title: Acid-base disturbances in nephrotic syndrome: analysis using the CO2/HCO3method (traditional Boston model) and the physicochemical method (Stewart model).
abstract: BACKGROUND
  The Stewart model for analyzing acid-base disturbances emphasizes serum albumin levels, which are ignored in the traditional Boston model. We compared data derived using the Stewart model to those using the Boston model in patients with nephrotic syndrome.
  
  
  METHODS
  Twenty-nine patients with nephrotic syndrome and six patients without urinary protein or acid-base disturbances provided blood and urine samples for analysis that included routine biochemical and arterial blood gas tests, plasma renin activity, and aldosterone. The total concentration of non-volatile weak acids (ATOT), apparent strong ion difference (SIDa), effective strong ion difference (SIDe), and strong ion gap (SIG) were calculated according to the formulas of Agrafiotis in the Stewart model.
  
  
  RESULTS
  According to the Boston model, 25 of 29 patients (90%) had alkalemia. Eighteen patients had respiratory alkalosis, 11 had metabolic alkalosis, and 4 had both conditions. Only three patients had hyperreninemic hyperaldosteronism. The Stewart model demonstrated respiratory alkalosis based on decreased PaCO2, metabolic alkalosis based on decreased ATOT, and metabolic acidosis based on decreased SIDa. We could diagnose metabolic alkalosis or acidosis with a normal anion gap after comparing delta ATOT[(14.09 - measured ATOT) or (11.77 - 2.64 × Alb (g/dL))] and delta SIDa [(42.7 - measured SIDa) or (42.7 - (Na + K - Cl)]). We could also identify metabolic acidosis with an increased anion gap using SIG > 7.0 (SIG = 0.9463 × corrected anion gap-8.1956).
  
  
  CONCLUSIONS
  Patients with nephrotic syndrome had primary respiratory alkalosis, decreased ATOTdue to hypoalbuminemia (power to metabolic alkalosis), and decreased levels of SIDa (power to metabolic acidosis). We could detect metabolic acidosis with an increased anion gap by calculating SIG. The Stewart model in combination with the Boston model facilitates the analysis of complex acid-base disturbances in nephrotic syndrome.
authors.affiliation: Division of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan. kasagi.tomomichi.284@mail.aichi-med-u.ac.jp.|Aichi Medical University School of Medicine, Nagakute, Aichi, 480-1195, Japan. kasagi.tomomichi.284@mail.aichi-med-u.ac.jp.
authors.forename: Tomomichi
authors.identifier: http://orcid.org/0000-0002-9150-1446
authors.initials: T
authors.lastname: Kasagi
authors.affiliation: Division of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Imai
authors.affiliation: Division of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
authors.forename: Naoto
authors.initials: N
authors.lastname: Miura
authors.affiliation: Division of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
authors.forename: Keisuke
authors.initials: K
authors.lastname: Suzuki
authors.affiliation: Division of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
authors.forename: Masabumi
authors.initials: M
authors.lastname: Yoshino
authors.affiliation: Division of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
authors.forename: Hironobu
authors.initials: H
authors.lastname: Nobata
authors.affiliation: Division of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
authors.forename: Takuhito
authors.initials: T
authors.lastname: Nagai
authors.affiliation: Division of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
authors.forename: Shogo
authors.initials: S
authors.lastname: Banno
mesh_terms: D000136:Acid-Base Equilibrium; D000137:Acid-Base Imbalance / Q000097:blood* / Q000175:diagnosis / Q000503:physiopathology / Q000652:urine; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001639:Bicarbonates / Q000097:blood*; D015415:Biomarkers / Q000097:blood / Q000652:urine; D002245:Carbon Dioxide / Q000097:blood*; D016022:Case-Control Studies; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D034141:Hypoalbuminemia / Q000097:blood / Q000503:physiopathology / Q000652:urine; D007668:Kidney / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D009404:Nephrotic Syndrome / Q000097:blood* / Q000175:diagnosis / Q000503:physiopathology / Q000652:urine; D011507:Proteinuria / Q000097:blood / Q000503:physiopathology / Q000652:urine; D012084:Renin-Angiotensin System; D000075462:Serum Albumin, Human / Q000378:metabolism
chemical_list: C422455:ALB protein, human; D001639:Bicarbonates; D015415:Biomarkers; D002245:Carbon Dioxide; D000075462:Serum Albumin, Human
keywords: Acid–base disturbance; Metabolic acidosis; Nephrotic syndrome; Renin–angiotensin–aldosterone system; Respiratory alkalosis