Metabolic Basis for Low Urine pH in Type 2 Diabetes

Maalouf, Naim M.; Cameron, Mary Ann; Moe, Orson W.; Sakhaee, Khashayar

doi:10.2215/cjn.08331109

Cited by 130 publications

(124 citation statements)

References 29 publications

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“…Unfortunately, since we did not measure glutathione or urinary NH 4 + in this study, we were unable to confirm any such changes in glutathione or reductions in NH 3 levels; these topics should be explored in future studies. Urinary NH 4 + is reported to decrease in association with diabetes, in which increased OS is observed (Maalouf et al 2010). In our report, we also noted that UpH correlated negatively with urinary OS markers (Ogawa et al 2015b).…”

Section: Discussionsupporting

confidence: 74%

The Reduction in Urinary Glutamate Excretion Is Responsible for Lowering Urinary pH in Pink Urine Syndrome

Ogawa

Takiguchi

Shimizu

et al. 2016

Tohoku J. Exp. Med.

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We frequently encounter brownish-red, cloudy urine in some obese subjects, which occurs due to pink urine syndrome (PUS). PUS is a phenomenon in which uric acid precipitates into the urine due to reduced urinary pH (UpH). The mechanism underlying urinary acidification has not been elucidated so far. UpH level is adjusted by urinary excretion of ammonia synthesized from glutamate or glutamine, suggesting that renal synthesis of ammonia from glutamate or glutamine is decreased in PUS. However, this hypothesis has not been examined yet. We therefore examined the changes in the urinary excretion of these amino acids in PUS. One-hundred-fifty male students who had undergone a physical examination were enrolled. To determine the presence [PUS (+), n = 72] or absence [PUS (−), n = 78] of PUS, urinary amino acid excretion and UpH were evaluated. Independent risk factors of lower UpH were determined using multiple regression analyses. The PUS (+) subjects, who had lower UpH values than PUS (-) subjects, showed lower urinary excretion of glutamate and some other glucogenic amino acids. Thus, UpH correlated positively with the urinary excretion of glutamate in the PUS (+) subjects. A reduction in urinary glutamate but not in glutamine excretion proved to be an independent risk factor for reduced UpH. In conclusion, PUS appears to occur when a reduction in the synthesis of ammonia from glutamate causes a decrease in UpH. Our results showed that urinary glutamate excretion was reduced in PUS because renal glutamate was consumed by a reaction different from ammonia production.

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Section: Discussionsupporting

confidence: 74%

The Reduction in Urinary Glutamate Excretion Is Responsible for Lowering Urinary pH in Pink Urine Syndrome

Ogawa

Takiguchi

Shimizu

et al. 2016

Tohoku J. Exp. Med.

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“…We next performed a multivariate analysis to adjust for known predictors of acid-base homeostasis, including sex, age, BMI, and dietary acid and alkali intake, taking between-center variability into account. [16][17][18] As shown in Table 4, after this adjustment, urinary pH on lowCa and low-Na diet remained significantly different between the two groups of patients. However, plasma bicarbonate under random outpatient diet was no longer different between the two groups.…”

Section: Multivariate Analysesmentioning

confidence: 88%

The Vacuolar H+-ATPase B1 Subunit Polymorphism p.E161K Associates with Impaired Urinary Acidification in Recurrent Stone Formers

Dhayat

Schaller

Albano

et al. 2015

JASN

Self Cite

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Mutations in the vacuolar-type H + -ATPase B1 subunit gene ATP6V1B1 cause autosomal-recessive distal renal tubular acidosis (dRTA). We previously identified a single-nucleotide polymorphism (SNP) in the human B1 subunit (c.481G.A; p.E161K) that causes greatly diminished pump function in vitro. To investigate the effect of this SNP on urinary acidification, we conducted a genotype-phenotype analysis of recurrent stone formers in the Dallas and Bern kidney stone registries. Of 555 patients examined, 32 (5.8%) were heterozygous for the p.E161K SNP, and the remaining 523 (94.2%) carried two wild-type alleles. After adjustment for sex, age, body mass index, and dietary acid and alkali intake, p.E161K SNP carriers had a nonsignificant tendency to higher urinary pH on a random diet (6.31 versus 6.09; P=0.09). Under an instructed low-Ca and low-Na diet, urinary pH was higher in p.E161K SNP carriers (6.56 versus 6.01; P,0.01). Kidney stones of p.E161K carriers were more likely to contain calcium phosphate than stones of wild-type patients. In acute NH 4 Cl loading, p.E161K carriers displayed a higher trough urinary pH (5.34 versus 4.89; P=0.01) than wild-type patients. Overall, 14.6% of wild-type patients and 52.4% of p.E161K carriers were unable to acidify their urine below pH 5.3 and thus, can be considered to have incomplete dRTA. In summary, our data indicate that recurrent stone formers with the vacuolar H + -ATPase B1 subunit p.E161K SNP exhibit a urinary acidification deficit with an increased prevalence of calcium phosphatecontaining kidney stones. The burden of E161K heterozygosity may be a forme fruste of dRTA.

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“…First, because proximal tubular reabsorption of most organic molecules occurs through sodium cotransport, excess filtered glucose may compete with other substrates, such as citrate, for reabsorption through this pathway. Second, it is possible that altered renal citrate handling leading to citrate wasting, like alterations in renal net acid excretion (14), is another manifestation of altered renal acid-base handling in diabetes.…”

Section: Discussionmentioning

confidence: 99%

“…However, these associations have yet to be explored on the population level. Furthermore, numerous other dietary and lifestyle factors and medical conditions are known to be associated with low urine pH, including obesity (12), diabetes mellitus (4,(13)(14)(15), and gout (16,17). However, the independent associations between these factors and urinary citrate excretion have not yet been reported.…”

Section: Introductionmentioning

confidence: 99%

Dietary and Lifestyle Factors and Medical Conditions Associated with Urinary Citrate Excretion

Mandel

Taylor

Curhan

2013

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Lower urinary citrate excretion is a risk factor for nephrolithiasis and associated with metabolic acidosis and higher prevalence of hypertension and insulin resistance. This study sought to quantify the independent predictors of urinary citrate excretion in population-based cohorts.Design, setting, participants, & measurements A cross-sectional study of 2561 individuals from the Health Professionals Follow-Up Study and Nurses' Health Studies I and II who provided two 24-hour urine collections was conducted. Dietary data were ascertained from the semiquantitative food frequency questionnaire. Lifestyle and disease data were derived from responses to biennial questionnaires. Multivariable linear regression was used to quantify the predictors of urinary citrate excretion. Conclusions Several dietary and lifestyle factors and medical conditions are independently associated with urinary citrate excretion. Results

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Metabolic Basis for Low Urine pH in Type 2 Diabetes

Cited by 130 publications

References 29 publications

The Reduction in Urinary Glutamate Excretion Is Responsible for Lowering Urinary pH in Pink Urine Syndrome

The Reduction in Urinary Glutamate Excretion Is Responsible for Lowering Urinary pH in Pink Urine Syndrome

The Vacuolar H+-ATPase B1 Subunit Polymorphism p.E161K Associates with Impaired Urinary Acidification in Recurrent Stone Formers

Dietary and Lifestyle Factors and Medical Conditions Associated with Urinary Citrate Excretion

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