Cellular Mechanisms of Renal Tubular Acidification
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Bicarbonate
Lumen (anatomy)
Kidney tubules
Acid–base homeostasis
Whether altered reabsorption of bicarbonate by the superficial distal nephron contributes to the renal response to a chronic dietary bicarbonate challenge is not known. These micropuncture studies were done in control, NaHCO3-loaded, and NaCl-loaded Munich-Wistar rats to determine whether this dietary maneuver altered acidification in this nephron segment as evaluated in situ. Urinary bicarbonate excretion of NaHCO3-loaded animals was higher than control for each day of a 7-day study period, but bicarbonate excretion for animals identically loaded with NaCl was not sustained above control. Bicarbonate transport by the superficial distal nephron was assessed using paired collections from this segment. Net bicarbonate reabsorption was observed in all three groups. Reabsorption was lower in NaHCO3-loaded vs. control (11 vs. 25 pmol/min, P less than 0.01) but that for NaCl-loaded animals was not. The data indicate that reduced reabsorption of bicarbonate by the superficial distal nephron of rats contributes to the renal response to a chronic dietary bicarbonate challenge as evaluated in situ.
Bicarbonate
Sodium bicarbonate
Renal physiology
Net acid excretion
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The kidney plays a major role in the regulation of acid-base balance. This process is mainly dependent on H+ secretion in the tubular lumen. Two acid extruder proteins are involved: the Na+/H+ exchanger and H(+)-ATPase. Studies using in vivo and in vitro microperfusion and isolated membrane vesicles have clearly demonstrated that the Na+/H+ exchanger is the main mechanism regulating H+ secretion/HCO3- reabsorption along the proximal nephron. Moreover, several reports indicate that this protein is involved in intracellular pH (pHi) regulation. Newer studies using molecular biology techniques have identified at least five isoforms of the Na+/H+ exchanger: NHE-1 is the housekeeping isoform, while NHE-3 seems to be implicated in transepithelial acid-base transport, although other isoforms could be involved too. H(+)-ATPase is the major acid extruder protein along the distal nephron, but it is also expressed along the proximal tubule, where a Na(+)-independent bicarbonate reabsorption has been described. There are a few studies indicating that the proton pump participates in pHi regulation, particularly in the presence of a large acid load. Its absence along the distal nephron may be one of the causes of distal tubular acidosis.
Sodium–hydrogen antiporter
Acid–base homeostasis
Intracellular pH
Bicarbonate
Loop of Henle
Renal physiology
Amiloride
Renal sodium reabsorption
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Electrolyte and acid-base balance was evaluated in 14 high UF (124 +/- 7 ml/min) hemodiafiltration sessions. The dialysate contained (in mEq/l): Na 138-140, K 2-3, Ca 3.5, Mg 0.5-0.7, Cl 106-110, acetate 38 or acetate 3 and bicarbonate 35-38. The fluid, infused in postdilutional mode, was 23.5 +/- 21 per session (session length 203 +/- 22 minuti), 80% containing Na 138, K 2, Ca 3.5, Mg 1, Cl 109.5, acetate 35 and 20% Na 145, HCO3 100, Cl 45. The balance was: negative for Na (-255 +/- 220 mEq), for K (-74 +/- 22 mEq) and for Mg (-166 +/- 141 mg), positive for Ca (215 +/- 147 mg) and for acetate (590 +/- 15 and 966 +/- 412 mmol); the electrolytes and bicarbonate plasma values were within of close to normal limits during the session. An unphysiological feature was the positive balance of acetate which, though, was metabolized during the interdialytic period as to return to normal predialytic values. Therefore, in high UF HDF, the above combination of dialysate and reinfusate allows a reasonable electrolyte and acid-base balance; however, bicarbonate should be the only buffer in order to avoid unphysiological levels of other buffers in the biological fluids.
Bicarbonate
Acid–base homeostasis
Ultrafiltration (renal)
Equivalent
Acid–base reaction
Base (topology)
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Unilateral pyelonephritis was induced in the rat and micropunture techniques were used to assess nephron function in individual nephrons from chronically diseased and normal kidneys in the same animals. Conventional clearances were performed simultaneously in the same kidneys. The clearance data indicated that the chronically diseased kidney of the rat, like that of the dog and man in a nonuremic environment, behaved in a predictable and organized manner. Analysis of data from micropuncture of the proximal tubules of individual nephrons from the chronically diseased kidneys indicated that salt and water reabsorption proceeded in a manner indistinguishable from that in nephrons of the contralateral control kidneys in the same animals. There was no evidence of intrinsic lesions affecting salt and water transport in the portions of the nephrons examined.
Kidney tubules
Kidney Glomerulus
Renal physiology
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Previous micropuncture studies utilizing indirect methods to estimate bicarbonate transport in the rat superficial distal tubule have indicated that the distal bicarbonate reabsorptive process normally operates well below the saturation level. Recent studies from our laboratory failed to demonstrate a spontaneous acid disequilibrium pH in this segment, implying that the bicarbonate reabsorptive rate was less than previously estimated. The purpose of the present experiments were 1) to measure the rate of absolute bicarbonate reabsorption by the rat superficial distal tubule while controlling bicarbonate delivery, and 2) to examine the effects of alterations in acid-base status on the rate of bicarbonate reabsorption. Five groups of rats in different states of acid-base balance were studied. No significant bicarbonate reabsorption was detected in the control hydropenic, combined respiratory acidosis-metabolic alkalosis, acute respiratory acidosis, or acute metabolic acidosis groups. In contrast, metabolic acidosis of 3 days duration resulted in a significant bicarbonate reabsorptive rate of 52.6 +/- 13.9 pmol . mm-1 . min-1. The observation of significant bicarbonate reabsorption in the distal tubule only during chronic metabolic acidosis of 3 days duration is compatible with adaptation of this normally low-capacity segment to chronic changes in systemic acid-base states.
Bicarbonate
Acid–base homeostasis
Respiratory acidosis
Alkalosis
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The low bath bicarbonate concentration ([ HCO3- ]) used by a nephrology group in Japan (25.5 mEq/L), coupled with a bath [acetate] of 8 mEq/L, provided an opportunity to study the acid-base events occurring during hemodialysis when HCO3- flux is from the patient to the bath. We used an analytic tool that allows calculation of HCO3- delivery during hemodialysis and the physiological response to it in 17 Japanese outpatients with an average pre-dialysis blood [ HCO3- ] of 25 mEq/L. Our analysis demonstrates that HCO3- addition is markedly reduced and that all of it comes from acetate metabolism. The HCO3- added to the extracellular fluid during treatment (19.5 mEq) was completely consumed by H+ mobilization from body buffers. In contrast to patients dialyzing with higher bath [ HCO3- ] values in the US and Europe, organic acid production was suppressed rather than stimulated. Dietary analysis indicates that these patients are in acid balance due to the alkaline nature of their diet. In a larger group of patients using the same bath solution, pre-dialysis blood [ HCO3- ] was lower, 22.2 mEq/L, but still in an acceptable range. Our studies indicate that a low bath [ HCO3- ] is well tolerated and can prevent stimulation of organic acid production.
Bicarbonate
Acid–base homeostasis
Acid–base reaction
Homeostasis
Organic acid
Nephrology
Sodium bicarbonate
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A study was conducted to determine the relative acidogenicities of dietary supplements of the anions, chloride, sulfate, and monohydrogen phosphate (HPO4−2) in diets of young Leghorn chicks. Chloride supplements ranged from 40 to 240 meq/kg, sulfate ranged from 100 to 240 meq/kg, and monohydrogen phosphate ranged from 120 to 240 meq/kg of diet. Anions were substituted on a charge-equivalent basis for dietary carbonate (CO3–2) at 7 to 10 days of age, and blood samples were taken for measurement of blood hydrogen ion concentration, carbon dioxide tension, and bicarbonate concentration (calculated) on the 1st day and after several (usually 8) days of experiment. The effects of anions on acid-base balance were evident on the 1st day and generally persisted for the duration of experiments. Chloride consistently depressed blood pH and blood bicarbonate concentration. Sulfate was acidogenic, but less so than chloride, whereas monohydrogen phosphate did not affect blood measures of acid-base balance.
Bicarbonate
Acid–base homeostasis
Base (topology)
Acid–base reaction
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Because maintaining a normal body pH is essential to the efficient functioning of many physiologic processes, the body has a number of mechanisms that prevent pH fluctuations. Some of these prevent minute-to-minute pH fluctuations over the course of the day, whereas others maintain pH balance from day to day. The kidney plays a key role in both processes. The renal process of bicarbonate reclamation prevents the loss of bicarbonate in the urine and, thus, maintains plasma levels of one substrate that is instrumental to preventing minute-to-minute pH fluctuations. The other renal process, bicarbonate regeneration, replenishes the body's supply of bicarbonate and, thus, maintains pH balance on a day-to-day basis. This article will discuss basic principles of acid-base physiology, the mechanisms that prevent fluctuations in body pH, and the renal processes involved in maintaining a homeostatic pH environment.
Bicarbonate
Acid–base homeostasis
Homeostasis
Net acid excretion
Renal physiology
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Bicarbonate
Acetazolamide
Convoluted tubule
Tubular fluid
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Bicarbonate
Carbonic acid
Tubule
Acid–base homeostasis
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