Las causas más frecuentes de SIADH son neoplasias (carcinoma microcítico de pulmón como el más frecuente), patología del SNC (tumores, accidentes. Alteraciones Metabólicas del Magnesio Alteraciones Metabólicas del Fósforo Soluciones de Uso Parenteral Hipocloremia Causas: Falta de. Manifestaciones clínicas. Signos vitales estables o inestables. Consiente Impotencia funcional. Dolor, anestesia superficial al estimulo.
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Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of clinical conditions.
The kidney plays an important role in the regulation of chloride concentration through a variety of transporters that are present along the nephron. Nevertheless, hyperchloremia can occur when water losses exceed sodium and chloride losses, when the capacity to handle excessive chloride caudas overwhelmed, or when the serum bicarbonate causaz low with a concomitant rise in chloride as occurs with a normal anion gap metabolic acidosis or respiratory alkalosis.
The varied nature of the underlying causes of the hyperchloremia will, to a large extent, determine how to treat this electrolyte disturbance. Chloride is the most abundant anion in the extracellular fluid ECF compartment.
Hyperchloremia is defined as an increase in the chloride concentration in the plasma water.
Acidose metabólica de intervalo aniônico elevado
Hyperchloremia hiopcloremia a relative excess of chloride in the body have been linked to the development of reduced renal blood flow, 12 increased interstitial edema including in the kidney and gastrointestinal system, 3 excess morbidity and mortality in critically ill patients, 45 and reduced survival and recovery in patients with acute kidney injury. The organ that is responsible for the maintenance of chloride balance in the body is the kidney. This article reviews the handling of chloride by the kidney and clinical situations in which hyperchloremia can occur.
The level of the chloride in the plasma is regulated by the kidney. The kidney causax filters chloride across the basement membranes of the glomeruli. The amount of chloride that is excreted into the urine is hipocloremoa by the chloride filtered by the glomeruli and by a series of transport processes hipocloremiq occur along the nephron.
In the early proximal tubule, sodium is absorbed with a proportional amount of water so that the concentration of sodium does not change. By contrast, bicarbonate and other non-chloride anions are rapidly absorbed with sodium and removed from the filtrate 7 Fig. As sodium and non-chloride anions are absorbed in the early proximal tubule segments S1 and S2the chloride concentration in the lumen of the proximal tubule increases. By the time the tubular fluid reaches the last segment of the proximal tubule S3uipocloremia chloride concentration is high with respect to its plasma concentration allowing chloride to be passively absorbed down its concentration gradient Fig.
The transepithelial permeability for chloride is higher than the permeability for bicarbonate so that despite the peritubular-to-lumen gradient for bicarbonate, the transport of chloride leaving the lumen exceeds the bicarbonate entering the tubular fluid. B Yipocloremia high chloride concentration in the lumen also favors transcellular and paracellular transport. Intercellular junctions in the later proximal tubule become more permeable to chloride facilitating paracellular transport.
The organic acid formic or oxalic acid is recycled into cells. Cahsas the early portion of the proximal tubule, chloride absorption also occurs via apical chloride-anion formate, oxalate, base exchangers and it exits the cell via basolateral membrane transporters 8 Fig.
Manifestaciones clínicas by Fernando Marein Reyes on Prezi
In hyperchloremic metabolic acidosis due to HCl- or ammonium chloride-loading, the chloride reabsorption in the proximal tubule is reduced, in part, because of the reduction in organic anion transporters that facilitate sodium chloride transport 9 as well as the reduction in lumen-to-peritubular gradient for chloride. Chloride enters the TALH cell and leaves its basolateral aspect down an electrogenic chloride channel or via the electroneutral potassium chloride co-transporter.
The movement of chloride through the basolateral chloride channel CLC-NKB contributes to the generation of a transepithelial positive lumen to negative basolateral potential gradient. ROMK potassium channels on the apical TALH cell membrane contributes to the lumen positive intracellular negative potential through the conductive jipocloremia of potassium ions from cell to lumen.
The tight coupling between sodium and chloride transport in the TALH is underscored by one of the varieties hipockoremia Bartter syndrome in which defects in basolateral chloride channels disrupt sodium chloride reabsorption and mimics the renal defect observed with abnormal NKCC2 proteins. Although other transporters on the peritubular side of the TAL cell such as the KCl co-transporter will transport chloride in a sodium-independent manner, most of the chloride that is absorbed by the TALH is coupled with sodium reabsorption.
Therefore, factors that increase sodium reabsorption in this segment will also increase chloride reabsorption. On the other hand, when chloride accumulates in the cell due to defects in basolateral chloride channel exit pathway, NKCC2 transport is blocked. When NKCC2 is stimulated, for example by antidiuretic hormone, chloride entry is increased, but basolateral Cl-conductance is also enhanced.
In the distal convoluted tubule, sodium and chloride are transported from the lumen into the cell by a sodium-chloride co-transporter NCC 11 Fig. Further regulation of NCC and NKCC may occur through WNK kinases, which may serve as chloride sensors 12 and can regulate these transporters by modifying trafficking or their phosphorylation state. Thus, the segments of distal convoluted tubule display direct coupling of sodium and chloride transport via the NCC and indirect coupling of transport via passive movement down an electrochemical gradient.
The collecting duct plays an important role in determining the chloride content of the hipocloremiq urine. Chloride reabsorption in this portion of the nephron helps to conserve chloride in response to low chloride intake and can contribute to the jipocloremia effects of a high sodium chloride diet.
Most of sodium that is reabsorbed in the collecting duct occurs in principal cells via aldosterone-regulated apical epithelial sodium channels. Chloride reabsorption in the collecting duct can occur via paracellular chloride absorption that is driven by the lumen negative transepithelial potential generated by lumen-to-cell sodium flow through ENaC Fig. In addition, in B-type and non-A non-B type intercalated cells, chloride can be transported via pendrin, a chloride-bicarbonate exchanger, with chloride moving from lumen-to-cell while bicarbonate secreted into the lumen Causzs.
The relationship between various sodium and chloride transport processes in this portion of the nephron was illustrated in a recent paper by Vallet and colleagues. A dissociation between sodium and chloride transport was observed, however, with the inhibition of the sodium-chloride co-transporter with hydrochlorothiazide, pendrin levels fell but ENaC levels increased. NaCl restriction increased pendrin expression. If NDCBE transport is coupled with pendrin-mediated chloride-bicarbonate exchange, the two transporters working together could result in net sodium chloride reabsorption from the lumen, as the bicarbonate recycles into and out of the cell while sodium and chloride enter the cell 17 Fig.
Factors which alter the ratio of the bipocloremia or activities of these two anion exchangers may determine the net impact on bicarbonate secretion and chloride reabsorption. Another transporter which may be involved in excretion of excessive chloride in the body is the Slc26A9 transporter which may act as a chloride channel in the medullary portions of xausas collecting duct.
Knockout of this gene results in a predisposition to hypertension. Hipoclorsmia deficient in this protein develop hypertension when exposed to a high sodium chloride load. A portion of chloride absorption is driven by a lumen negative potential and paracellular movement. The net result would be the transport of 1 sodium and 1 chloride into the cell. The serum chloride level is generally measured as a concentration of chloride in a volume of serum.
The biologically active chloride concentration is the concentration of free chloride in the plasma water. Chloride is most frequently measured by using a silver-chloride electrode either in a direct or diluted serum sample.
When the solid components of the serum are very high, as can occur with hypertriglyceridemia and multiple myeloma, pseudohypochloremia can occur. Pseudohyperchloremia can also be seen in bromide or iodide intoxication. The interaction of bromide or iodide with the silver-chloride electrode generates a greater voltage change than does chloride giving the impression of excessive chloride in the blood.
Hyperchloremia can result from a number of mechanisms Table 1. Water loss in excess of chloride loss can raise the chloride concentration. As there may also be a component of volume depletion with more severe degrees of dehydration, conservation of chloride as well as sodium occurs via increased proximal tubule reabsorption of chloride and other solutes, and reduced delivery of chloride and sodium to more distal nephron segments.
The enhanced proximal tubular reabsorption of tubular fluid and its contents will not necessarily change the chloride concentration as the absorption of fluid occurs isotonically. The treatment of water deprivation is the judicious administration of electrolyte-free water which will reduce both the sodium and chloride concentrations.
Hyperchloremia can occur when the body is exposed to fluids that are high in chloride. The sudden large input of seawater average salinity is 3. A less extreme example of hyperchloremia with an excessive sodium chloride load is the administration of large volumes of isotonic 0. It hipovloremia noteworthy that when a normal individual is given a large bolus of isotonic saline, it may take up to 2 days to return to the pre-treatment state of sodium and chloride balance.
The relatively slow excretory response to isotonic saline may be related to effects of chloride loads on renal blood flow and on glomerular filtration tubuloglomerular feedback. Although down-regulation of chloride reabsorptive transporter activities occur with sodium chloride loading, 142526 the rapidity of the reduction of these transporters is not well defined.
With isotonic saline administration, the bicarbonate concentration may also fall as the chloride concentration rises. Besides dilution of the plasma bicarbonate with administration of supraphysiologic chloride-containing, base-free solutions such as normal saline, other factors may play roles in the fall in bicarbonate and rise in chloride levels.
Urinary bicarbonate losses may contribute hipocloremix the fall in serum bicarbonate hkpocloremia as there may be a reduction in the reabsorptive threshold for bicarbonate with volume expansion. The reduced excretion of chloride in comparison to sodium and potassium suggested the urinary loss of other anions such as bicarbonate and other organic anions that may also contribute to a fall in the serum bicarbonate concentration.
Nevertheless, certain hipocloreima situations may favor the use of normal saline including in patients with hypochloremic metabolic alkalosis or those with cerebral edema. Hyperchloremia also occurs when hydrochloric acid HCl is added to the blood.
HCl is rarely given as a direct acidifying agent but can be created from the metabolism of ammonium chloride or cationic amino acids such as lysine and arginine.
Thus for every milliequivalent of HCl added, a milliequivalent of bicarbonate is consumed and converted to CO 2 so that the chloride level rises to the same extent as the bicarbonate level falls. In proximal RTA type 2bicarbonate reabsorption in the proximal tubule is impaired resulting in increased losses of bicarbonate out of this segment. There is also some disruption of chloride reabsorption because the lack of the extraction of bicarbonate prevents the normal rise in luminal chloride concentration.
Nevertheless, in proximal RTA, the reduction in bicarbonate transport is greater hpiocloremia the reduction in chloride transport so that there is relatively more chloride reabsorbed causae bicarbonate. If carbonic anhydrase inhibition is used as a model for proximal RTA, chloride reabsorption appears to be less impaired than bicarbonate reabsorption as is reflected by a relatively modest increase in the urinary chloride excretion rate while the rates of excretion of sodium, potassium and, presumably, bicarbonate are markedly increased.
As a result, the HCl generated by metabolism results in a fall in bicarbonate that is not compensated for by the generation and hlpocloremia of bicarbonate and excretion of chloride. As long as renal function cauaas preserved, non-chloride acid anions do not accumulate in the systemic circulation maintaining a relatively normal anion gap. Indeed, the renal excretion of phosphate and sulfate anions generated from the metabolism of phosphorus- and sulfur-containing amino acids 31 is actually stimulated by acidosis.
Another cause of hyperchloremic metabolic acidosis casas with diarrhea.
In many segments of the gastrointestinal tract and associated exocrine organs such as the pancreas, bicarbonate is secreted into the gut in hipoclorejia for chloride so that loss of bicarbonate, especially in secretory forms of diarrhea, can be associated with bicarbonate losses which are associated with chloride retention. Repair of hyperchloremic forms of metabolic acidosis involves stopping the ongoing cause of bicarbonate loss or HCl generation while giving the patient bicarbonate or base equivalents e.
During the generation of metabolic acidosis, there are initially net sodium losses and volume contraction. With more prolonged acidosis, there may be sodium retention due to high aldosterone levels and upregulation of ENaC in the collecting duct. The associated volume re-expansion with bicarbonate may contribute to the fall in chloride.
When the kidneys repair the metabolic acidosis, ammonium hopocloremia is excreted in the urine while bicarbonate that is made in the proximal tubule as a byproduct of the glutamine metabolism is returned to the blood. The kidney plays a key role in maintaining chloride balance in the body.
Although renal chloride transport is coupled with sodium transport, chloride transport may sometimes diverge from sodium transport. Hyperchloremia can result from a variety of conditions including water depletion, excessive chloride exposure and metabolic acidosis. The pathogenic cause of hyperchloremia will provide guidance on how the disturbance should be treated: Regulation of renal blood flow by plasma chloride.
Chloride regulates afferent arteriolar contraction in response to depolarization. Resuscitation-induced intestinal edema and related dysfunction: Is hyperchloremia associated with mortality in critically ill patients? A prospective cohort study. Association of hyperchloremia with hospital mortality in critically ill septic patients. Fluid accumulation, survival and recovery of kidney function in critically ill patients with acute kidney injury.
Sodium, bicarbonate, and chloride absorption by the hopocloremia tubule.