Measurement of total CO2 in microliter samples of urine and other biological fluids using infrared detection of CO2

Trepiccione, Francesco; Iena, Francesco Maria; Catalini, Laura; Carpi, Francesco M.; Koed, Mogens; Frische, Sebastian

doi:10.1007/s00424-017-1997-8

Cited by 13 publications

(10 citation statements)

References 19 publications

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“…Urine bicarbonate was measured by an in-house developed device as described (Trepiccione et al, 2017 ). Briefly 20 μl of urine was placed in a hermetically closed chamber.…”

Section: Methodsmentioning

confidence: 99%

Deficiency of Carbonic Anhydrase II Results in a Urinary Concentrating Defect

et al. 2018

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Carbonic anhydrase II (CAII) is expressed along the nephron where it interacts with a number of transport proteins augmenting their activity. Aquaporin-1 (AQP1) interacts with CAII to increase water flux through the water channel. Both CAII and aquaporin-1 are expressed in the thin descending limb (TDL); however, the physiological role of a CAII-AQP1 interaction in this nephron segment is not known. To determine if CAII was required for urinary concentration, we studied water handling in CAII-deficient mice. CAII-deficient mice demonstrate polyuria and polydipsia as well as an alkaline urine and bicarbonaturia, consistent with a type III renal tubular acidosis. Natriuresis and hypercalciuria cause polyuria, however, CAII-deficient mice did not have increased urinary sodium nor calcium excretion. Further examination revealed dilute urine in the CAII-deficient mice. Urinary concentration remained reduced in CAII-deficient mice relative to wild-type animals even after water deprivation. The renal expression and localization by light microscopy of NKCC2 and aquaporin-2 was not altered. However, CAII-deficient mice had increased renal AQP1 expression. CAII associates with and increases water flux through aquaporin-1. Water flux through aquaporin-1 in the TDL of the loop of Henle is essential to the concentration of urine, as this is required to generate a concentrated medullary interstitium. We therefore measured cortical and medullary interstitial concentration in wild-type and CAII-deficient mice. Mice lacking CAII had equivalent cortical interstitial osmolarity to wild-type mice: however, they had reduced medullary interstitial osmolarity. We propose therefore that reduced water flux through aquaporin-1 in the TDL in the absence of CAII prevents the generation of a maximally concentrated medullary interstitium. This, in turn, limits urinary concentration in CAII deficient mice.

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“…Urine bicarbonate was measured by an in-house developed device as described (Trepiccione et al, 2017 ). Briefly 20 μl of urine was placed in a hermetically closed chamber.…”

Section: Methodsmentioning

confidence: 99%

Deficiency of Carbonic Anhydrase II Results in a Urinary Concentrating Defect

et al. 2018

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“…Measurements were performed by a Corning 960 analyzer 23 calibrated to small volume samples in the pendrin mice series and by a custom-built infrared CO 2 sensor-based system in the rest of the experimental series. 24 In urine samples from human participants, the same principle was applied, but the system was redesigned using a GM70 Carbon Dioxide Meter (Vaisala, Helsinki, Finland) and 5 ml sample sizes.…”

Section: Urine Hcomentioning

confidence: 99%

Impaired Renal HCO3 - Excretion in Cystic Fibrosis

Berg

Svendsen

Sørensen

et al. 2020

JASN

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BackgroundPatients with cystic fibrosis (CF) do not respond with increased urinary HCO3− excretion after stimulation with secretin and often present with metabolic alkalosis.MethodsBy combining RT-PCR, immunohistochemistry, isolated tubule perfusion, in vitro cell studies, and in vivo studies in different mouse models, we elucidated the mechanism of secretin-induced urinary HCO3− excretion. For CF patients and CF mice, we developed a HCO3- drinking test to assess the role of the cystic fibrosis transmembrane conductance regulator (CFTR) in urinary HCO3-excretion and applied it in the patients before and after treatment with the novel CFTR modulator drug, lumacaftor-ivacaftor.Resultsβ-Intercalated cells express basolateral secretin receptors and apical CFTR and pendrin. In vivo application of secretin induced a marked urinary alkalization, an effect absent in mice lacking pendrin or CFTR. In perfused cortical collecting ducts, secretin stimulated pendrin-dependent Cl−/HCO3− exchange. In collecting ducts in CFTR knockout mice, baseline pendrin activity was significantly lower and not responsive to secretin. Notably, patients with CF (F508del/F508del) and CF mice showed a greatly attenuated or absent urinary HCO3−-excreting ability. In patients, treatment with the CFTR modulator drug lumacaftor-ivacaftor increased the renal ability to excrete HCO3−.ConclusionsThese results define the mechanism of secretin-induced urinary HCO3− excretion, explain metabolic alkalosis in patients with CF, and suggest feasibility of an in vivo human CF urine test to validate drug efficacy.

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“…Fasting urine pH was measured using a standard pH meter [16]. Urinary bicarbonate was evaluated by acid base titration according to previous studies [17,18].…”

Section: Patient Recruitment and Renal Function Analysismentioning

confidence: 99%

Urinary Metabolic Profile of Patients with Transfusion-Dependent β-Thalassemia Major Undergoing Deferasirox Therapy

Capolongo

Zacchia

Beneduci

et al. 2020

Kidney Blood Press Res

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Introduction: Renal dysfunction is a frequent complication in patients suffering from β-thalassemia major (β-TM). The aim of this study was to analyze the renal function and urine metabolomic profile of β-TM patients undergoing transfusions and deferasirox (DFX) therapy, in order to better characterize and shed light on the pathogenesis of renal disease in this setting. Methods and Subjects: 40 patients affected by β-TM treated with DFX and 35 age-and gender-matched healthy controls were enrolled in the study. Renal function was assessed. Glomerular filtration rate (GFR) was estimated with CKD-EPI and Schwartz formula for adults and children, respectively. Renal tubular function and maximal urine concentration ability were tested. Urine specimens were analyzed by nuclear magnetic resonance spectroscopy to identify the urinary metabolite profiles. Results: The study of renal function in β-TM patients revealed normal estimated (e)GFR mean values and the albumin-to-creatinine ratio was < 30 mg/g. The analysis of tubular function showed normal basal plasma electrolyte levels; 60% of patients presented hypercalciuria and many subjects showed defective urine concentration. Several amino acids, N-methyl compounds, and organic acids were overexcreted in the urine of thalassemic patients compared with controls. Discussion: The major finding of this work is that β-TM patients and controls exhibit different concentrations of some metabolites in the urine. Early recognition of urinary abnormalities may be useful to detect and prevent kidney damage.

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Measurement of total CO2 in microliter samples of urine and other biological fluids using infrared detection of CO2

Cited by 13 publications

References 19 publications

Deficiency of Carbonic Anhydrase II Results in a Urinary Concentrating Defect

Deficiency of Carbonic Anhydrase II Results in a Urinary Concentrating Defect

Impaired Renal HCO3 - Excretion in Cystic Fibrosis

Urinary Metabolic Profile of Patients with Transfusion-Dependent β-Thalassemia Major Undergoing Deferasirox Therapy

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