Effects of acid-base disturbances on renal handling of magnesium in the dog

1986 ◽  
Vol 70 (3) ◽  
pp. 277-284 ◽  
Author(s):  
Norman L. M. Wong ◽  
Gary A. Quamme ◽  
John H. Dirks
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Indirect Effect ◽  
Metabolic Alkalosis ◽  
Distal Tubule ◽  
Acid Base ◽  
Renal Handling ◽  
Chronic Metabolic Acidosis ◽  
Magnesium Transport

1. Clearance and micropuncture studies were performed in four groups of acutely thyropara-thyroidectomized animals to study the effects of alkalosis and acidosis on the renal handling of magnesium. 2. Our results indicate that chronic metabolic acidosis reduces, whereas acute metabolic alkalosis enhances, magnesium reabsorption. 3. The site within the nephron where absorption of magnesium increases or decreases during acid-base disturbances was beyond the late proximal tubule. 4. Tubular fluid bicarbonate was also measured in these experiments, and the results indicated that magnesium reabsorption in the distal tubule correlated to bicarbonate delivery. However, whether this was a direct or an indirect effect of bicarbonate on magnesium transport could not be delineated.

Ureagenesis: evidence for a lack of hepatic regulation of acid-base equilibrium in humans

2004 ◽  
Vol 286 (1) ◽  
pp. F94-F99 ◽  
Author(s):  
Markus Hosch ◽  
Juergen Muser ◽  
Henry N. Hulter ◽  
Reto Krapf
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Acid Base ◽  
Chronic Metabolic Acidosis ◽  
Base Equilibrium ◽  
Acid Base Equilibrium ◽  
Wide Range ◽  
Per Se ◽  
Hepatic Regulation ◽  
Bicarbonate Infusion

Ureagenesis in the liver consumes up to 1,000 mmol of [Formula: see text]/day in humans as a result of [Formula: see text] + [Formula: see text] → urea + CO2 + 3H2O. Whether the liver contributes to the regulation of acid-base equilibrium by controlling the rate of ureagenesis and, therefore, [Formula: see text] consumption in response to changes in plasma acidity has not been adequately evaluated in humans. Rates of ureagenesis were measured in eight healthy volunteers during control, chronic metabolic acidosis (induced by oral administration of CaCl2 3.2 mmol·kg body wt-1·day-1 for 11 days), and recovery as well as during bicarbonate infusion (200 mmol over 240 min; acute metabolic alkalosis). Rates of ureagenesis were correlated negatively with plasma [Formula: see text] concentration both during adaption to metabolic acidosis and during the chronic, steady-state phase. Thus ureagenesis, an acidifying process, increased rather than decreased in metabolic acidosis. During bicarbonate infusion, rates of ureagenesis decreased significantly. Thus ureagenesis did not appear to be involved in the regulated elimination of excess [Formula: see text]. The finding of a negative correlation between ureagenesis and plasma [Formula: see text] concentration over a wide range of [Formula: see text] concentrations, altered both chronically and acutely, suggests that the ureagenic process per se is maladaptive for acid-base regulation and that ureagenesis has no discernible homeostatic effect on acid-base equilibrium.

Relative influence of respiratory and metabolic acid-base changes on renal acid excretion

1960 ◽  
Vol 198 (2) ◽  
pp. 237-243 ◽  
Author(s):  
Daniel H. Simmons ◽  
Nicholas A. Assali ◽  
Melvin Avedon
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Time Lag ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Acid Excretion ◽  
Acid Base ◽  
Urine Ph ◽  
Renal Handling ◽  
Anesthetized Dogs

Arterial pH of anesthetized dogs was maintained constant for 90 minutes during continuous infusion of 0.15 m HCl or NaHCO3 (0.3 cc/kg/min.) by adjusting alveolar ventilation with a respiration pump. This resulted in simultaneous metabolic acidosis and respiratory alkalosis (acid infusion) or metabolic alkalosis and respiratory acidosis (base infusion) equal in degree with respect to their effect on blood pH. Since urine pH dropped and renal acid excretion increased during metabolic acidosis and respiratory alkalosis, while pH rose and acid excretion decreased during metabolic alkalosis and respiratory acidosis, metabolic acid-base disturbances appear to exert more influence on renal acid excretion than do respiratory disturbances comparable in terms of their effect on pH. This difference in response was shown not to be due to a time lag in renal response to respiratory disturbances, nor could it be explained by effects on urine flow, renal hemodynamics or renal handling of sodium.

Effects of pH on potassium transport by renal distal tubule

1982 ◽  
Vol 242 (5) ◽  
pp. F544-F551 ◽  
Author(s):  
B. A. Stanton ◽  
G. Giebisch
Keyword(s):  
Metabolic Acidosis ◽  
Distal Tubule ◽  
Potassium Transport ◽  
Free Flow ◽  
Acid Base Balance ◽  
Acid Base ◽  
Solution Ph ◽  
Fluid Delivery ◽  
Urinary Potassium ◽  
Potassium Secretion

To determine the relative importance of plasma and luminal pH changes as factors regulating potassium secretion by rat distal tubule, superficial tubules were continuously microperfused in vivo. The effects of changes in plasma pH were examined by producing acute systemic metabolic acidosis or alkalosis and holding luminal flow rate, solute composition, and pH constant by microperfusion. Alternatively, the effect of luminal solution pH was evaluated by microperfusing tubules with solutions buffered to either pH 6.5 or 8.0 at constant systemic acid-base balance. Net transport of Na and K and the pH of the luminal fluid were measured. Results showed that metabolic acidosis inhibited and metabolic alkalosis stimulated potassium secretion. Increased luminal fluid pH, in contrast, did not stimulate potassium transport. In experiments in which metabolic acidosis produced a diuresis, urinary potassium excretion was enhanced compared with hydropenic controls. Free-flow micropuncture studies revealed that the rate of fluid delivery to the distal tubule was 45% greater during acidosis compared with control and that potassium secretion increased in both the distal and collecting tubule. Since the rate of fluid delivery is a potent stimulus of potassium secretion in the distal tubule, it is concluded that the stimulus of increased delivery of fluid, observed in free-flow conditions, masked the inhibitory effect of acidosis on potassium transport. Potassium transport by the distal tubule, during acid-base disorders, is regulated by plasma pH and the rate of delivery of fluid but is not stimulated by alkalinization of the luminal fluid.

Basolateral membrane H-OH-HCO3 transport in the proximal tubule

1989 ◽  
Vol 256 (5) ◽  
pp. F751-F765
Author(s):  
P. A. Preisig ◽  
R. J. Alpern
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Basolateral Membrane ◽  
Respiratory Acidosis ◽  
Cell Voltage ◽  
Transport Mechanisms ◽  
Transport Capacity ◽  
Chronic Metabolic Acidosis

This review focuses on the basolateral membrane mechanisms of H-OH-HCO3 transport in the proximal tubule. The mechanism that has the greatest transport capacity and mediates most of transepithelial H-HCO3 transport is the electrogenic, Na-3HCO3 cotransporter. This transporter has been extensively characterized in the salamander, rat, and rabbit proximal tubule, and has now been found in a number of other epithelia that effect transepithelial NaHCO3 transport. Transporter rate is sensitive to intra- and extracellular [Na], intra- and extracellular [HCO3]/pH, and cell voltage. Adaptations in transporter activity have been demonstrated in chronic metabolic acidosis and alkalosis, chronic respiratory acidosis and alkalosis, and chronic hyperfiltration. In addition to the Na-3HCO3 cotransporter, the basolateral membrane possesses both Na-dependent and -independent Cl-HCO3 exchangers, a H leak, and in the S3 proximal tubule an Na-H antiporter. The role of these H-OH-HCO3 transport mechanisms in transcellular HCO3 and Cl absorption and pHi defense is discussed.

Chronic metabolic acidosis upregulates rat kidney Na-HCO 3 − cotransporters NBCn1 and NBC3 but not NBC1

2002 ◽  
Vol 282 (2) ◽  
pp. F341-F351 ◽  
Author(s):  
Tae-Hwan Kwon ◽  
Christiaan Fulton ◽  
Weidong Wang ◽  
Ira Kurtz ◽  
Jørgen Frøkiær ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Rat Kidney ◽  
Free Access ◽  
Thick Ascending Limb ◽  
Acid Base Balance ◽  
Acid Base ◽  
Chronic Metabolic Acidosis ◽  
Daily Water Intake ◽  
Base Balance ◽  
Access To Water

Several members of the Na-HCO[Formula: see text] cotransporter (NBC) family have recently been identified functionally and partly characterized, including rkNBC1, NBCn1, and NBC3. Regulation of these NBCs may play a role in the maintenance of intracellular pH and in the regulation of renal acid-base balance. However, it is unknown whether the expressions of these NBCs are regulated in response to changes in acid-base status. We therefore tested whether chronic metabolic acidosis (CMA) affects the abundance of these NBCs in kidneys using two conventional protocols. In protocol 1, rats were treated with NH4Cl in their drinking water (12 ± 1 mmol · rat−1 · day−1) for 2 wk with free access to water ( n = 8). Semiquantitative immunoblotting demonstrated that whole kidney abundance of NBCn1 and NBC3 in rats with CMA was dramatically increased to 995 ± 87 and 224 ± 35%, respectively, of control levels ( P < 0.05), whereas whole kidney rkNBC1 was unchanged (88 ± 14%). In protocol 2, rats were given NH4Cl in their food (10 ± 1 mmol · rat−1 · day−1) for 7 days, with a fixed daily water intake ( n = 6). Consistent with protocol 1, whole kidney abundances of NBCn1 (262 ± 42%) and NBC3 (160 ± 31%) were significantly increased compared with controls ( n = 6), whereas whole kidney rkNBC1 was unchanged (84 ± 17%). In both protocols, immunocytochemistry confirmed upregulation of NBCn1 and NBC3 with no change in the segmental distribution along the nephron. Consistent with the increase in NBCn1, measurements of pH transients in medullary thick ascending limb (mTAL) cells in kidney slices revealed two- to threefold increases in DIDS- sensitive, Na+-dependent HCO[Formula: see text] uptake in rats with CMA. In conclusion, CMA is associated with a marked increase in the abundance of NBCn1 in the mTAL and NBC3 in intercalated cells, whereas the abundance of NBC1 in the proximal tubule was not altered. The increased abundance of NBCn1 may play a role in the reabsorption of NH[Formula: see text] in the mTAL and increased NBC3 in reabsorbing HCO[Formula: see text].

scholarly journals Renal ATP Citrate Lyase (ATP CL) Protein Localizes throughout the Nephron and Increases Only in the Proximal Tubule with Chronic Metabolic Acidosis (CMA)

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 336A-336A
Author(s):  
Krishna Puttaparthi ◽  
Thomas Rogers ◽  
Nabil A Elshourbagy ◽  
Moshe Levi ◽  
Joel Z Melnick
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Atp Citrate Lyase ◽  
Chronic Metabolic Acidosis ◽  
Citrate Lyase

Effects of Intraluminal sulfate on electrolyte transfers along the perfused rat nephron

1981 ◽  
Vol 59 (2) ◽  
pp. 122-130 ◽  
Author(s):  
Gary A. Quamme
Keyword(s):  
Proximal Tubule ◽  
Chloride Transport ◽  
Distal Tubule ◽  
Phosphate Transport ◽  
Loop Of Henle ◽  
Magnesium Transport ◽  
Calcium And Magnesium ◽  
A Site ◽  
Distal Delivery

Superficial nephrons were perfused in vivo to determine the effect of intraluminal sulfate (1–20 mM) on electrolyte reabsorption in the rat with special reference to calcium and magnesium transport. This technique allowed us the opportunity of investigating separate electrolyte transfers without alteration of extrarenal influences. The major amount of perfused sulfate was absorbed in the proximal tubule with little absorption distal to the late proximal collection site. Phosphate transport was not affected by high luminal sulfate concentrations indicating distinct reabsorptive mechanisms for these two anions. Intraluminal sulfate significantly inhibited calcium and magnesium reabsorption in the proximal tubule, loop of Henle, and superficial distal tubule, in distinction to modest effects on sodium transport in these nephron segments. Chloride transport was not altered. The inhibition of divalent cation transfer was not quantitively similar in the different tubule segments. Small amounts of sulfate completely inhibited proximal calcium and magnesium reabsorption with little effect on transport within the loop of Henle. Enhanced distal delivery of sulfate significantly inhibited calcium and magnesium reabsorption in the distal tubule, a site where the sulfate anion is not reabsorbed. These results demonstrate the importance of distal delivery of anionic ligands capable of forming nonreabsorbable complexes. Thus distal calcium and magnesium transport may be greatly modified by proximal control of anion reabsorption.

scholarly journals Acid base status of prevalent peritoneal dialysis patients

2018 ◽  
Vol 1 (1) ◽  
pp. 21-25
Author(s):  
Raymond Azar ◽  
Vincent Coevoet
Keyword(s):  
Peritoneal Dialysis ◽  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Lower Probability ◽  
Individual Choice ◽  
Dietary Intakes ◽  
Dialysis Patients ◽  
Acid Base Balance ◽  
Acid Base ◽  
Acid Base Status

Acid-base status of patients on peritoneal dialysis is influenced by multiple factors. Metabolic acidosis is a common feature of chronic renal failure and dialysis treatment provides alkali in the dialysate in order to maintain a normal acid-base balance. This paper reports the prevalence of acid-base disorders in peritoneal dialysis patients and their associations with clinical and laboratory parameters. This is a cross-sectional retrospective study that included all PD patients registered in the RDPLF database. Metabolic acidosis was found in 20.4% of patients while 27.8% of patients had metabolic alkalosis. There is a significant relationship between age, protein intake estimated by nPNA and the level of alkaline reserve pleading in favor of the influence of dietary intakes in the maintenance of metabolic acidosis. Low residual renal function is associated with a lower probability of being in metabolic alkalosis. These results could allow an individual choice of the dialysate buffer in order to permanently obtain stable acid-base status in patients on peritoneal dialysis.

scholarly journals P0004REDUCED EXPRESSION OF PROXIMAL ACID-BASE TRANSPORT PROTEINS IN KIDNEY TRANSPLANT PATIENTS WITH METABOLIC ACIDOSIS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Anna Wiegand ◽  
Arezoo Daryadel ◽  
Pedro Henrique Imenez da Silva ◽  
Ariana Gaspert ◽  
Rudolf Peter Wuthrich ◽  
...  
Keyword(s):  
Kidney Transplantation ◽  
Metabolic Acidosis ◽  
Kidney Disease ◽  
Proximal Tubule ◽  
Kidney Transplant ◽  
Transport Proteins ◽  
Transplant Recipients ◽  
Kidney Transplant Recipients ◽  
Acid Base ◽  
Alkali Therapy

Abstract Background and Aims Metabolic acidosis (MA) is a frequent complication of chronic kidney disease and an independent risk factor for kidney disease progression and mortality. MA is highly prevalent after kidney transplantation (12%-58%)(1). However, there are scarcely any data available on the underlying pathomechanisms and in particular molecular mechanisms involved in metabolic acidosis after kidney transplantation. Thus, we wanted to investigate the expression of key acid base transport proteins in kidney biopsies of kidney transplant recipients with and without metabolic acidosis. Method We evaluated 22 kidney transplant biopsies including 9 biopsies from kidney transplant recipients (KTR) with MA, nine biopsies from KTRs without MA (control) and four biopsies from KTRs with MA that were consequently subjected to alkali therapy (Alkali therapy). Immunofluorescence staining was used to identify key renal acid-base transport proteins. Additionally, six control kidneys were analyzed. Immunofluorescence staining was used to identify key renal acid-base transport proteins along the nephron. In addition, RNA extraction and full RNA sequencing analysis of all biopsies –where available- was performed. Results In the proximal tubule, we observed reduced immunostaining for the sodium bicarbonate cotransporter NBCe1 (SLC4A4) in the MA group compared to the control and alkali group, whereas the alkali group demonstrated the strongest staining of all three groups. In the distal nephron, expression of the chloride/bicarbonate exchanger Pendrin (SLC26A4) and the B1 subunit of the V-ATPase (ATP6V1B1) were markedly stronger in the alkali and control group compared to the MA group. Expression of other acid base proteins such as Renal ammonia transporter RhCG (SLC42A3), Carbonic Anhydrase II, Glutamate dehydrogenase, anion exchanger AE1 (SLC4A1) and the B2 subunit of the V-ATPase (ATP6V1B2) showed no difference among all groups. Interestingly, the B2 subunit was absent in the proximal tubule in transplant biopsies of all groups. In kidney biopsies of transplant recipients with metabolic acidosis RNA abundance of NBCe1, CAII and Pendrin was lower while RhCG and B1 RNA counts were not different when compared to recipients without metabolic acidosis. Conclusion Our data demonstrate altered protein and mRNA expression of several key acid base transporters in kidney biopsies of transplant recipients with metabolic acidosis. Treatment with alkali may have the potential to reverse or prevent these changes in renal allografts after transplantation.

Ventilatory response to chronic metabolic acidosis and alkalosis in the dog

1984 ◽  
Vol 56 (6) ◽  
pp. 1640-1646 ◽  
Author(s):  
N. E. Madias ◽  
W. H. Bossert ◽  
H. J. Adrogue
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Ventilatory Response ◽  
Wide Spectrum ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Plasma Bicarbonate ◽  
Oral Sodium ◽  
Chronic Change

Systematic data are not available with regard to the anticipated appropriate responses of arterial PCO2 to primary alterations in plasma bicarbonate concentration. In the present study, we attempted to rigorously characterize the ventilatory response to chronic metabolic acid-base disturbances of graded severity in the dog. Animals with metabolic acidosis produced by prolonged HCl feeding and metabolic alkalosis of three different modes of generation, i.e., diuretics (ethacrynic acid or chlorothiazide), gastric drainage, and administration of deoxycorticosterone acetate (alone or in conjunction with oral sodium bicarbonate), were examined. The results indicate the existence of a significant and highly predictable ventilatory response to chronic metabolic acid-base disturbances. Moreover, the magnitude of the ventilatory response appears to be uniform throughout a wide spectrum of chronic metabolic acid-base disorders extending from severe metabolic acidosis to severe metabolic alkalosis; on average, arterial PCO2 is expected to change by 0.74 Torr for a 1-meq/l chronic change in plasma bicarbonate concentration of metabolic origin. Furthermore, the data suggest that the ventilatory response to chronic metabolic alkalosis is independent of the particular mode of generation.

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