Dietary Acid Load and Urinary Health: The Impact of Animal vs Plant Protein

References

I said I used MDCalc but I was mistaken I use MedCalX which is nice but getting dated. 

We talked about this out of print book that we love: Cohen, J. J., Kassirer, J. P. (1982). Acid-base. United States: Little, Brown.

Josh mentioned this article that looked at over 17,000 samples with simultaneous measured and calculated bicarbonate and found a very small difference. Comparison of Measured and Calculated Bicarbonate Values | Clinical Chemistry | Oxford Academic

Base deficit or excess- Diagnostic Use of Base Excess in Acid–Base Disorders | NEJM (check out the accompanying letter to the editor from Melanie challenging this article! Along with colleagues Lecker and Zeidel Diagnostic Use of Base Excess in Acid-Base Disorders )

Melanie loves this paper which shows a nice correlation between arterial and venous pH but the rest of the comparisons are disappointing - Comparison of arterial and venous pH, bicarbonate, Pco2 and Po2 in initial emergency department assessment - PMC

A nomogram for the interpretation of acid-base data is figure 17-1 in the book, this manuscript with the ! in the conclusion creates the acid-base map. 

We debated about whether we like Winter’s formula: Quantitative displacement of acid-base equilibrium in metabolic acidosis (melanie does b/c it used real patients). 

Amy’s Voice of God on Dietary Acid Load

Review of dietary acid load: https://pubmed.ncbi.nlm.nih.gov/23439373/, https://pubmed.ncbi.nlm.nih.gov/38282081/, https://pubmed.ncbi.nlm.nih.gov/33075387/

Survey data from kidney stone formers regarding sources of dietary acid load: https://pubmed.ncbi.nlm.nih.gov/35752401/

Urine profile for vegans and omnivories (urine pH and cations/anions): https://pubmed.ncbi.nlm.nih.gov/36364731/

SWAP-MEAT pilot trial: https://pubmed.ncbi.nlm.nih.gov/39514692/ looked at urine profile on plant based meat diet (Beyond Meat) versus animal based meat diet

Not all plant meat substitutes are the same in terms of net acid load: https://pubmed.ncbi.nlm.nih.gov/38504022/

Frassetto paper showing that the dietary acid load effect is mostly from sodium chloride: https://pubmed.ncbi.nlm.nih.gov/17522265/

Healthy eating is probably more important than plant based diet for CKD: https://pubmed.ncbi.nlm.nih.gov/37648119/, https://pubmed.ncbi.nlm.nih.gov/32268544/

KDIGO 2024 guidelines: https://kdigo.org/guidelines/ckd-evaluation-and-management/

Association (or lack thereof) of a pro-vegetarian diet and sarcopenia/protein energy wasting in CKD: https://pubmed.ncbi.nlm.nih.gov/39085942/

Outline Chapter 17 Introduction to simple and mixed acid-base disorders

Introduction to Simple and Mixed Acid-Base Disorders

Disturbances of acid-base homeostasis are common clinical problems

Discussed in Chapters 18-21

This chapter reviews:

Basic principles of acid-base physiology

Mechanisms of abnormalities

Evaluation of simple and mixed acid-base disorders

Acid-Base Physiology

Free hydrogen is maintained at a very low concentration

40 nanoEq/L

1 millionth the concentration of Na, K, Cl, HCO3

H+ is highly reactive and must be kept at low concentrations

Compatible H concentration: 16 to 160 nanoEq/L

pH range: 7.8 to 6.8

Buffers prevent excessive variation in H concentration

Most important buffer: HCO3

Reaction: H+ + HCO3 <=> H2CO3 <=> H2O + CO2

H2CO3 exists at low concentration compared to its products

Henderson-Hasselbalch Equation (HH Equation)

Understanding acid-base can use both H+ concentration and pH

Measurement of pH

Must be measured anaerobically to prevent CO2 loss

Measurement methods:

pH: Electrode permeable to H+

PCO2: CO2 electrode

HCO3: Calculated using HH Equation

Alternative: Add strong acid, measure CO2 released

PCO2 * 0.03 gives mEq of CO2

Measured vs. Calculated HCO3

pKa of 6.1 and PCO2 coefficient (0.03) vary

Measurement of CO2 prone to error

Debate remains unresolved

Differences affect anion gap calculations

Arterial vs. Venous Blood Gas (ABG vs. VBG)

Venous pH is lower due to CO2 retention

Venous blood may be as accurate as arterial for pH if well perfused

Pitfalls in pH Measurement

Must cool ABG quickly to prevent glycolysis

Air bubbles affect gas readings

Heparin contamination lowers pH

Arterial pH may not reflect tissue pH

Reduced pulmonary blood flow skews results

End tidal CO2 > 1.5% indicates adequate venous return

Regulation of Hydrogen Concentration

HCO3/CO2 as the Principal Buffer

High HCO3 concentration

Independent regulation of HCO3 (renal) and PCO2 (lungs)

Renal Regulation of HCO3

H secretion reabsorbs filtered bicarbonate

Loss of HCO3 in urine equates to H retention

H combines with NH3 or HPO4, forming new HCO3

Pulmonary Regulation of CO2

CO2 is not an acid but forms H2CO3

Lungs excrete 15,000 mmol of CO2 daily

Kidneys excrete 50-100 mmol of H daily

H = 24 * (PCO2 / HCO3)

pH compensation via respiratory and renal adjustments

Acid-Base Disorders

Definitions

Acidemia: Decreased blood pH

Alkalemia: Increased blood pH

Acidosis: Process lowering pH

Alkalosis: Process raising pH

Primary PCO2 abnormalities: Respiratory disorders

Primary HCO3 abnormalities: Metabolic disorders

Compensation moves in the same direction as the primary disorder

Diagnosis requires extracellular pH measurement

Metabolic Acidosis

Low HCO3 and low pH

Causes:

HCO3 loss (e.g., diarrhea)

Buffering of non-carbonic acid (e.g., lactic acid, sulfuric acid in renal failure)

Compensation: Increased ventilation lowers PCO2

Renal excretion of acid restores pH over days

Metabolic Alkalosis

High HCO3 and high pH

Causes:

HCO3 administration

H loss (e.g., vomiting, diuretics)

Compensation: Hypoventilation

Renal HCO3 excretion corrects pH unless volume or chloride depleted

Respiratory Acidosis

Due to decreased alveolar ventilation, increasing PCO2

Compensation: Increased renal H excretion raises HCO3

Acute phase: Large pH drop, small HCO3 increase

Chronic phase: Small pH drop, large HCO3 increase

Respiratory Alkalosis

Due to hyperventilation, reducing CO2 and raising pH

Compensation: Decreased renal H secretion, leading to bicarbonaturia

Time-dependent compensation (acute vs. chronic phases)

Mixed Acid-Base Disorders

Multiple primary disorders can coexist

Example:

Low arterial pH with:

Low HCO3 → Metabolic acidosis

High PCO2 → Respiratory acidosis

Combination indicates mixed disorder

Extent of renal and respiratory compensation clarifies diagnosis

Compensation does not fully restore pH

Example: pH 7.4, PCO2 60, HCO3 36 → Combined respiratory acidosis & metabolic alkalosis

Acid-Base Map illustrates normal responses to disturbances

Clinical Use of Hydrogen Concentration

H+ vs. pH Relationship

H = 24 * (PCO2 / HCO3)

Normal HCO3 cancels out 24, so H = 40 nMol/L

pH to H conversion:

Increase pH by 0.1 → Multiply H by 0.8

Decrease pH by 0.1 → Multiply H by 1.25

Example: Salicylate Toxicity

7.32 / 30 / xx / 15

Goal: Alkalinize urine to pH 7.45 (H+ = 35 nMol/L)

Bicarb needs to reach 20 for compensation

Potassium Balance in Acid-Base Disorders

Metabolic Acidosis

H+ buffered in cells, causing K+ to move extracellularly

K+ rises ~0.6 mEq/L per 0.1 pH drop

Less predictable in lactic or ketoacidosis

DKA-associated hyperkalemia due to insulin deficiency

Hyperkalemia can induce mild metabolic acidosis

Respiratory Acid-Base Disorders

Minimal effect on potassium levels