You may also need dialysis. This treatment takes over for your damaged kidneys. It removes wastes, salt, extra water, and chemicals like phosphate from your blood. A few drugs help reduce the amount of phosphate your intestines absorb from foods you eat. These include:. Hyperphosphatemia is often a complication of chronic kidney disease.
One way to reduce your risk is by slowing kidney damage.
Protect your kidneys by treating the cause of your kidney disease. High phosphate levels in your blood can increase your risk for serious medical problems and other complications.
- Phosphorus | Linus Pauling Institute | Oregon State University.
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Treating hyperphosphatemia with dietary changes and medication as soon as possible can prevent these complications. Getting treated can also slow bone problems linked to chronic kidney disease.
Learn how to keep your kidneys healthy and prevent kidney disease. Find information on kidney disease, including causes, symptoms, diagnosis, and…. In end-stage kidney disease, also known as end-stage renal disease ESRD , the kidneys are functioning below 10 percent of their normal function.
Chronic kidney disease CKD is progressive and irreversible damage to the kidneys. The most common causes of CKD are high blood pressure and diabetes. Kidneys perform essential functions in your body, filtering waste and producing hormones. Read more on how to maintain good kidney health.
Phosphorus in Your Diet
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Food Sources of Phosphorus
Identifying your triggers can take some time and self-reflection. This anomaly in phosphate homeostasis was evidently shown by elevated fibroblast growth factor 23 FGF23 levels hormone-regulating phosphate excretion in early stages of CKD 4. The two main homeostatic mechanisms that regulate circulating phosphates are intestinal absorption and renal excretion. While intestinal absorption depends on the dietary pattern, renal excretion promotes removal of excess phosphates even in case of phosphate-rich diet through regulation of FGF23 and PTH 5 , 6.
In individuals with normal renal function, this is facilitated by decreased reabsorption of phosphates, which is mediated by downregulation of sodium phosphate cotransporters in the proximal tubule of the nephrons 7 , 8. However, in case of patients with CKD, the progressive reduction in glomerular filtration leads to further decrease in phosphate reabsorption, which compensates the renal insufficiency during the early stages of CKD. Elevated PTH induces excess bone resorption of phosphates, which exceeds bone formation, leading to osteoporosis and other skeletal structure abnormalities.
Furthermore, since skeletal structures could no longer act as phosphate reservoirs, soft tissues and vasculatures become secondary reservoirs, thereby leading to their calcification and increasing CV morbidity and mortality in patients with CKD 11 , 12 , 13 , Hyperphosphatemia in patients with CKD, apart from inducing secondary hyperparathyroidism and renal osteodystrophy, CV calcification is also an important prognostic factor for morbidity and mortality in patients with end-stage renal disease ESRD undergoing dialysis 15 , 16 , 17 , 18 , 19 , The prognostic role of serum phosphorous as a modifiable risk factor has also been reported in multiple observational studies, highlighting the potential effect of lowering blood phosphorous Pi and phosphates in CKD-MBD 17 , 21 , The therapeutic management of hyperphosphatemia includes decreasing intestinal absorption of phosphorus and increasing its renal removal.
The former includes dietary restriction to reduce phosphorus intake 24 , 25 , 26 , 27 and a phosphorus binder to reduce oral phosphorus absorption 15 , 16 , The latter includes regular dialysis to remove blood phosphorus, which is considered to be of limited value in removal of phosphates, highlighting the importance of dietary restriction 29 , Owing to the fact that proteins are the main source of dietary phosphates, which is difficult to restrict, dietary control of phosphates has its own pitfalls. To the best of our knowledge, this is the first review highlighting the phosphorus content in medications prescribed to patients with CKD.
Other than dairy or protein-based food products, which are rich in dietary phosphates, there is yet another source of dietary phosphorus that has remained unrecognized, i. In pharmaceutical preparation, phosphates are used both as an active pharmaceutical ingredient API; such as bisphosphonates or as a drug counterion e. This also includes some of the available drugs used for the treatment of CKD in which the most common role of phosphorus is as an excipient 34 , The largely unrecognized role of phosphorus content in medication is mainly due to its role in pharmaceutical preparations.
It is mostly used as a pharmaceutical excipient, which in most cases is reported on the packaging label without the precise concentration Phosphates as excipients are most commonly used as diluents, buffers to prevent pH fluctuations, and provide the required density for the preparation, thereby facilitating appropriate route of administration 32 , Although excipients are often considered as pharmacologically inert ingredients, they could also have iatrogenic effects as shown by diethylene glycol in sulfanilamide, which caused acute kidney injury, killing more than people in the US The phosphorus-containing excipients in drugs are not inert as they increase the phosphorus intake and thereby increase the blood phosphorus levels that could have potential iatrogenic effects Although the phosphorus content in excipients usually contribute to only a small fraction of the recommended daily intake, it is still clinically significant in terms of treating patients with CKD because most of these patients will be on multiple medications Polypharmacy is a major problem for patients with ESRD due to the burden of multiple comorbidities and dialysis-related complications caused by it 38 , If most of the medications consumed by patients undergoing dialysis contain phosphate, then this will significantly contribute to daily phosphorus intake of these patients, which may contribute to the progression of CKD-MBD.
Although the number of phosphate-binder pills taken by the patient is not accounted for in this study, the phosphate burden due to medication is significant Patients with CKD are usually prescribed a daily dose of multiple medications, and hence, drugs are an important source of phosphorus intake that cannot be ignored. Commonly used drugs for long-term oral administration in patients with CKD alleviate comorbidities related to CV system and central nervous system CNS.
The different medications include antihypertensives, anticoagulants, immunosuppressants, hypoglycemic agents, lipid-lowering drugs, analgesics, antihistamines, antidepressants, anti-gout drugs, and gastrointestinal drugs 35 , A potential confounder in estimating the medicinal phosphorus content is the wide variation observed with different formulations of the same drug from different manufactures, which has been highlighted in previous studies 31 , Although the label usually mentions that the drug contains phosphorus usually shown in the excipient list , the label does not specify the exact quantity of phosphorous present The extent of the problem was highlighted by a landmark study by Sherman et al.
They analyzed different doses of both the branded and generic forms of multiple drugs and reported dose-independent variations in phosphorus content between branded and generic formulations. Phosphorus was identified in both branded and generic forms of amlodipine, lisinopril, paroxetine, and bisoprolol. On the basis of their preliminary study, they also hypothesized that when the branded form of a drug is phosphorus-free, then the generic form may also be phosphorus-free.
Although contrary to their hypothesis, they observed generic form of paroxetine to contain lower concentration of phosphorus than the branded version In a subsequent large-scale analysis by the same authors, most commonly prescribed branded medications used in the dialysis centers of the US-based Dialysis Clinic, Inc. Nashville, TN were analyzed and reported 23 branded formulations As they could not ascertain the phosphorus content from the drug manufacturers, they estimated the phosphorus content of multiple doses of branded and generic formulations by spectroscopy-based method.
They reported the amount of phosphorus to vary from 1. The branded versus generic comparison revealed results similar to their earlier study. Furthermore, in order to confirm their hypothesis with respect to the absence of phosphorus in generic form, provided the branded form is phosphorus-free, they analyzed 91 generic drugs and found phosphorus in only 1 generic drug Pravachol, Eon despite the absence of phosphorus in its branded form 31 , The phosphorus content of branded versus generic formulation issue was also addressed by a similar study conducted by Shimoishi et al.
They also reported branded formulations such as amlodipine and paroxetine to be rich in phosphorus content among the study drugs. In case of paroxetine, all the generic formulations contained lower levels of phosphorus compared with the branded formulations, which was in concurrence to the study by Sherman et al. However, as the number of drugs examined by Shimoishi et al. In a similar study, Nelson et al. In order to find the precise amount of phosphorus, they contacted 26 drug manufacturers, out of which 18 manufacturers revealed the phosphorus content.
The quantum of phosphate-containing CKD drugs was also reported by a retrospective database analysis by Sultana et al. They utilized the PubChem and other publicly available databases to confirm the presence of phosphate in the medicinal products used to treat patients with CKD. Further investigations revealed that in majority of those medications phosphate was derived from the excipient One important observation made in all the above studies was the diverse amounts of phosphorus present in different formulations of the same drug, which highlights the difficulty in controlling medicinal phosphorus intake.
In view of the KDIGO guideline recommendations for dietary phosphorus intake in patients with CKD, the intestinal load of phosphorus through oral medications took precedence. Moreover, due to the practical difficulty involved with other routes of administration in patients with CKD, a bulk of the medicines were administered via oral route, which increases intestinal load of phosphorus.
Although a few previous studies had reported a serious concern with phosphorus content of medications, they did not report the precise nature of the phosphorus organic or inorganic as it may have potential ramifications in intestinal load. Moreover, the previous reports analyzed only the phosphorus content in the medicines prescribed to individual patient cohorts 31 , In order to address this issue, Cupisti et al. Moreover, it was observed that oral hypoglycemic drug formulations were the most phosphorus-containing drugs The major finding of the study was that the widely used form of phosphorus in excipient was calcium hydrogen phosphate On the basis of their finding and review of previous reports, they concluded that the phosphorus load in medications may be of concern only in a minor population with distinct medicinal requirements However, a comprehensive perspective on the potential effects of the additional medicinal phosphorus load in case of the phosphorus absorption and renal clearance by HD has to be considered.
Sodium salts of phosphorus are generally used as food quality-modifying, -emulsifying, -dispersing, -buffering, -chelating, -leavening, and -rehydrating agents and others On the contrary, calcium phosphate and calcium hydrogen phosphate are often used as a filler to combine pharmaceutical ingredients to form a tablet-based solid preparation 43 , 44 , The amount of phosphorus contributed by medications is minor in most patients; however, in some, it is notable.
Therefore, even a minor increase in phosphorus intake may have a disproportional effect, which could be seen from two perspectives.
Phosphorus - P
From the perspective of phosphorus-binding pills, the reported medicinal phosphorus load requires four additional doses of sevelamer or calcium acetate to counter the medicinal phosphorus load. Another important aspect of significance is the phosphorus content of vitamin supplements prescribed for patients with CKD Nevertheless, medicinal drugs as a hidden source of phosphorus in patients with CKD cannot be neglected.
If alternative drugs with similar safety, efficacy, and cost exist, they are preferable to be used in place of drugs with high-phosphorus content such as lisinopril, amlodipine, and bisoprolol in order to reduce oral phosphorus intake. The probable efficacy of low-phosphorus-containing alternatives could be seen from the perspective of daily phosphorus intake and its removal by dialysis.