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Why take GI friendly enteric coated Bicarbi.

Clinical Studies show that around 35% of CKD patients taking uncoated sodium bicarbonate for Metabolic Acidosis cannot tolerate the therapeutic dose needed to reach their serum bicarbonate (TCO2) goal. The primary reason is excessive bloating, belching or burping and acid reflux. Bicarbi is GI friendly enteric coated sodium bicarbonate, designed of offer the benefits of bicarbonate, without the GI side effects of uncoated sodium bicarbonate.

Cutting the number of pills needed in half with Bicarbi Double Strength.

Each enteric coated capsule of Bicarbi has 650mg of sodium bicarbonate. Each enteric coated capsule of Bicarbi Double Strength has 1300mg of sodium bicarbonate. Bicarbi Double Strength is designed to control Metabolic Acidosis due to CKD with half the pills versus 650mg capsules.

Chronic Kidney Disease.

30 million people in the United States have Chronic Kidney Disease or CKD per the US Centers for Disease Control (CDC). Chronic kidney disease ranges between Stage 1 when the kidneys start to have mild disfunction to Stage 5, sometimes called ESRD or End Stage Renal Disease, where the kidneys have complete or near complete loss of function, requiring dialysis or kidney transplant.

About Metabolic Acidosis due to CKD, and why proper treatment is important.

Metabolic acidosis is a condition which occurs in a significant number of people who develop chronic kidney disease (CKD). Our body produces acid as part of daily functioning. This acid which is found in the serum (a component of blood) is removed by the kidneys. When kidney function declines, this metabolic or serum acid can build up in the body and cause problems like the faster progression of kidney disease, muscle wasting, bone disease, inflammation and malnutrition. This serum acid is called metabolic acid, because it is produced from everyday body function and the metabolism of food. This acid has no relation to stomach acid.

The kidneys are a key part in keeping serum acid in balance. When serum acid is too high and the kidneys don't have the ability to reduce this acid, metabolic acidosis can occur. Uncontrolled metabolic acidosis has been clinically proven to further damage the kidneys, causing a faster decline in kidney function.

Controlling metabolic acidosis is one of the most profound factors in slowing the progression of CKD, retaining kidney function, and avoiding or delaying kidney dialysis. Clinical studies have shown that in people with CKD, lowering serum acid to raise serum bicarbonate from 19.9 mEq/l to 24mEq/l can slow the progression of kidney disease by 2-3 fold (200-300%). Click on the HCP section and the Bicarbonate Case Studies section for more information.

How Metabolic Acidosis is Diagnosed

Metabolic acidosis in chronic kidney disease is diagnosed with a routine blood test which is included as part of the kidney function panel or metabolic panel. The test is called many things including: Serum Bicarbonate, Serum TCO2, Total CO2, TCO2, CO2, or Carbon Dioxide. All of these tests are measuring the amount of bicarbonate in the serum. The optimal value of serum bicarbonate ranges between 23-29 mEq/L. A serum bicarbonate of less than 22 mEq/L in individuals with kidney disease is usually considered significant enough to require treatment with an acid buffering agent or base, such as sodium bicarbonate, the active ingredient in enteric coated Bicarbi.

Correcting elevated serum acid levels can slow kidney disease and the loss of kidney function.

Correcting metabolic acidosis or elevated serum acid levels with sodium bicarbonate has been shown to delay the progression of kidney disease and loss of kidney function. Correcting metabolic acidosis may be one of the most profound and important factors in protecting your kidneys. For more information on the importance of managing serum bicarbonate levels and reducing serum acid levels, please see the Bicarbonate Case studies page. This page compares the rate of kidney function decline with different levels of serum Bicarbonate or serum TCO2.

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Frequently Asked Questions about Bicarbi

Click on any question to expand the answer

  • Each capsule of Bicarbi contains 650 mg of sodium bicarbonate in an enteric coated capsule. Bicarbi is used to treat metabolic acidosis or elevated blood acid levels. The acid in blood with metabolic acidosis is different from stomach acid. Elevated blood acid occurs when the body produces excessive quantities of acid or the kidneys aren't removing enough acid from the blood.
  • Yes, several studies have clearly shown that reducing elevated serum or blood acid or raising serum bicarbonate with sodium bicarbonate, the active ingredient in Bicarbi, can slow the progression of kidney disease by 2-3 fold. Properly treating metabolic acidosis is one of the most profound factors in slowing the progression of kidney disease.

    One study even showed not only did reducing serum acid levels (the same as raising low serum bicarbonate levels) reduce the risk of kidney failure but it also improved the nutritional status of people with kidney disease.

    This said, lowering serum or blood acid (or raising low bicarbonate levels) is only one part in improving outcomes for those with chronic kidney disease. Your health care provider will give you guidance on controlling blood pressure, controlling glucose, potential weight loss and some dietary requirements. All of these and more are modifiable factors in improving the outcome of chronic kidney disease or CKD. See 'References' in the 'About Metabolic Acidosis' section if you are interested in some of the published clinical data about improving bicarbonate levels in CKD.
  • Sodium bicarbonate is an acid buffer or a base. Sodium Bicarbonate is often used in clinical settings. It is widely used to treat metabolic acidosis due to CKD.
  • Bicarbi is new and many Health Care Providers don't yet know about it.
  • Bicarbi has an enteric coating so the sodium bicarbonate in Bicarbi won’t react with stomach acid. When un-coated raw sodium bicarbonate is taken, some of it reacts with the acid in the stomach and is lost and turned into carbon dioxide gas before it can enter the small intestine. When the bicarbonate is lost to carbon dioxide gas some potency is lost. The production of carbon dioxide gas from uncoated sodium bicarbonate reacting with stomach acid may also increase gastric discomfort, boating, belching or burping.
  • Your healthcare provider will guide you on your specific dosing for Bicarbi. The typical dose for Bicarbi is one capsule twice daily. Dosing can vary depending on your current needs. The need for bicarbonate supplementation and adjustment can change.
  • Resources where you can learn more about Metabolic Acidosis and Chronic Kidney disease include the NKF-National Kidney Foundation, the AAKP-American Association of Kidney Patients and UpToDate.


  1. Kraut JA, Madias NE. Metabolic Acidosis of CKD: An Update.
    Am J Kidney Dis. 2015 Oct 15
  2. Starke A, Corsenca A, Kohler T, Knubben J, Kraenzlin M, Uebelhart D, et al. Correction of metabolic acidosis with potassium citrate in renal transplant patients and its effect on bone quality.
    Clin J Am Soc Nephrol. 2012 Sep. 7(9):1461-72
  3. Abramowitz MK, Melamed ML, Bauer C, Raff AC, Hostetter TH. Effects of oral sodium bicarbonate in patients with CKD.
    Clin J Am Soc Nephrol. 2013 May. 8(5):714-20
  4. De Brito-Ashurst L, Varagunam M, Raferty J, Yaqoob M. Bicarbonate Supplementation Slows Progression of CKD and Improves Nutritional Status.
    J Am Soc Nephrol. 2009 , 20: 2075-2084
  5. Phisikul S, Khanna A, Simon J, Amelioration of metabolic acidosis in patients with low GFR reduced kidney endothelin production and kidney injury, and better preserved GFR
    Kidney Int. 2010; 77:617-623
  6. Kraut J, Madias N, Retarding progression of chronic kidney disease : use of modalities that counter acid retention.
    Curr Opin Nephrol Hypertens 2018 27:94-101
  7. Kovesdy CP, Anderson JE, Kalantar-Zadeh K. Association of serum bicarbonate levels with mortality in patients with non-dialysis dependent CKD.
    Nephrol Dial Tranplant 2009; 24:1232.