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The Generation and Maintenance of Metabolic Alkalosis

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The Generation and Maintenance of Metabolic Alkalosis View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 1 (1972), p. 306—321 The generation and maintenance of metabolic alkalosis DONALD W. SELDIN and FLOYD C. RECTOR JR. Department ofInternal Medicine,The University of Texas Southwestern Medical School atDallas, Dallas, Texas The pathogenesis of chronic metabolic alkalosis involves of hydrogen ions, both in the proximal and distal portions two distinct physiologic derangements. First, there must of the nephron [1, 2]. According to this model, hydrogen be a loss of acid or gain of alkali in order to generate the ions are secreted into the tubular lumen in exchange for alkalosis. Renal or extra-renal factors may be responsible. filtered sodium. It is not clear whether hydrogen secretion If the alkalosis is generated by the kidney, the net excretion and sodium reabsorption are tightly coupled in an ob- of acid in the form of titratable acid and ammonia must be ligatory fashion or only loosely coupled through electrical increased, at least transiently, to a level greater than the forces. Malnic and de Mello-Aires [3] have recently pre- sum of the acid load originating from both dietary and sented evidence that in the absence of sodium in luminal metabolic acid production and from alkali loss into the fluid, the secretion of hydrogen continues at a near normal feces. For each mEq of excess net acid excretion by the rate. Presumably under these conditions (tubular fluid kidney, one mEq of new bicarbonate will be generated and containing principally choline bicarbonate) the secretion of added to the blood. The kidney is not the only source for hydrogen would be accompanied by the inward movement the generation of metabolic alkalosis. Extra-renal factors, of chloride along its electrochemical gradient. Their results, such as vomiting, special types of diarrhea, and the like, therefore, would suggest that under normal physiologic may be the source of the alkali load. conditions, the reabsorption of sodium and the secretion The generation of alkali by either renal or extra-renal of hydrogen are only very loosely coupled. mechanisms may not be sufficient to produce sustained The process of hydrogen secretion by the tubule may metabolic alkalosis. Under normal circumstances the kidney involve a number of reduced substrates in oxidation- has an enormous capacity to excrete NaHCO3. In conse- reduction reactions, but ultimately the hydrogen must be quence, increased amounts of NaHCO3 which gain access derived from the splitting of water with the liberation of to the blood may be promptly excreted into the urine. hydroxyl ions into the cell. The hydroxyl ions subsequently Clearly, then, in order to maintain metabolic alkalosis, the react with C02, under the catalytic impact of the enzyme increased amounts of bicarbonate in the glomerular filtrate carbonic anhydrase, to form bicarbonate. In this respect, must be reclaimed by a commensurate rise in tubular it is of interest that recent evidence indicates that the reabsorption. During chronic stable metabolic alkalosis, hydroxyl ion, not water or carbonic acid, is the primary the tubular reabsorption of bicarbonate will be persistently substrate for carbonic anhydrase [4]. The bicarbonate ions elevated, while the net excretion of acid will have returned formed by this process leave the cell, presumably by passive to a level equal to the net acid load. The present paper will diffusion down their clectrochemical gradient, along with be concerned with the factors involved in the generation the reabsorbed sodium. Thus for each hydrogen secreted, and maintenance of metabolic alkalosis. Physiologic deter- one sodium bicarbonate is added to renal venous blood, minants will be explored. Clinical derangements will then The fate of the secreted hydrogen depends upon the be examined. composition of the tubular fluid. As long as bicarbonate is present in the luminal fluid, it will preferentially react with the hydrogen to form H2O and CO2. However, as the The Maintenance of Metabolic Alkalosis by the Kidney removal of bicarbonate nears completion, the pH of the There is now abundant evidence that both the reabsorp- tubular fluid will begin to fall and the secreted hydrogen tion of bicarbonate and the excretion of titratable acid and will react with filtered buffers to form titratable acid, and ammonium are mediated primarily by the tubular secretion with ammonia to form ammonium. From a quantitative standpoint, the formation of titratable acid and ammonium © 1972, by the International Society of Nephrology ions normally accounts for only 2 to 3 % of total hydrogen 306 Metabolic alkalosis 307 secretion, while the remainder is consumed in the con- or threshold level, reabsorption is complete, and no bi- servation of filtered bicarbonate. carbonate is lost into the urine. Below this critical plasma The level at which the plasma bicarbonate concentration concentration, reabsorption is a linear function of the will be maintained is dependent in some manner on the filtered load. However, as the plasma concentration is total or maximal hydrogen secretory capacity of the kidney. raised above this threshold level, reabsorption does not Since the rate of hydrogen secretion is influenced by the pH increase proportionately and excretion of bicarbonate into of the tubular fluid, the maximal capacity of the system can the urine begins. Further increases in plasma concentration only be assessed when the tubular fluid is maintained produce only slight changes in reabsorption and the system relatively alkaline. This requires that the plasma bicarbonate exhibits an apparent transport maximum. concentration be progressively elevated by infusions of There is, however, no true transport maximum for sodium bicarbonate solutions, and, as a consequence, a bicarbonate reabsorption (via hydrogen secretion). Pitts highly distorted physiologic state is induced: alkaline blood and Lotspeich [5] found the maximum rate of bicarbonate pH, elevated P02, hypernatremia, expanded extracellular reabsorption is not constant, but varies proportionately to fluid volume, variable glomerular filtration rate. The spontaneous or chronically induced changes in GFR. method of measuring the maximal rate of hydrogen secre- Bicarbonate reabsorption, expressed as mEq/liter GFR, tion, therefore, introduces a number of variables which however, appeared to be constant. Thompson and Barrett could independently influence the rate of secretion and [6], on the other hand, observed that acutely reducing GFR obscure the true capacity of the system. by partial obstruction of the aorta above the renal arteries The hydrogen secretory system operates in such a manner did not change the absolute rate of bicarbonate reabsorp- that when the plasma bicarbonate is below a certain critical tion, but reabsorption expressed as mEq/liter GFR rose. 5 . S 0 S • • • S S. •.. S . 0. 0 E 03 0. 0 Mean concentration of bicarbonate in -c glomerular filtrate during control period C) C) 0C2 -D C) 0 10 20 30 40 50 60 70 Concentration of bicarbonate in glomerular filtrate in mEcj]liter Fig. 1. Maximum bicarbonate reabsorptive capacity in normal ruts. 308 Seldin/Rector Lemieux et al [7] have recently reexamined the relation ate concentration would stabilize at a concentration be- between bicarbonate reabsorption and GFR by constricting tween the threshold level and the maximal capacity, even either one or both renal arteries acutely and chronically. in the face of fairly large loads of sodium bicarbonate. In both the acute and chronic experiments, absolute reab- This assumption, however, is clearly an over-simplifica- sorption paralleled the changes in GFR and reabsorption tion, particularly with respect to the rat. Fig. 1, based on expressed as mEq/liter GFR remained constant. Thus, unpublished data from our laboratory, shows a bicarbonate with the exception of the studies of Thompson and Barrett titration study in a group of normal rats. As bicarbonate [6], the observed relation between bicarbonate reabsorption concentration in the glomerular filtrate is progressively and GFR is similar to that observed between total sodium raised, reabsorption is complete until the concentration reabsorption and GFR, and indicates that the mechanisms exceeds 35 mEq/liter. The maximal capacity in these animals responsible for glomerulotubular balance involve not only was approximately 42 mEq/liter. It would be predicted, sodium reabsorption, but also the secretion of hydrogen therefore, that rats given chronic sodium bicarbonate loads ions. would stabilize their plasma bicarbonate concentration The participation of hydrogen secretion in glomerulo- somewhere between 35 and 42 mEq/liter. tubular balance has much the same physiologic significance To examine this question, awake rats were placed in as does the participation of total sodium reabsorption. The restraining cages and infused continuously with sodium roughly proportionate changes between the rate of hydro- bicarbonate at a rate of 1.46 mEq/l0 hr. As shown in gen secretion and GFR serve to prevent both marked Fig. 2, the bicarbonate concentration in glomerular filtrate augmentation of titrable acid and ammonium excretion, was approximately 30 mEq/liter (comparable to a plasma with the subsequent production of metabolic alkalosis when bicarbonate of 27 mEq/liter) at the beginning of the in- GFR is reduced, and bicarbonate wastage and metabolic fusion and rose to 36 mEq/liter during the next 20 hours.
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