ライフサイエンスコーパス: metabolic acidosis

1 pH 6.8, followed by 2 h at pH 7.4 (in vitro metabolic acidosis).

2 y acidosis) or through lactic acid infusion (metabolic acidosis).

3 bicarbonate therapy for patients with severe metabolic acidosis.

4 used in resuscitation can themselves produce metabolic acidosis.

5 e mixed acid-base disorders in patients with metabolic acidosis.

6 a further decrease of PMo2 by 68% and worse metabolic acidosis.

7 ponatremia, but in large volumes may lead to metabolic acidosis.

8 s led to new ways of managing hyperchloremic metabolic acidosis.

9 terone, with salt wasting, hyperkalemia, and metabolic acidosis.

10 al Lowe syndrome, none of these patients had metabolic acidosis.

11 ren deficient in enzyme activity have severe metabolic acidosis.

12 rbonate load, but there was no effect during metabolic acidosis.

13 d at rest, likely compensating for a chronic metabolic acidosis.

14 ertension, hyperkalemia, hyperchloremia, and metabolic acidosis.

15 w-grade, pathogenically significant systemic metabolic acidosis.

16 y impaired renal acid secretion resulting in metabolic acidosis.

17 potension, decreased urine output (UOP), and metabolic acidosis.

18 higher than that of controls, indicative of metabolic acidosis.

19 adaptation helps maintain homeostasis during metabolic acidosis.

20 e inner stripe of renal outer medulla during metabolic acidosis.

21 rupt acid-base balance, particularly causing metabolic acidosis.

22 Veverimer effectively and safely corrected metabolic acidosis.

23 l outcome (progression to hemodialysis), and metabolic acidosis.

24 evations in CBF induced via the ACZ-mediated metabolic acidosis.

25 r blood ketoacids; and 'A', a high anion gap metabolic acidosis.

26 unmeasured anions were the leading cause of metabolic acidosis.

27 sis in the whole cohort and in patients with metabolic acidosis.

28 arterial hypertension and hyperkalemia with metabolic acidosis.

29 evented IC subtype alterations and magnified metabolic acidosis.

30 I)--features hypertension, hyperkalemia, and metabolic acidosis.

31 ith weight loss, hypertonic dehydration, and metabolic acidosis.

32 luding hyperkalemia, hyperaldosteronism, and metabolic acidosis.

33 n in the papilla, and chronic hyperchloremic metabolic acidosis.

34 ely low in alphaICs, even when stimulated by metabolic acidosis.

35 ociated with hyperkalemia and hyperchloremic metabolic acidosis.

36 ogical tissue damage despite more pronounced metabolic acidosis.

37 ssium channel activation and respiratory and metabolic acidosis.

38 nd increased urinary acid elimination during metabolic acidosis.

39 c4a7) in rat brain is upregulated by chronic metabolic acidosis.

40 d plexus epithelia was unaffected by chronic metabolic acidosis.

41 ule reabsorption of bicarbonate resulting in metabolic acidosis.

42 tion of breathing elicited by hypercapnia or metabolic acidosis.

43 and hippocampal neurones was in response to metabolic acidosis (22 mm--> 14 mm HCO(3)(-)), which cau

44 l manifestations: cardiac (3.8 [2.88-4.91]), metabolic acidosis (3.7 [2.7-5.0]), renal failure (1.9 [

45 ackground ventilatory drive, increasing with metabolic acidosis (-6.7 mm Hg) and nonhypoxic periphera

46 During metabolic acidosis (a reduction in systemic pH caused by

47 Patients who have metabolic acidosis, a bicarbonate or inotrope/vasopresso

48 Metabolic acidosis, a complication of chronic kidney dis

49 have alkaline urine but do not exhibit overt metabolic acidosis, a renal phenotype similar to that of

50 on disease, metabolism abnormalities such as metabolic acidosis, abnormal fatty acid metabolism, hype

51 ular acidoses (dRTA), whose features include metabolic acidosis accompanied by disturbances of potass

52 udy randomized 1480 individuals with CKD and metabolic acidosis, across 320 sites to placebo or vever

53 cytokines and did not exhibit hypothermia or metabolic acidosis after CLP.

54 at administration of AM/AMBP-1 would prevent metabolic acidosis after uncontrolled hemorrhage via dow

55 d with endothelial dysfunction (L-arginine), metabolic acidosis (alanine and lactate), and disease se

56 Metabolic acidosis alone induces neovascularization simi

57 Chronic metabolic acidosis also stimulates ammoniagenesis that i

58 lood pressure, core temperature, and greater metabolic acidosis (analysis of variance, P < 0.0001).

59 out the study period; 1,609 met criteria for metabolic acidosis and 145 had normal acid-base values.

60 tal renal tubular acidosis, as manifested by metabolic acidosis and alkaline urine pH.

61 nal, bone and mineral metabolism, correcting metabolic acidosis and anemia, achieving excellent blood

62 ised by more severe inflammation, shock, and metabolic acidosis and by worse clinical outcomes.

63 on was then compared between rats in chronic metabolic acidosis and control rats.

64 ts in energy supply and demand can result in metabolic acidosis and diminished delivery and/or availa

65 eatures of MetS while also causing low-grade metabolic acidosis and elevating natriuretic peptides.

66 cause high-protein (HP) Western diets induce metabolic acidosis and hypercalciuria.

67 ensue from a mitochondrial dysfunction (e.g. metabolic acidosis and hyperthermia) and that MH-suscept

68 , veverimer safely and effectively corrected metabolic acidosis and improved subjective and objective

69 The findings suggest that diet-induced metabolic acidosis and its sequelae in humans eating con

70 Metabolic acidosis and lactatemia resolved significantly

71 H(3)), an environmental pollutant leading to metabolic acidosis and liver and kidney toxicity; dimeth

72 tation with Hextend was associated with less metabolic acidosis and longer survival in this experimen

73 e prevents the development of hyperchloremic metabolic acidosis and may reduce the need for vasopress

74 dded benefits but alleviated the severity of metabolic acidosis and mortality after LNA.

75 rongly associated with mortality were severe metabolic acidosis and need for endotracheal intubation.

76 ciated with mortality, whereas patients with metabolic acidosis and noncardiac structural or chromoso

77 n reduced glycogen accumulation and improved metabolic acidosis and phosphaturia in the animals by no

78 ammonia excretion (UNH(4)) in patients with metabolic acidosis and postulated that UAG could be used

79 Ethylene glycol poisoning causes metabolic acidosis and renal failure and may cause death

80 Hypertension, anaemia, metabolic acidosis and secondary hyperparathyroidism con

81 Mild hyperchloremia, metabolic acidosis and suppressed plasma renin activity

82 HF patients experienced faster correction of metabolic acidosis and tended to be more rapidly weaned

83 oplasty in childhood can lead to significant metabolic acidosis and that compensation with bone buffe

84 ive anions responsible for the main types of metabolic acidosis and the outcome.

85 rinary citrate excretion fourfold in chronic metabolic acidosis and threefold in K+-depletion.

86 olloids are associated with a hyperchloremic metabolic acidosis, and a hypocoagulable state although

87 lloids) are associated with a hyperchloremic metabolic acidosis, and a hypocoagulable state, although

88 The patient developed cardiac arrhythmia, metabolic acidosis, and cardiac failure, which resulted

89 decreased mean arterial pressure, increased metabolic acidosis, and decreased urine output.

90 Persistent systolic hypotension, acidemia/metabolic acidosis, and elevated Pao2) after 24 hours of

91 ominal tenderness, severe hepatic cytolysis, metabolic acidosis, and hemodynamic dysfunction.

92 dyspnea, peripheral edema), worsening eGFR, metabolic acidosis, and hyperkalemia inform the timing o

93 nal function, longer scene-to-hospital time, metabolic acidosis, and hyperkalemia.

94 n, increased blood oxygen content, prevented metabolic acidosis, and improved 6-hour survival (42% in

95 d hyponatremia, hyperkalemia, hypercalcemia, metabolic acidosis, and increased serum lithium concentr

96 issive hypercapnia in the presence of shock, metabolic acidosis, and multi-organ system dysfunction m

97 %) patients died due to acute kidney injury, metabolic acidosis, and multiple organ dysfunction syndr

98 membrane oxygenation, development of severe metabolic acidosis, and number of early extubations in t

99 increased expression in response to chronic metabolic acidosis, and originally was cloned as a tumor

100 ed by processes other than the post-exercise metabolic acidosis, and that changes in peripheral chemo

101 scle protein breakdown include inflammation, metabolic acidosis, angiotensin II, and neural and hormo

102 id excretion and bicarbonate reabsorption in metabolic acidosis are closely similar to those operativ

103 Although the protein catabolic effects of metabolic acidosis are well established, it is unclear w

104 -center prospective studies identify chronic metabolic acidosis as an independent and modifiable risk

105 provement in hemodynamics, urine output, and metabolic acidosis, as well as a perceived increase in s

106 The mice developed metabolic acidosis, as well as profound acidemia and hyp

107 The models predict that the graded metabolic acidosis associated with mild renal failure af

108 erely injured trauma patients, the degree of metabolic acidosis at the time of admission identified t

109 Treatment of chronic metabolic acidosis attenuates these adaptive responses;

110 n two study groups: children presenting with metabolic acidosis (base deficit >8) and children withou

111 During metabolic acidosis, basolateral Na(+)/HCO(3) (-) cotrans

112 Patient diagnosis, absence of severe metabolic acidosis before ECMO support, and uncomplicate

113 n with hyperkalemia/potassium level and with metabolic acidosis/bicarbonate level.

114 Methanol poisoning may result in metabolic acidosis, blindness, and death.

115 provide control data with a varying level of metabolic acidosis, but with no prior exercise.

116 Chronic metabolic acidosis caused hypocitraturia in rats and inc

117 Metabolic acidosis causes a reversal of polarity of HCO(

118 d acidotic rats is mediated by NHE3 and that metabolic acidosis causes increased expression of renal

119 lp to preserve muscle oxygenation and reduce metabolic acidosis compared with CLE at the same average

120 odds for receiving palliative care service, metabolic acidosis, compared with White race.

121 A subsequent renally mediated compensatory metabolic acidosis corrects pH toward baseline values, w

122 ral markers of cardiovascular compromise and metabolic acidosis correlate with mortality.

123 l metabolism, in addition to roles played by metabolic acidosis, cytokines, and degradation of parath

124 cluding urinary tract infections, hematuria, metabolic acidosis, dehydration, and reflux pancreatitis

125 Evaluation II score, mechanical ventilation, metabolic acidosis, delirium on the prior day, and coma

126 acidosis with blood pH </= 7.15, persistent metabolic acidosis despite adequate supportive measures

127 dehydration, hypotension, hyperkalaemia and metabolic acidosis, despite elevated aldosterone levels.

128 nd shock refractory to inotropic agents, and metabolic acidosis developed in the patient within 2 hou

129 er of pathophysiologic conditions, including metabolic acidosis, diabetes, sepsis, and high angiotens

130 Acute metabolic acidosis did not affect the PTH-iCa curve.

131 ated by liver failure, renal failure, severe metabolic acidosis, disseminated intravascular coagulopa

132 ences, is characterized by hyperglycemia and metabolic acidosis due to the accumulation of ketone bod

133 y as capable as control livers in correcting metabolic acidosis during the first 24 hr posttransplant

134 During metabolic acidosis, electrodialysis reduced plasma chlor

135 weaning grew to adulthood; however, they had metabolic acidosis, elevated blood concentrations of Na(

136 nate synthesis from glutamine during chronic metabolic acidosis facilitate the excretion of acids and

137 gh energy phosphate stores and correction of metabolic acidosis following brief periods of global isc

138 rough feedback inhibition, likely to prevent metabolic acidosis from occurring.

139 acidosis (pRTA), a disease characterized by metabolic acidosis, growth retardation, ocular abnormali

140 NBC1-/- mice exhibited severe metabolic acidosis, growth retardation, reduced plasma N

141 y massive urinary excretion of 5-oxoproline, metabolic acidosis, haemolytic anaemia and central nervo

142 ll alkali supplementation trials, correcting metabolic acidosis has a strikingly broad array of poten

143 known to decrease bone mineral density, and metabolic acidosis has been shown to increase glucocorti

144 In vitro, metabolic acidosis has been shown to initially induce ph

145 me featuring hypertension, hyperkalaemia and metabolic acidosis, has revealed previously unrecognized

146 Children with severe malaria and metabolic acidosis have evidence of hypovolemia and evid

147 and proinflammatory mediators and correcting metabolic acidosis, high-volume hemofiltration (HVHF) mi

148 renal insufficiency, high plasma potassium, metabolic acidosis, hydronephrosis of varying severity,

149 erventions specifically targeting hypoxemia, metabolic acidosis, hyperglycemia, and cardiovascular in

150 disease (CKD), such as anemia, hypertension, metabolic acidosis, hyperkalemia, or persistent secondar

151 complications of CKD, such as hyperkalemia, metabolic acidosis, hyperphosphatemia, vitamin D deficie

152 This was associated with prevention of metabolic acidosis, hypocalcemia, hyperkalemia, and card

153 ning, Atp6v0a4(-/-) mice demonstrated severe metabolic acidosis, hypokalemia, and early nephrocalcino

154 These results suggest that during acute metabolic acidosis, IMCD 11 beta-HSD2 is inhibited and m

155 Uremic metabolic acidosis impairs insulin signaling, which norm

156 definitive trial testing whether correcting metabolic acidosis improves clinical outcomes has not be

157 only transiently for 1 hr, and caused severe metabolic acidosis in all animals.

158 E-subunit; however, the greater severity of metabolic acidosis in Atp6v1b1(-/-) mice after oral acid

159 Metabolic acidosis in CKD stimulates production of intra

160 abrogation of weight loss, dehydration, and metabolic acidosis in inoculated pigs, and LT complement

161 y and safety of veverimer as a treatment for metabolic acidosis in patients with chronic kidney disea

162 symptoms, secondary hyperparathyroidism, and metabolic acidosis in patients with chronic renal failur

163 with higher risks of long-term dialysis and metabolic acidosis in patients with POAG and pre-dialysi

164 a demonstrating the benefits of azotemia and metabolic acidosis in survival of patients with metastat

165 tion (H+ secretion) in OMCD is stimulated by metabolic acidosis in vivo and in vitro by an increase i

166 that the osteopenia observed in response to metabolic acidosis in vivo is not due to an increase in

167 chemical and cell-mediated bone responses to metabolic acidosis, in addition to an acidosis-induced i

168 n after hemorrhagic shock is associated with metabolic acidosis, in which the up-regulated endothelin

169 to assess other deleterious consequences of metabolic acidosis including progression of chronic kidn

170 In conclusion, metabolic acidosis increases ET-1 expression, which incr

171 Chronic metabolic acidosis increases proximal tubular citrate up

172 Metabolic acidosis increases urine calcium excretion wit

173 etion by the kidney and resulted in a nongap metabolic acidosis, indicating that GPR4 is required to

174 Understanding the role of OGR1 in metabolic acidosis-induced bone resorption will provide

175 ng osteoclast OGR1 is important in mediating metabolic acidosis-induced bone resorption.

176 of osteoclast OGR1 decreased both basal and metabolic acidosis-induced osteoclast activity indicatin

177 NH4Cl gavage in the neonatal rat produces a metabolic acidosis-induced retinopathy which serves as a

178 Metabolic acidosis induces osteoclastic bone resorption

179 strated that saline may cause hyperchloremic metabolic acidosis, inflammation, hypotension, acute kid

180 li that initiate muscle protein loss include metabolic acidosis, insulin and IGF1 resistance, changes

181 Metabolic acidosis is a common complication of CKD and i

182 Chronic metabolic acidosis is an independent risk factor for chr

183 In summary, the hypocitraturia of chronic metabolic acidosis is associated with an increase in ATP

184 Metabolic acidosis is associated with impaired physical

185 Metabolic acidosis is associated with increased urinary

186 Metabolic acidosis is associated with poor outcomes in C

187 entifying these individuals with subclinical metabolic acidosis is challenging, but recent results su

188 Metabolic acidosis is common in CKD, but whether its tre

189 Metabolic acidosis is common in septic shock, yet few da

190 In CKD, metabolic acidosis is commonly treated with alkali in th

191 sed brush border Na+-H+ exchange observed in metabolic acidosis is due to increased expression of NHE

192 The intraoperative development of metabolic acidosis is frequently attributed to hypovolem

193 f the rat renal glutaminase (GA) mRNA during metabolic acidosis is mediated by a pH-response element

194 Urine pH is more alkaline and metabolic acidosis is more severe in Atp6v1b1(-/-) mice

195 Metabolic acidosis is not uncommon in CKD and is linked

196 Metabolic acidosis is partially compensated by a pronoun

197 hloride levels should be assessed whenever a metabolic acidosis is seen perioperatively.

198 ock, as measured by systemic hypotension and metabolic acidosis, is significantly associated with a h

199 Our data also support the idea that metabolic acidosis itself can lead to impaired intrapulm

200 tomy and urinary diversion may cause chronic metabolic acidosis, leading to long-term bone loss in pa

201 Induction of metabolic acidosis led to a significantly augmented abun

202 intractable myocardial failure preceded by a metabolic acidosis, lipaemic plasma, fatty infiltration

203 Metabolic acidosis (MA) contributes to the development o

204 Metabolic acidosis (MA) is associated with alterations i

205 Metabolic acidosis (MA) upregulates the pathway that mit

206 NH(4) Cl-induced metabolic acidosis (MAc) substantially increases protein

207 During metabolic acidosis (MAc), AE3 speeds initial acidificati

208 ular acidification during the early phase of metabolic acidosis (MAc), not just in neurons but, surpr

209 Dietary patterns that promote mild metabolic acidosis may have a negative effect on bone de

210 paired acid excretion in CKD, with potential metabolic acidosis, may contribute to the progression of

211 opics and the prevalence and risk factors of metabolic acidosis, mechanisms of acid-mediated organ in

212 cate that AM/AMBP-1 administration prevented metabolic acidosis, mitigated organ injury, down-regulat

213 mal babies, and those with mixed respiratory/metabolic acidosis (more profound and prolonged hypoxia)

214 the shock-related lactic acidosis but caused metabolic acidosis, most likely resulting from reduced c

215 During metabolic acidosis, NBCn1 is required for the upregulate

216 y urine, variable hyperchloremic hypokalemic metabolic acidosis, nephrocalcinosis, and nephrolithiasi

217 e of a normal salt intake led to a degree of metabolic acidosis not significantly different from that

218 Although metabolic acidosis occurs in both hypovolaemia and malar

219 Atp6v1b1vxt/vtx mice do not recapitulate the metabolic acidosis of dRTA patients, they provide a new

220 In patients with CKD, untreated chronic metabolic acidosis often leads to an accelerated reducti

221 resent study addressed the effect of chronic metabolic acidosis on a cytosolic enzyme of citrate meta

222 omized trials testing the effect of treating metabolic acidosis on slowing CKD progression have not b

223 abolism; it was confounded by the effects of metabolic acidosis on the CO(2)-hemoglobin dissociation

224 Therefore, the effect of pure metabolic acidosis on the developing retinal vasculature

225 s shifted from secretion to absorption after metabolic acidosis or acid incubation of the CCD.

226 ECLS, patients who develop renal failure or metabolic acidosis or undergo venoarterial ECLS should b

227 rnatremia, hypomagnesemia, hypophosphatemia, metabolic acidosis, or metabolic alkalosis.

228 In response to metabolic acidosis, osteoclasts from knockout mice had d

229 g-term dialysis, and cumulative incidence of metabolic acidosis over time between CAI users and CAI n

230 tions include volume overload, hyperkalemia, metabolic acidosis, overt uremia, and even progressive a

231 s of dehydration, electrolyte imbalance, and metabolic acidosis (P < 0.05).

232 Mice infected with P. berghei exhibit (i) metabolic acidosis (pH < 7.3) associated with elevated p

233 icipated events were categorized as isolated metabolic acidosis (pH <7.20), hypercapnia (P(CO2), >70

234 petitive substrate methylaminoisobutyrate or metabolic acidosis (pH 7.1) depleted intracellular L-Gln

235 asma urea nitrogen (6.7 +/- 2.53 mmol/L), or metabolic acidosis (pH: 7.36 +/- 0.05).

236 igh urea serum levels [>= 150 mg/dL], severe metabolic acidosis [pH <= 7.15], oliguria [urinary outpu

237 of a trauma patient with severe unexplained metabolic acidosis, possibly attributable to the vasocon

238 creased urinary calcium excretion induced by metabolic acidosis predominantly results from increased

239 Paco2 and Pao2 remained stable, but metabolic acidosis progressed, as expected, throughout t

240 Metabolic acidosis promotes muscle wasting, and the net

241 3 days included hyperglycemia with resultant metabolic acidosis, pulmonary dysfunction, nausea, vomit

242 owing criteria was met: severe hyperkalemia, metabolic acidosis, pulmonary edema, blood urea nitrogen

243 onate administration to patients with severe metabolic acidosis remains controversial.

244 rdiac symptoms, rhabdomyolosis, hypotension, metabolic acidosis, renal failure, and age each affected

245 Profound hypotension, leukopenia, metabolic acidosis, renal impairment, thrombocytopenia,

246 per 1 mg/dl increase in total bilirubin) and metabolic acidosis (RR, 0.95; 95% CI, 0.90 to 0.99 per 1

247 tration rate 20-40 mL/min per 1.73 m(2)) and metabolic acidosis (serum bicarbonate 12-20 mmol/L), who

248 tion rate of 20-40 mL/min per 1.73 m(2)) and metabolic acidosis (serum bicarbonate concentration of 1

249 CKD (eGFR of 20-40 ml/min per 1.73 m 2 ) and metabolic acidosis (serum bicarbonate of 12-20 mEq/L) fr

250 Metabolic acidosis significantly influenced the PCO(2)/C

251 effects on osteoclast OGR1 are critical for metabolic acidosis stimulated bone resorption, we genera

252 Water supplementation with NH(4)Cl to induce metabolic acidosis stimulated Piezo1 activity in ICs but

253 In rats and humans, metabolic acidosis stimulates protein degradation and gl

254 Chronic metabolic acidosis stimulates the catabolism of bone and

255 One complication of uremia, metabolic acidosis, stimulates the degradation of branch

256 A metabolic acidosis study was performed in rats with 1, 4

257 xcrete endogenous acid, resulting in chronic metabolic acidosis that increases the risk of disease pr

258 kidney dysfunction include hyperkalemia and metabolic acidosis that occur at higher eGFR thresholds

259 ation of trauma patients, may exacerbate the metabolic acidosis that occurs with injury, and this aci

260 current oral sodium bicarbonate therapy for metabolic acidosis that only neutralises accumulated aci

261 The disease manifests as metabolic acidosis that significantly slows the growth r

262 ervation of visual acuity, the resolution of metabolic acidosis, the inhibition of formic acid produc

263 During the response to metabolic acidosis, the intercalated cell of the collect

264 urones indicates that, except in response to metabolic acidosis, the neurones from the chemosensitive

265 In patients with metabolic acidosis, the results were similar.

266 eating Western diets have chronic, low-grade metabolic acidosis, the severity of which is determined

267 During long-term studies to model chronic metabolic acidosis, there is also inhibition of osteobla

268 During short-term studies to model acute metabolic acidosis, there is initial physiochemical bone

269 rates, but it is not clear if it responds to metabolic acidosis to increase H+ secretion.

270 Among patients with CKD and metabolic acidosis, treatment with veverimer did not slo

271 SS(Kcnj16-/-) rats displayed metabolic acidosis under a normal salt diet.

272 arterial hypertension with hyperkalemia and metabolic acidosis, unmasked a complex multiprotein syst

273 The effects of low (metabolic acidosis) versus normal bicarbonate dialysis w

274 In patients with chronic kidney disease and metabolic acidosis, veverimer safely and effectively cor

275 g acid-base balance (control); (2) following metabolic acidosis via 2 days of oral acetazolamide at 2

276 Acetazolamide induces a metabolic acidosis via an alternative biochemical mechan

277 ed stepwise alterations in PaCO(2) following metabolic acidosis (via 2 days of oral acetazolamide; AC

278 In treated animals, urine output was higher, metabolic acidosis was attenuated, and renal tubular arc

279 Metabolic acidosis was common at presentation (mean base

280 lated from rats with 5 days of NH4Cl-induced metabolic acidosis was increased 1.5-fold compared with

281 Metabolic acidosis was induced in wild-type and NBCn1 kn

282 Metabolic acidosis was one of the earliest complications

283 Metabolic acidosis was prevented in the 4-aminopyridine

284 antibody-treated animals, UOP was decreased, metabolic acidosis was worsened, and median survival tim

285 on, as reflected by a hyperosmolar anion gap metabolic acidosis, was observed in critically ill adult

286 Hospital admissions due to metabolic acidosis were higher in CAI users compared wit

287 base deficit (as a reflection of severity of metabolic acidosis) were recorded immediately before the

288 Mild metabolic acidosis, which can be caused by diet, may res

289 locking muscle wasting include correction of metabolic acidosis, which can suppress muscle protein lo

290 onia metabolism in the kidney in response to metabolic acidosis, which provides mechanistic insights

291 He developed a significant metabolic acidosis with a lactic acid level of 10.9 mmol

292 osis in humans, a condition characterized by metabolic acidosis with an inappropriately alkaline urin

293 thanol: coma, seizures, new vision deficits, metabolic acidosis with blood pH </= 7.15, persistent me

294 denced by a high anion gap (> or =15 mmol/L) metabolic acidosis with elevated osmol gap (> or =10 mOs

295 s of autosomal recessive dRTA include severe metabolic acidosis with inappropriately alkaline urine,

296 spiratory alkalosis developed, followed by a metabolic acidosis with increased levels of blood lactat

297 phalopathy, failure to thrive, and recurrent metabolic acidosis with intercurrent infections.

298 oad, whereas Rhcg(-/-) mice developed severe metabolic acidosis with reduced ammonuria and high morta

299 actic, unmeasured anions, and hyperchloremic metabolic acidosis with that of patients without acid-ba

300 associated with neurological recovery while metabolic acidosis x TTI 5.7 min (OR: 3.63, 95% CI 1.36-