach, retina and ear. [Pg.216]

Although the kidneys are not considered endocrine glands per se, they are involved in hormone production. Erythropoietin is a peptide hormone that stimulates red blood cell production in bone marrow. Its primary source is the kidneys. Erythropoietin is secreted in response to renal hypoxia. Chronic renal disease may impair the secretion of erythropoietin, leading to development of anemia. The kidneys also produce enzymes. The enzyme renin is part of the renin-angiotensin-aldosterone system. As will be discussed, these substances play an important role in the regulation of plasma volume and therefore blood pressure. Other renal enzymes are needed for the conversion of vitamin D into its active form, 1,25-d i hyd ro xyv itamin D3, which is involved with calcium balance. [Pg.309]

The balance between renal clearance and metabohsm is readily predicted by physicochemical properties [36]. Rate of metabolism and formation of metabolic products can be screened for, using Ever microsomal systems and mass spectrometry. The... [Pg.137]

While most lipophilic and large molecules are primarily excreted by the hepatobiliary system, the kidney is the major excretory organ for many small organic and inorganic molecules, drugs and hydrophilic metabolites, maintenance of fluid balance, and bone metabolism. These functions expose the kidney to a number of clinical, physiological, and pathological conditions that may compromise renal function. Some renal disorders that necessitate clinical intervention are listed in Table 2. [Pg.52]

The few animal studies located appear to be in general agreement with the human findings (Gardner et al. 1925 Korsrud et al. 1972). Effects of carbon tetrachloride ingestion on blood pressure are sometimes observed, but these are likely secondary to effects on the central nervous system, or to effects on fluid and electrolyte balance following renal injury. [Pg.52]

Renal lithium excretion sensitive to changes in sodium balance. (Sodium depletion tends to cause lithium retention.) Susceptible to drugs enhancing central nervous system lithium toxicity. [Pg.1396]

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. [Pg.455]

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. 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.
Aluminium hydroxide reacts with HCl to form aluminium chloride this in turn reacts with intestinal secretions to produce insoluble salts, especially phosphate. The chloride is released and reabsorbed so systemic acid-base balance is not altered. It tends to constipate. Sufficient aluminium may be absorbed from the intestine to create a risk of encephalopathy in patients with chronic renal failure. Hypophosphataemia and hypophosphaturia may result from impaired absorption due to phosphate binding. [Pg.626]

Impairment of cerebral functions and disturbances of the water and electrolyte balance are the two most important and most common manifestations of decompensated liver cirrhosis. They may be reliably detected at an early stage by means of daily body weight control and simple psychometric tests. A documentation sheet filled in by the patient has proved to be worthwhile latent oedemas or the onset of ascites as well as latent encephalopathy can be detected in this way and thus treated at an early stage. Longterm standing leads to a reduction of natriuresis with subsequent water retention and a deterioration of renal blood flow (like a vicious circle). This is caused by activation of the RAAS and the sympathetic nervous system. Such a dangerous situation (which can arise for example after two hours of standing at a sports event with excessive emotional participation) is often underrated, as we ourselves observed in several patients (s. p. 292) (s. fig. 15.3) (see chapter 16 )... [Pg.733]

The indication for administering BCAA in patients with hepatic encephalopathy to compensate amino-acid imbalance was proposed by J.E. Fischer et al. in 1974, and implemented parenterally. However, oral application of BCAA for an adequate treatment period also has beneficial effects on cirrhosis and HE (7.) improvement in protein tolerance and the nutritional condition, (2.) improvement in cerebral functions (II8, 122), probably due to an amelioration of liver function, (2.) stimulation of ammonia detoxification with a positive nitrogen balance (118), (4.) reduction in or normalization of AAA levels, and (5.) promotion of glutamine synthesis with a favourable effect on the cells of the immune system and on renal function. By means of BCAA, it was possible to prolong the survival time and delay the occurrence of liver failure in rats with CC -induced cirrhosis. (123, 126) However, there are diverging results, which need further clarification. In principle, the use of BCAA is considered to be a necessary form of supplementary treatment for catabolic metabolism in cirrhosis (124,125, 127, 128, 130-132), in (also latent) HE and after curative resection of hepatocellular carcinoma. (I2l) (s. p. 280)... [Pg.861]

The pathophysiology of ciclosporin-induced hypertension is complex and not yet fully elucidated. Increased systemic vascular resistance subsequent to altered vascular endothelium function, renal vasoconstriction with reduced glomerular filtration and sodium-water retention, and/or increased activity of the sympathetic nervous system were suggested, while only a minor role or none was attributed to the renin-angiotensin system (10). However, hypertension often occurs before changes in renal function or sodium balance can be demonstrated, and ciclosporin nephrotoxicity alone does not explain ciclosporin-associated hypertension (8,11). [Pg.744]


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See also in sourсe #XX -- [ Pg.169 , Pg.170 , Pg.171 , Pg.172 , Pg.173 , Pg.174 ]




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