Renal Compensation, Kidney Disease and Nutrition: What To Eat and What To Avoid

Individuals with end-stage renal disease are often prompted to follow a special diet and pay special attention to what they eat and what they should especifically avoid. As per discussed in previous articles by Joe Cosgrove, a renal diet is always recommendable for those patients with any sort of renal disease or kidney failure. End-stage renal disease and kidney failure patients often, if not always, are required to follow a specific nutrition plan and diet simply because their kidneys are not working properly, thusly making it more difficult for the organs to process certain foods. Thus, following a tailored diet puts less effort on the kidneys and, moreover, may actually improve the individual’s overall health.

Even if an individual suffers from any type of kidney disease, it is of high importance to stick with a renal nutrition plan specially tailored to improve the individual’s kidney function in order to prevent further decay. A renal nutrition plan seeks to reduce the intake of several nutrients such as protein and phosphorus alongside other elements such as potassium, calcium, and sodium. By sticking with a renal diet, individuals and patients with kidney disease can definitely lower the amount of toxins and waste products the body accumulates in order to improve organ function.

Pay special attention to minerals

Sodium

Sodium can be found in the vast majority of the foods, and, moreover, it is often added to highlight some flavors. Most individuals believe that salt and sodium are the same; however, salt is actually the compound byproduct of chloride and sodium. Sodium is one of the body’s most important electrolytes and it helps monitor and control the balance of the body and its cells. It helps the body carry out some of its basic functions: it regulates blood pressure, nerve function and muscle contraction, acid-base balance, balances the amount of fluids that the body needs to either keep or eliminate, among others. In order to keep an eye on sodium intake, there are some things individuals can do: they can always go through food labels in order to determine the amount of sodium, they can pay attention to servings and, of course, abstain themselves from buying prepackaged meat and all types of processed foods. Choosing to cook at home using fresh ingredients is also a good way to monitor mineral intake.

Potassium

Aside from sodium, potassium is one of the body’s basic needs. This mineral plays a major role in keeping a regular heartbeat and the muscles working as they should. Potassium also helps the body maintain fluid and electrolyte balance in the blood. Kidneys help the body keep an adequate balance of this mineral in the body. Individuals with renal disease and end-stage kidney failure often struggle to maintain these levels, and since the kidney can no longer complete this task properly, the accumulation and buildup of potassium may lead to a condition commonly referred to as hyperkalemia, which can be diagnosed should the patient start showing symptoms such as muscle weakness and irregular heartbeat. In order to better monitor potassium intake, individuals can always come up with a diet plan with the help of a dietitian, limit foods with high a high potassium content, limit all sorts of dairy products, eat fruits and vegetables and stay away from any salt substitute and seasonings with high potassium content.

Phosphorus

Phosphorus stands out as one of the body’s most important mineral as it is responsible for bone maintenance and development. It also plays a key role in developing other organs and connective tissue. Phosphorus is also involved in muscle movement. People with end-stage kidney disease or any issue related with kidney function often experience imbalances in the mineral which has been related to worsening kidney function as it may lead the body to accumulate phosphorus in the blood. An increase in phosphorus levels can take calcium away from the bones, thusly making them much weaker, and the subsequent increase of calcium in the bloodstream often ends up being allocated in other organs or blood vessels.

In order to better monitor the intake of this mineral, patients, and individuals, in general, can start learning which foods are rich in phosphorus—such as meat, fast food, canned fish, and cheese—, eat smaller servings and pay special attention to PHOS in labels.

 

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What foods should individuals with renal disease include in their diet plans?

According to a study, and aside from the aforementioned words of advice, adding fruits and vegetables to an individual’s diet may help protect the organs from further deterioration. In the western hemisphere, a diet commonly consists of animal and grain foods, which are highly acidic. When an individual suffers from any type of kidney disease, the body is unable to get rid of the toxins and the excess acid found in the body, which is why some patients suffer episodes of metabolic acidosis. The idea is to increase the intake of less-acidic foods in hopes of alkalizing the body, thusly helping patients preserve, to some extent, a much better organ function.

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Acid-Base Compensation: What is it, and how to prevent it?

Acid-base Compensation is the relative constancy of the acid-base relationship of the internal environment of a living organism, particularly when it comes to the renal system. Also called acid-base balance, acid-base balance, equilibrium of acids and bases. It is an integral part of homeostasis. Quantitatively it is characterized either by the concentration of hydrogen ions in moles per one liter or by the hydrogen pH. The tissues of a living organism are very sensitive to fluctuations in the pH value – outside the permissible range, protein denaturation occurs: cells are destroyed, enzymes lose their ability to perform their functions, and the body can die. Therefore, the acid-base balance in the body is tightly regulated. There are several buffer systems that reversibly bind hydrogen ions and prevent any changes in pH. The bicarbonate buffer system (the most powerful and most controllable among buffer systems) is particularly important: an excess of protons interacts with bicarbonate ions (metabolic alkalosis) to form carbonic acid. Further decrease in the amount of carbonic acid occurs as a result of an accelerated release of carbon dioxide as a result of hyperventilation of the lungs (concentration is determined by the pressure in the alveolar gas mixture.)

There are several approaches for the evaluation and classification of acid-base balance alterations. The physicochemical proposal is the most recent and is based on the difference of strong ions, the total concentration of weak plasma acids and the partial pressure of arterial carbon dioxide. Of great acceptance among anesthesiologists and intensivists, it is a tremendous complex approach, both technical and interpretation. Therefore, in this post, the physiological approach will be used, based on pH, and plasma bicarbonate, which is the simplest, most rigorous and practical way to systematically classify and treat alterations in the acid-base balance.

First of all acid-base disorder must answer three basic questions. The first has to do with what disorder it is. The second, if the secondary response is adequate. The third, about the cause of the disorder. Metabolic acidosis is divided according to the value of the anionic hiatus. Acidosis with increased anionic hiatus: acid gain, endogenous or exogenous, predominates. They are normochloremic acidosis. Acidosis with normal anionic hiatus: the loss of bicarbonate outside the body predominates. They are called hyperchloremic acidosis.

Approximately three-quarters of the value of the anion hiatus correspond to serum albumin, which is an anion, so in the assessment of the anion, hiatus should be taken into account if hypoalbuminemia, as well as other circumstances.

The acid-base balance of the organism is possible thanks to the interrelation of three systems: intracellular and extracellular tampons, which cushion in a minute the acute changes of acid-base balance; respiratory compensation, which starts in minutes and is completed in hours, and renal excretion of excess acids, which takes more time. The total buffer capacity of the organism is about one thousand mMol (forty percent in the extracellular space, and sixty in the intracellular space.)

To plan an adequate treatment, and as in any acid-base disorder, it is essential to identify secondary responses (compensation mechanisms), whether these are adequate or not, and whether there are other acid-base mixed disorders or associated electrolyte disorders.

Read also: How to reduce the chances of suffering renal failure, by Joe Cosgrove

In metabolic acidosis, the key aspect of treatment lies in blocking the source of acid production (eg, by providing insulin in diabetic ketoacidosis,) always taking into account the compensations that exist, the rate of acid production and its cause (lactic acidosis due to hypoxia or alcohol intoxication are more serious due to its rapid evolution.) Special caution when planning treatment deserves the detection of hypokalemia since it implies a serious potassium deficit. The replacement of bicarbonate should be very cautious, applied only in certain circumstances (eg, extreme hyperkalemia, potentially fatal drops in pH,) and always assessing the risks and benefits. The only objective is to gain time until the homeostatic mechanisms manage to increase the pH.

To the problem of acidosis due to keto acids caused by insulin deficiency, water deficit, circulating volume deficit, the coexistence of lactic acidosis and potassium deficit, which in turn depends on the duration and magnitude of polyuria secondary to poor glycemic control, and the degree of replacement of losses.

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The general treatment plan should include, therefore: Insulin, re-expansion of the extracellular volume, correction of possible potassium deficit, and the decision to administer or not bicarbonate should be valued with great caution. The alterations in the bicarbonate concentration or the partial pressure of carbon dioxide in the arterial blood are accompanied by a compensatory response in the other element. If the compensation is adequate or it will not allow detecting if there is a second or third associated disorder, in what constitute the mixed disorders that are very frequent in clinical practice and that implies a greater severity.

In order to detect mixed disorders, it must be taken into account that a compensation will never be able to normalize the pH. Its treatment and the priority of the actions to follow will depend on the cause and predominant acid-base disorder, always taking into account the associated electrolyte alterations.

Recommended: Acid-Base Disorders

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Understanding Acid-Base Disorders: Metabolic Acidosis

Pentec Health CEO Joe Cosgrove has addressed before the topic of dialysis in several occasions; however, and given the variety of health issues related to renal failure, it is also important to discuss and clarify the doubts people may have about other renal pathologies such as acid-base disorders.

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Since acid-base disorders entails the deep study of kidneys, and every case depends on the patient, if one were to fully understand this topic, one would need to go through all the formulas in order to completely get the full picture of a given case, nevertheless, there is a way for readers to understand what is this thing commonly referred to as “compensation”—or renal compensation in an acid-base disorder, for this matter—, and furthermore understand what is going on under these circumstances. To understand compensation, it is advisable to take a few steps back in order to see a depiction of what is happening in the blood when it has a lot of acid as in metabolic acidosis, for instance.

Actually, acid-base disorders comprise four scenarios: metabolic acidosis, metabolic alkalosis, respiratory acidosis and respiratory alkalosis, however, and since each scenario demands a succinct study, this article focuses on metabolic acidosis. In a metabolic acidosis, what normally happens is that patients experience a drop in their serum bicarbonate, and what physicians strive to assess is how far the patients’ CO2 will fall, since it is expected to drop. This might sound very technical, so for people to understand this much easier, simply put, metabolic acidosis refers the condition where there is too much acid in the body fluids—which causes the bicarbonate drop mentioned before—; and, as in every pathology, there are some possible causes that can ultimately result in metabolic acidosis, specially three main categories: either patients have a lot of acid being produced in the body: patients suffering from DKA (Diabetic Ketoacidosis) are more likely to suffer from metabolic acidosis given their increased and extremely high blood sugar levels and ketones production which causes bicarbonate to go down; or patients experience a decreased acid excretion: patients who suffer from kidney failure cannot filter all the waste products and byproducts causing the acid to stay in the body and consequently rise its levels; and the another cause is the loss of bicarbonate: people can lose bicarbonate from diarrhea, for instance, and as consequence the acid stays in the body. In general, metabolic acidosis causes the arterial blood gases values to exceed their normal levels while the body struggles to compensate: the respiratory system sees that there is too much acid in the body and starts to breathe more rapidly so that the CO2 can be expelled out of the body in hopes of raising the blood pH back to normal, and consequently increase the bicarbonate level.

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Patients suffering from severe metabolic acidosis are commonly seen doing deep rapid breaths in order to expel all the CO2 (which is an acid) so that the blood pH can get to its normal values. Other causes that can result in metabolic acidosis can be found aside the three mentioned before. For example, aspirin toxicity has been correlated with metabolic acidosis: patients who have taken a lot of aspirin accidentally will experience a dramatic rise in their acid levels once the body has absorbed it. This will likely cause them to hyperventilate since, as explained before, the respiratory system will try to get rid of the excess of acid by expelling CO2 (causing, furthermore, respiratory alkalosis). Another cause has been linked to carbohydrates not being properly metabolized: there are plenty of metabolic issues and it is often seen the case where patients struggle to metabolize carbohydrates which in turn prevents the body to break down pyruvic acids due to the lack of oxygen. Not being able to break down the pyruvic acid, the body turns it into lactic acid, which almost shuts down the body and causes the bicarbonate levels to drop.

A third cause is inherently related to kidney failure: the kidneys, which are responsible for filtering the waste out of the body, fail to do so causing the body to store waste and acids in the blood. As readers might have already imagined, having increased acid levels causes the bicarbonate levels to fall. Actually, every single thing that causes either a loss of bicarbonate or alkaline fluids, or retention of acids, might result in metabolic acidosis, moreover, even a wrong diet can be directly linked with this pathology: an intake of high-fat diet increases the likelihood of increasing the waste, acids, and ketones in the body. Since the body is not a perfect machine and sometimes fail, one can certainly assert that an excess of fat, or any excess, results in something bad for the body: having a good and healthy lifestyle will surely help patients to keep their kidneys functioning for much longer.