For Health Care Professionals
- Buffers 40% more acid than 650mg sodium bicarbonate
- Lower sodium load per milliequivalent of buffer
- Enteric coated tablet:
- Easy to swallow which improves patient compliance
- Will not neutralize stomach acid and cause bloating
- Maximizes delivery of buffer to the serum
Managing Metabolic Acidosis in CKD patients
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Take control of acid imbalance
Improve outcomes
Slowing chronic kidney disease progression by correcting serum bicarbonate levels <22 mEq/L is well described 1, 2, 3 and in accordance with KDIGO guidelines 4.
However, to prevent compensatory damage which occurs within the kidney (as GFR declines) requires early alkaline intervention to reduce progressive retention of hydrogen ion. In early CKD, acid accumulation may not reduce serum bicarbonate levels (eubicarbonatemic metabolic acidosis); however it can result in initiation of pathologic consequences such as bone loss, muscle protein catabolism, and GFR decline 5, 6, 7.
It is important to treat the acid load and prevent pathologic homeostatic response in CKD patients even when serum bicarbonate and blood pH are within normal range 8.
Slow CKD progression
When kidney function declines, acid accumulates which necessitates alkali intervention. With the administration of alkali to CKD patients, we can slow progression of chronic kidney disease in both eubicarbonatemic and hypobicarbonatemic patients 7, 9, 10.
Metabolic acidosis has been found to be an independent risk factor for CKD progression 11.
Initiate alkali before clinical consequences occur
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Early Intervention Improves Outcomes 10, 12, 13
Acidosis – When to intervene
Normal
Acid Balance
- Normal blood pH
- Normal serum bicarb
Early Intervention
Initiate by Stage 2 CKD
Eubicarbonatemic Metabolic Acidosis
Acid load exceeds base reclamation and generation
- Early acid accumulation
- Compensatory response initiated
- Muscle catabolism and bone demineralization
- Normal blood pH
- Normal serum bicarb
Classical Intervention
Hypobicarbonatemic Metabolic Acidosis
Acid load overwhelms base reclamation and generation
- Acidemic
- Increased compensatory responses
- Muscle catabolism and bone demineralization
- Low blood pH
- Serum bicarb <22 mEq
Early intervention improves outcomes
Proton accumulation is present prior to the decline of serum bicarbonate. Early intervention with alkali may mitigate compensatory responses which promote kidney damage 14. Addressing acid imbalance in CKD patients with normal serum bicarbonate has been shown to preserve eGFR 7, 10.
What other nephrologists have said about acid balance management.
Acid balance has become the fourth leg of classical intervention.
Acid imbalance is part of the CKD condition
Classical interventions15
- BP lowering
- ACE inhibitors
- Glycemic control
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Why is RenaCarb the right alkali for your patients?
RenaCarb is a Low Sodium Alkali
40% more buffer with 25% less sodium than 650 mg sodium bicarbonate
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RenaCarb yields a lower sodium load per milliequivalent of buffer
Research has recast an 'old school' concern
Recent studies support magnesium’s beneficial effects on vascular calcification 16, 17. Improvement in T50 (serum calcification propensity)18 values and cardiovascular health19, 20, all support the selection of this cation to offset the sodium load from sodium bicarbonate while increasing the buffering capacity without hypermagnesemia.
“The replacement of the classical magnesium hydroxide by the carbonate congener yields a substrate for hepatic bicarbonate generation that is additionally less diarrheagenic.” 21
Magnesium carbonate is a more potent buffer than sodium bicarbonate
Various magnesium salts have differing degrees of buffering capacity and patient tolerance profiles. Magnesium carbonate provides a high acid neutralizing capacity. In addition, it also provides an excellent patient tolerance profile. Since magnesium carbonate has nearly twice the buffering capacity of sodium bicarbonate, the resulting tablet (magnesium carbonate and sodium bicarbonate) provides more total buffer with a lower sodium load than the standard 650 mg sodium bicarbonate.
Enteric coating improves GI tolerance
Generic sodium bicarbonate rapidly dissolves in the stomach which has been shown to cause gas production and bloating. By applying an enteric coating to RenaCarb, the alkali is delivered into the more neutral environment of the intestine.
Bypassing the stomach allows for less interference with digestion and scheduled medications. It is important to remember when taking an antacid (such as immediate release sodium bicarbonate) it is recommended not to take scheduled medications an hour prior to or two hours after an antacid dose. This is because antacids are known to interfere with certain medications.
By delivering the buffer past the stomach to the intestine, patients do not experience unpleasant GI side effects which improves patient compliance and will not impact digestion or medication schedules.
RenaCarb is a medical food formulated to be administered under the supervision of a physician in accordance with FDA regulations.
Dosing schedule
When initiating RenaCarb for an eubicarbonatemic patient, the starting dose should be based upon the amount of estimated base deficit. For guidance, the western diet typically produces 50 to >70 mEq/d of acid6.
To minimize the compensatory base generation from muscle and bone, supplementing with 10-20 mEq of base would be an appropriate starting dose. This translates to 1 to 2 tablets of RenaCarb daily without regard to meals or scheduled medication.
For hypobicarbonatemic patients, an initial starting dose of 2 to 3 tablets of RenaCarb daily without regard to meals or scheduled medication would be appropriate.
RenaCarb Ingredients: 470 mg sodium bicarbonate, 260 mg magnesium carbonate, microcrystalline cellulose, magnesium stearate, hydroxypropyl methyl cellulose, mica/titanium dioxide, polyethylene glycol, FD&C red #40, FD&C blue #2.
NephroTech
