Proportion calcium to phosphorous

[hazel]

Ray says that the proportion of calcium that is higher than phosphorous in meals ... does he mean at each meal or throughout the day? I mean, can I have calcium as a snack to make up for a meat and potato meal? or should I include a dairy in that meal?

 

[Ben.]

Ray says that the proportion of calcium that is higher than phosphorous in meals ... does he mean at each meal or throughout the day? I mean, can I have calcium as a snack to make up for a meat and potato meal? or should I include a dairy in that meal?

I am no expert, but i would assume calcium with the phosphorus would be ideal to bind it intestinally.

But getting adequate calcium troughout the day is certainly good aswell if not contraindicated. Hormones and vitamin d matters in these equations however. So i do not want to make generalizating statements.


Maybe check these 2 links, out Basically vitamin b3 and sodium bicarbonate helps against phosphorus and calcium can be a helpful binder apparantly:

Reversing Chronic Kidney Disease with Niacin and Sodium Bicarbonate

"...
Recently, I had been putting together a new treatment algorithm with substantial literature support, data, on CKD. I was lucky to have been mentored by Dr. William F. Finn. [46]. Even if a patient has not already been scheduled for dialysis, he explained, and especially if they are currently on dialysis, you must get the serum phosphorus down. Excessive phosphorous is toxic to the kidneys as well as virtually every organ system and the entire body. [47,48] Phosphorus is a primary initiator of vascular calcification, among several other pathologies. If the kidneys start to lose a certain fraction of their normal function, the body can no longer efficiently clear phosphorous. When phosphorous serum levels reach abnormal levels, then you begin to saturate the tissues. Then phosphorous binds to calcium and it's the phosphorous, not the calcium that starts the pathology leading to calcium phosphate stones.

Niacin helps to get the phosphorous down.​

Even after you bring serum phosphate down you still have it in the tissues. The only biomarker available in a clinical setting, Fibroblast Growth Factor-23 (FGF-23), reflects the pathology behind long-term exposure to elevated phosphorus. FGF-23 can be decreased, simply by administering niacin. [14] However, the sodium phosphorous transporter works through a feedback mechanism to make more receptors to compensate.


So, calcium carbonate (from an antacid tablet) is commonly used first to bind the readily available intestinal phosphorous. This is among the cheapest and most effective phosphorus chelator approaches. Calcium carbonate should not be used above 2g/day elemental calcium, which is 40% of most of the formulations: Total 5g/day as calcium-carbonate. This should be administered at mealtime. The idea is to 'treat the meal', as there is generally very little phosphorous available to bind, outside of mealtime. When the kidney is in 'failure', after meals, excess phosphorous remains uncleared and leads to deposition in the tissues: valve leaflets; at the endothelial barrier; arterial subendothelial space (Mönckeberg's medial calcification: arteriosclerosis). [49] When sodium bicarbonate (baking soda) is administered, based on the landmark study, [50,51] the transition from stages-3 & 4 to Stage-5/ESRD/Dialysis, can be reduced by ~80%, with just 1.8 grams sodium bicarbonate, alone. Mealtime dosing BID, (1X 600mg at lunch & 2X 600mg at dinner each day, i.e 1.8g total per day), optimizes the therapy.


In that study, the fraction of people of people that went to dialysis by the end of two years was roughly 35% on placebo, but the fraction that went to dialysis with the modest dose of sodium bicarbonate, was reduced roughly > 80%. [50] However, the concerns about sodium intake are frequently expressed. The literature is quite clear on this. The chloride salt of sodium is the issue, not the bicarbonate salt of sodium. This a key point. We just need to do a better job of identifying them early on. Do not assume the patient is stage 1 or 2 if the creatinine indicated that. We need better, more reliable biomarkers (EXAMP: Cystatin-C) and should insist the insurance companies reimburse for it.


This approach worked amazingly well for my father, because he reversed his CKD, by more than two stages! I calculated it incrementally based on where he was at each stage. He was nearing end-stage renal disease (stage 5) and he reverted back to stage 2, which was a virtual miracle at that time! I had never heard or seen of anything similar.


Niacin interested me when I came across a company that was working on a new chelator for phosphorus. I had already seen some literature on an extended-release niacin (ER-niacin) study showing a phosphorus-lowering effect and IR-Niacin having an antiproteinuric effect. Niacin was so effective that it moved the GFR up enough to reverse the baseline status by a full stage, even at very low doses. This seemed to be the plausible explanation for this net result.


Niacin (as well as no-flush niacinamide/nicotinamide) inhibits the sodium phosphate transporter. There are at least twenty peer-reviewed publications demonstrating this. [5-41,52-59] What was discovered was, if you want to control phosphorus, niacin is one the most effective methods and its efficacy is not affected by timing relative to meals. As little as 100mg of niacin will effectively reduce the serum phosphorus.


Some studies refer to this niacin-mediated effect as the "phosphorous fix". The additional CKD benefits of niacin include the antiproteinuric, as well. If you compare a blood test vs. urine test, then the urine is probably a much more reliable indicator, because when the basement membrane is damaged, filtration is impaired such that the basement membrane between the podocyte processes no longer conserves plasma proteins & the amount lost, 'leaked' is present in the urine. The appearance of albumin (protein) in the urine is a 'flag' that loss of serum protein due to impaired renal function. Often, this is one of the earliest markers. Blood biomarkers have some variables that could result in misclassification of CKD stages. Protein leaking from the kidneys, is a direct correlate to the podocyte/basement-membrane damage. This is the gold-standard measure of endothelial function. I always like to use at least one blood marker (ideally CystatinC) in addition to the urine test, to facilitate extrapolating, "pinpointing" the true stage at baseline and where they are at follow-up.

Phosphate Binders: Hold the Calcium?​

" ... Phosphorus is ubiquitous in our daily diet, and its absorption is poorly regulated. We continue to absorb approximately 60 to 70% of dietary phosphorus regardless of bodily needs or renal function (5). As our renal excretory capacity diminishes, unrelenting absorption coupled with impaired excretion results in phosphorus retention. Dialysis effectively removes a single day’s worth of absorbed phosphorus (6); our patients generally receive dialysis only 3 d/wk, but they continue to eat on all 7 days. Therefore, to prevent phosphorus retention, we must first decrease dietary phosphorus, which results in less absorption and is always worthwhile but limited by the necessity to provide simultaneously adequate protein; second, inhibit intestinal phosphorus transport, which, although promising, has not reached the clinical arena; third, prescribe more frequent dialysis, which effectively prevents phosphorus retention but is not yet practicable for the majority of patients; and/or fourth, lessen absorption by binding intestinal phosphorus, which leads to increased fecal excretion, an approach used in the vast majority of dialysis patients.

How, then, should we bind intestinal phosphorus in dialysis patients? The ideal agent should selectively and irreversibly bind large amounts of phosphorus, require only a few relatively small pills, have no absorption or toxicity, and be inexpensive. None of the currently marketed phosphorus binders entirely satisfies these parameters. Because of toxicity, we have effectively eliminated aluminum as a binder. We are left with calcium-containing agents—calcium carbonate and calcium acetate—and non–calcium-containing agents—sevelamer hydrochloride and lanthanum carbonate—and others such as iron and magnesium that are infrequently used.

The current controversy revolves not around the need to bind phosphorus, for which there is broad agreement, but around the contribution of elemental calcium in calcium-containing phosphorus binders, if any, to vascular calcification and death. Moe and Chertow (7) argue that phosphorus is a uremic toxin; that serum calcium levels do not reflect calcium balance; that vascular calcification is a cell-mediated process accelerated by hyperphosphatemia and excess calcium load; and that in prospective, randomized studies, calcium-based phosphorus binders lead to increased arterial calcification, whereas the non–calcium-based phosphate binder sevelamer does not. Friedman (8) argues that the clinical trials that favor sevelamer are flawed, that the evidence that oral calcium intake modulates vascular and/or cardiac calcification is weak, that clinical trials reinforce the safety and the efficacy of the calcium-based phosphate binders, and that sevelamer is inordinately expensive.

In adult, nonpregnant humans, if net calcium absorption exceeds urine calcium excretion, then calcium must be retained (5). Dialysis patients absorb approximately 20% of dietary calcium, which increases with exogenously administered vitamin D3, and have essentially no urine calcium excretion, although there are small extrarenal losses (9). If the dialysis treatment itself results in no net calcium flux, then any absorbed calcium must be retained. Once bone calcium stores are replete, excess calcium must accumulate, with phosphorus as the preferred anion, in extraosseous sites with potential detrimental consequences. Indeed, repeated studies have shown excess calcium deposition in dialysis patients (10,11). Elevated serum phosphorus, which has the potential to transform vascular smooth muscle cells into collagen-secreting osteoblasts (12) and to bond with normal or perhaps elevated serum calcium, leads invariably to an elevated calcium × phosphorus product. The elevated product increases supersaturation for calcium phosphorus solid phases, potentially overwhelming inhibitors of calcification (13,14) and leading to deposition of calcium and phosphorus on this extraosseous, collagen matrix. Once the initial solid phase is formed, thermodynamics favor rapid crystal growth. This analysis argues against addition of oral calcium, especially when given with vitamin D3, the principal hormonal regulator of calcium and phosphorus absorption (5).

One should always support hypothetical arguments with facts. Two carefully performed, randomized, prospective studies demonstrated that use of the non–calcium-containing phosphate binder sevelamer attenuated progression of vascular calcification compared with calcium-based phosphate binders (15,16). Neither study was powered to demonstrate differences in mortality nor immune to thoughtful critique; however, the converse, that calcium-containing phosphate binders retard the progression of calcification compared with non–calcium-containing binders, has yet to be presented."

 

[Cloudhands]

people who need calcium should check out calcium acetate, its cheap to buy or make, and it has very potent phosphorus binding capabilities