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Describe How The Kidneys Respond To Respiratory Acidosis

Molecular Mechanisms Of Acid-base Sensing By The Kidney

Molecular Mechanisms Of Acid-base Sensing By The Kidney

Go to: Abstract A major function of the kidney is to collaborate with the respiratory system to maintain systemic acid-base status within limits compatible with normal cell and organ function. It achieves this by regulating the excretion and recovery of bicarbonate (mainly in the proximal tubule) and the secretion of buffered protons (mainly in the distal tubule and collecting duct). How proximal tubular cells and distal professional proton transporting (intercalated) cells sense and respond to changes in pH, bicarbonate, and CO2 status is a question that has intrigued many generations of renal physiologists. Over the past few years, however, some candidate molecular pH sensors have been identified, including acid/alkali-sensing receptors (GPR4, InsR-RR), kinases (Pyk2, ErbB1/2), pH-sensitive ion channels (ASICs, TASK, ROMK), and the bicarbonate-stimulated adenylyl cyclase (sAC). Some acid-sensing mechanisms in other tissues, such as CAII-PDK2L1 in taste buds, might also have similar roles to play in the kidney. Finally, the function of a variety of additional membrane channels and transporters is altered by pH variations both within and outside the cell, and the expression of several metabolic enzymes are altered by acid-base status in parts of the nephron. Thus, it is possible that a master pH sensor will never be identified. Rather, the kidney seems equipped with a battery of molecules that scan the epithelial cell environment to mount a coordinated physiologic response that maintains acid-base homeostasis. This review collates current knowledge on renal acid-base sensing in the context of a whole organ sensing and response process. A major unresolved issue in renal physiology is how renal epithelial cells sense extracellular acid-base status to initiate their homeos Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory acidosis is a medical emergency in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood's pH (a condition generally called acidosis). Carbon dioxide is produced continuously as the body's cells respire, and this CO2 will accumulate rapidly if the lungs do not adequately expel it through alveolar ventilation. Alveolar hypoventilation thus leads to an increased PaCO2 (a condition called hypercapnia). The increase in PaCO2 in turn decreases the HCO3−/PaCO2 ratio and decreases pH. Terminology[edit] Acidosis refers to disorders that lower cell/tissue pH to < 7.35. Acidemia refers to an arterial pH < 7.36.[1] Types of respiratory acidosis[edit] Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.36). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO3− >30 mm Hg). Causes[edit] Acute[edit] Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation. Chronic[edit] Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation Continue reading >>

Response To Disturbances

Response To Disturbances

The body tries to minimize pH changes and responds to acid-base disturbances with body buffers, compensatory responses by the lungs and kidney (to metabolic and respiratory disturbances, respectively) and by the kidney correcting metabolic disturbances. Body buffers: There are intracellular and extracellular buffers for primary respiratory and metabolic acid-base disturbances. Intracellular buffers include hemoglobin in erythrocytes and phosphates in all cells. Extracellular buffers are carbonate (HCO3–) and non-carbonate (e.g. protein, bone) buffers. These immediately buffer the rise or fall in H+. Compensation: This involves responses by the respiratory tract and kidney to primary metabolic and respiratory acid-base disturbances, respectively. Compensation opposes the primary disturbance, although the laboratory changes in the compensatory response parallel those in the primary response. This concept is illustrated in the summary below. Respiratory compensation for a primary metabolic disturbance: Alterations in alveolar ventilation occurs in response to primary metabolic acid-base disturbances. This begins within minutes to hours of an acute primary metabolic disturbance. Note that complete compensation via this mechanism may take up to 24 hours. Renal compensation for a primary respiratory disturbance: Here, the kidney alters excretion of acid (which influences bases as well) in response to primary respiratory disturbances. This begins within hours of an acute respiratory disturbance, but take several days (3-5 days) to take full effect. Correction of acid-base changes: Correction of a primary respiratory acid-base abnormality usually requires medical or surgical intervention of the primary problem causing the acid-base disturbance, e.g. surgical relief of a colla Continue reading >>

Acidosis

Acidosis

The kidneys and lungs maintain the balance (proper pH level) of chemicals called acids and bases in the body. Acidosis occurs when acid builds up or when bicarbonate (a base) is lost. Acidosis is classified as either respiratory or metabolic acidosis. Respiratory acidosis develops when there is too much carbon dioxide (an acid) in the body. This type of acidosis is usually caused when the body is unable to remove enough carbon dioxide through breathing. Other names for respiratory acidosis are hypercapnic acidosis and carbon dioxide acidosis. Causes of respiratory acidosis include: Chest deformities, such as kyphosis Chest injuries Chest muscle weakness Chronic lung disease Overuse of sedative drugs Metabolic acidosis develops when too much acid is produced in the body. It can also occur when the kidneys cannot remove enough acid from the body. There are several types of metabolic acidosis: Diabetic acidosis (also called diabetic ketoacidosis and DKA) develops when substances called ketone bodies (which are acidic) build up during uncontrolled diabetes. Hyperchloremic acidosis is caused by the loss of too much sodium bicarbonate from the body, which can happen with severe diarrhea. Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Lactic acidosis is a buildup of lactic acid. Lactic acid is mainly produced in muscle cells and red blood cells. It forms when the body breaks down carbohydrates to use for energy when oxygen levels are low. This can be caused by: Cancer Drinking too much alcohol Exercising vigorously for a very long time Liver failure Low blood sugar (hypoglycemia) Medications, such as salicylates MELAS (a very rare genetic mitochondrial disorder that affects energy production) Prolonged lack of oxygen from shock, heart failure, or seve Continue reading >>

Merck And The Merck Manuals

Merck And The Merck Manuals

Acidosis is caused by an overproduction of acid in the blood or an excessive loss of bicarbonate from the blood (metabolic acidosis) or by a buildup of carbon dioxide in the blood that results from poor lung function or depressed breathing (respiratory acidosis). If an increase in acid overwhelms the body's acid-base control systems, the blood will become acidic. As blood pH drops (becomes more acidic), the parts of the brain that regulate breathing are stimulated to produce faster and deeper breathing (respiratory compensation). Breathing faster and deeper increases the amount of carbon dioxide exhaled. The kidneys also try to compensate by excreting more acid in the urine. However, both mechanisms can be overwhelmed if the body continues to produce too much acid, leading to severe acidosis and eventually heart problems and coma. The acidity or alkalinity of any solution, including blood, is indicated on the pH scale. Metabolic acidosis develops when the amount of acid in the body is increased through ingestion of a substance that is, or can be broken down (metabolized) to, an acid—such as wood alcohol (methanol), antifreeze (ethylene glycol), or large doses of aspirin (acetylsalicylic acid). Metabolic acidosis can also occur as a result of abnormal metabolism. The body produces excess acid in the advanced stages of shock and in poorly controlled type 1 diabetes mellitus (diabetic ketoacidosis). Even the production of normal amounts of acid may lead to acidosis when the kidneys are not functioning normally and are therefore not able to excrete sufficient amounts of acid in the urine. Major Causes of Metabolic Acidosis Diabetic ketoacidosis (buildup of ketoacids) Drugs and substances such as acetazolamide, alcohols, and aspirin Lactic acidosis (buildup of lactic acid Continue reading >>

Renal Regulation Of Metabolic Acidosis And Alkalosis

Renal Regulation Of Metabolic Acidosis And Alkalosis

1. 06/21/14 1 Normal Acid-Base Balance • Normal pH 7.35-7.45 • Narrow normal range • Compatible with life 6.8 - 8.0 ___/______/___/______/___ 6.8 7.35 7.45 8.0 Acid Alkaline 2. 06/21/14 2 PH Scale 3. 06/21/14 3 Acid & Base • Acid: • An acid is "when hydrogen ions accumulate in a solution" • It becomes more acidic • [H+] increases = more acidity • CO2 is an example of an acid. Base: A base is chemical that will remove hydrogen ions from the solution Bicarbonate is an example of a base. 4. 06/21/14 4 Acid and Base Containing Food: • To maintain health, the diet should consist of 60% alkaline forming foods and 40% acid forming foods. To restore health, the diet should consist of 80% alkaline forming foods and 20% acid forming foods. • Generally, alkaline forming foods include: most fruits, green vegetables, peas, beans, lentils, spices, herbs,seasonings,seeds and nuts. • Generally, acid forming foods include: meat, fish, poultry, eggs, grains, and legumes. 5. 06/21/14 5 Citric Acid And Lactic Acid Although both citric acid and lactic acid are acids BUT Citric acid leads to Alkalosis while Lactic acid to Acidosis due to metabolism 6. 06/21/14 6 Acidoses & Alkalosis • An abnormality in one or more of the pH control mechanisms can cause one of two major disturbances in Acid-BaseAcid-Base balance – AcidosisAcidosis – AlkalosisAlkalosis 7. 06/21/14 7 Acidosis • Acidosis is excessive blood acidity caused by an overabundance of acid in the blood or a loss of bicarbonate from the blood (metabolic acidosis), or by a buildup of carbon dioxide in the blood that results from poor lung function or slow breathing (respiratory acidosis). • Blood acidity increases when people ingest substances that contain or produce acid or when the lungs do not expel enou Continue reading >>

Regulation Of Blood Ph

Regulation Of Blood Ph

Although many people are unaware of the fact, maintaining the acid/base balance of your blood is actually vital to your survival. If the pH of your blood drops below 7.2 or rises above 7.6, then very soon your brain will no longer be able to function normally and you will be in dire straits1. As luck would have it, although you cannot consciously detect your blood pH, the human body does in fact have an elegant but effective means of coping with every change in pH, large or small. This relies on three interlinking objects: buffers, the lungs and the kidneys. Buffers pH is a measurement of the concentration of hydrogen H+ ions and buffers are molecules which take in or release ions in order to maintain the H+ ion concentration at a certain level. Buffers in the blood include haemoglobin (Hb), certain proteins (Prot) and phosphates, and are the first line of defence whenever sudden changes in pH occur. When the pH is too low and the blood becomes too acidic, it is due to the presence of too many H+ ions in the blood. The buffers will attempt to mop up the excess. Conversely, a lack of H+ ions leads to the blood becoming too basic, and so the buffers release H+ ions. Buffers therefore help to maintain the pH of the blood by either sacrificing or accepting H+ ions as necessary to maintain the number of free H+ ions floating around in the blood. ← Buffer taking up excess H+ Buffer releasing H+ → H-Hb ↔ Hb- + H+ Prot-H ↔ Prot- + H+ H2PO4- ↔ HPO42- + H+ The Lungs Through these buffer reactions, the pH can be quickly corrected before any damage is done, but this does not provide a long-term solution to the problem. The buffers can only mop up or release so many H+ ions before they reach their capacity and are no longer of any use, and then the situation will once agai Continue reading >>

Intro To Arterial Blood Gases, Part 2

Intro To Arterial Blood Gases, Part 2

Arterial Blood Gas Analysis, Part 2 Introduction Acute vs. Chronic Respiratory Disturbances Primary Metabolic Disturbances Anion Gap Mixed Disorders Compensatory Mechanisms Steps in ABG Analysis, Part II Summary Compensatory Mechanisms Compensation refers to the body's natural mechanisms of counteracting a primary acid-base disorder in an attempt to maintain homeostasis. As you learned in Acute vs. Chronic Respiratory Disturbances, the kidneys can compensate for chronic respiratory disorders by either holding on to or dumping bicarbonate. With Chronic respiratory acidosis: Chronic respiratory alkalosis: the kidneys hold on to bicarbonate the kidneys dump bicarbonate With primary metabolic disturbances, the respiratory system compensates for the acid-base disorder. The lungs can either blow off excess acid (via CO2) to compensate for metabolic acidosis, or to a lesser extent, hold on to acid (via CO2) to compensate for metabolic alkalosis. With Metabolic acidosis: Metabolic alkalosis: ventilation increases to blow off CO2 ventilation decreases to hold on to CO2 The body's response to metabolic acidosis is predictable. With metabolic acidosis, respiration will increase to blow off CO2, thereby decreasing the amount of acid in the blood. Recall that with metabolic acidosis, central chemoreceptors are triggered by the low pH and increase the drive to breathe. For now, it is only important to learn (qualitatively) that there is a predictable compensatory response to metabolic acidosis. Later, during your 3rd or 4th year rotations, you might learn how to (quantitatively) determine if the compensatory response to metabolic acidosis is appropriate by using the Winter's Formula. The body's response to metabolic alkalosis is not as complete. This is because we would need to hypov Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Practice Essentials Respiratory acidosis is an acid-base balance disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly and failure of ventilation promptly increases the partial pressure of arterial carbon dioxide (PaCO2). [1] The normal reference range for PaCO2 is 35-45 mm Hg. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3–)/PaCO2 ratio, thereby decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the respiratory system is less than the production of carbon dioxide in the tissues. Lung diseases that cause abnormalities in alveolar gas exchange do not typically result in alveolar hypoventilation. Often these diseases stimulate ventilation and hypocapnia due to reflex receptors and hypoxia. Hypercapnia typically occurs late in the disease process with severe pulmonary disease or when respiratory muscles fatigue. (See also Pediatric Respiratory Acidosis, Metabolic Acidosis, and Pediatric Metabolic Acidosis.) Acute vs chronic respiratory acidosis Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, >45 mm Hg) with an accompanying acidemia (ie, pH < 7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate levels (ie, >30 mEq/L). Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may result from depression of the central respiratory center by one or another of the foll Continue reading >>

4.5 Respiratory Acidosis - Compensation

4.5 Respiratory Acidosis - Compensation

Acid-Base Physiology 4.5.1 The compensatory response is a rise in the bicarbonate level This rise has an immediate component (due to a resetting of the physicochemical equilibrium point) which raises the bicarbonate slightly. Next is a slower component where a further rise in plasma bicarbonate due to enhanced renal retention of bicarbonate. The additional effect on plasma bicarbonate of the renal retention is what converts an "acute" respiratory acidsosis into a "chronic" respiratory acidosis. As can be seen by inspection of the Henderson-Hasselbalch equation (below), an increased [HCO3-] will counteract the effect (on the pH) of an increased pCO2 because it returns the value of the [HCO3]/0.03 pCO2 ratio towards normal. pH = pKa + log([HCO3]/0.03 pCO2) 4.5.2 Buffering in Acute Respiratory Acidosis The compensatory response to an acute respiratory acidosis is limited to buffering. By the law of mass action, the increased arterial pCO2 causes a shift to the right in the following reaction: CO2 + H2O <-> H2CO3 <-> H+ + HCO3- In the blood, this reaction occurs rapidly inside red blood cells because of the presence of carbonic anhydrase. The hydrogen ion produced is buffered by intracellular proteins and by phosphates. Consequently, in the red cell, the buffering is mostly by haemoglobin. This buffering by removal of hydrogen ion, pulls the reaction to the right resulting in an increased bicarbonate production. The bicarbonate exchanges for chloride ion across the erythrocyte membrane and the plasma bicarbonate level rises. In an acute acidosis, there is insufficient time for the kidneys to respond to the increased arterial pCO2 so this is the only cause of the increased plasma bicarbonate in this early phase. The increase in bicarbonate only partially returns the extracel Continue reading >>

Shared Flashcard Set

Shared Flashcard Set

Details Title Acid Base Balance Description Acid Base Balance Total Cards 214 Subject Nursing Level Undergraduate 2 Created 10/14/2012 Click here to study/print these flashcards. Create your own flash cards! Sign up here. Additional Nursing Flashcards Cards Term An opioid drug overdose would put a patient at most risk for what acid/base imbalance? Definition Respiratory Acidosis Term Pulmonary Edema would put a patient at most risk for what acid/base imbalance? Definition Respiratory Acidosis Term Chest trauma would put a patient at most risk for what acid/base imbalance? Definition Respiratory Acidosis Term Neuromuscular disease would put a patient at most risk for what acid/base imbalance? Definition Respiratory Acidosis Term COPD would put a patient at most risk for what acid/base imbalance? Definition Respiratory Acidosis Term Airway obstruction would put a patient at most risk for what acid/base imbalance? Definition Respiratory Acidosis Term Pneumonia would put a patient at most risk for what acid/base imbalance? Definition Respiratory Acidosis Term TB would put a patient at most risk for what acid/base imbalance? Definition Respiratory Acidosis Term Emphysema would put a patient at most risk for what acid/base imbalance? Definition Respiratory Acidosis Term Asthma would put a patient at most risk for what acid/base imbalance? Definition Respiratory Acidosis Term Cigarrette smoking would put a patient at most risk for what acid/base imbalance? Definition Respiratory Acidosis Term Pleural effusion would put a patient at most risk for what acid/base imbalance? Definition Respiratory Acidosis Term What is pleural effusion? Definition excess fluid that accumulates in the pleura, the fluid-filled space that surrounds the lungs Pleural effusion is excess fluid that accu Continue reading >>

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Acid-Base Physiology Buffers H+ A- HCO3- CO2 Buffers H+ A- CO2 Cells Blood Kidney Lungs Fluids, Electrolytes, and Acid-Base Status in Critical Illness Blood Gas Analysis--Insight into the Acid-Base status of the Patient The blood gas consists of pH-negative log of the Hydrogen ion concentration: -log[H+]. (also, pH=pK+log [HCO3]/ 0.03 x pCO2). The pH is always a product of two components, respiratory and metabolic, and the metabolic component is judged, calculated, or computed by allowing for the effect of the pCO2, ie, any change in the pH unexplained by the pCO2 indicates a metabolic abnormality. CO +H 0ºº H CO ººHCO + H2 2 2 3 3 - + CO2 and water form carbonic acid or H2CO3, which is in equilibrium with bicarbonate (HCO3-)and hydrogen ions (H+). A change in the concentration of the reactants on either side of the equation affects the subsequent direction of the reaction. For example, an increase in CO2 will result in increased carbonic acid formation (H2CO3) which leads to an increase in both HCO3- and H+ (\pH). Normally, at pH 7.4, a ratio of one part carbonic acid to twenty parts bicarbonate is present in the extracellular fluid [HCO3-/H2CO3]=20. A change in the ratio will affect the pH of the fluid. If both components change (ie, with chronic compensation), the pH may be normal, but the other components will not. pCO -partial pressure of carbon dioxide. Hypoventilation or hyperventilation (ie, minute2 ventilation--tidal volume x respitatory rate--imperfectly matched to physiologic demands) will lead to elevation or depression, respectively, in the pCO2. V/Q (ventilation/perfusion) mismatch does not usually lead to abnormalities in PCO2 because of the linear nature of the CO2 elimination curve (ie, good lung units can make up for bad lung units). Diffus Continue reading >>

Regulation Of Acid-base Balance

Regulation Of Acid-base Balance

There is precise regulation or maintenance of ‘free H+ ions’ in body fluids. Balance is Achieved by Three Defense Mechanisms:- • First defense: Chemical buffering • 2nd defense: Respiratory (alteration in arterial CO2) • 3rd defense: Renal (alteration in HCO-3 excretion) Acid Base Regulation/Balance 1. Chemical Buffer system: – Responds within seconds – Does not eliminate or add H+ from body – Operates by binding or to tied up H+ till balance is reestablished. a. In ECF: – Mainly HCO-3/CO2 Buffer system – Plasma Proteins – HPO–4/H2PO-4 Buffer system b. In ICF: – Proteins Mainly e.g.: Hb in RBCs – HPO–4/H2PO-4 Buffer system Routes of excretion of acids; lungs & kidneys 2. Respiratory Mechanisms: – Responds within minutes – Takes 6-12 hours to be fully effective – Operates by excreting CO2 or (adding H2CO3/HCO-3) 3. Renal Mechanisms: • Responds slowly (effectively in 3-5 days) • Eliminates excess Acids or Base from body • The most powerful mechanism e.g. i. HCO-3/CO2 Buffer system ii. NH3/NH+4 Buffer system iii. HPO–4/H2PO-4 Buffer system Chemical Buffer System • Consists of a ‘pair of substances’ present in a mixture of a solution that ‘minimizes pH changes’ when an ‘acid or base’ is ‘added or removed’ from the solution. • Consists of; 1. Carbonic Acid – Bicarbonate Buffer System 2. Phosphate Buffer system 3. Protein Buffer system Chemical Buffer System of ECF 1. Bicarbonate Buffer System: H2CO3/NaHCO3 consists of H2CO3 (weak Acid) + NaHCO3 (Bicarbonate salt) – CO2 + H2O ↔H2CO3 ↔ H+ + HCO-3 – NaHCO3 ↔ Na+ + HCO-3 → H2CO3 → CO2 + H2O Bicarbonate buffer system is quantitatively the most powerful ECF buffer system Its two components HCO-3 & CO2 are precisely regulated by kidneys & lungs. 2. Phos Continue reading >>

Acid–base Homeostasis

Acid–base Homeostasis

Acid–base homeostasis is the homeostatic regulation of the pH of the body's extracellular fluid (ECF).[1] The proper balance between the acids and bases (i.e. the pH) in the ECF is crucial for the normal physiology of the body, and cellular metabolism.[1] The pH of the intracellular fluid and the extracellular fluid need to be maintained at a constant level.[2] Many extracellular proteins such as the plasma proteins and membrane proteins of the body's cells are very sensitive for their three dimensional structures to the extracellular pH.[3][4] Stringent mechanisms therefore exist to maintain the pH within very narrow limits. Outside the acceptable range of pH, proteins are denatured (i.e. their 3-D structure is deranged), causing enzymes and ion channels (among others) to malfunction. In humans and many other animals, acid–base homeostasis is maintained by multiple mechanisms involved in three lines of defence.[5][6] The first line of defence are the various chemical buffers which minimize pH changes that would otherwise occur in their absence. They do not correct pH deviations, but only serve to reduce the extent of the change that would otherwise occur. These buffers include the bicarbonate buffer system, the phosphate buffer system, and the protein buffer system.[citation needed] Physiological corrective measures make up of the second and third lines of defence. This is because they operate by making changes to the buffers, each of which consists of two components: a weak acid and an weak base.[5][7] It is the ratio of weak acid to weak base that determines the pH of the solution.[8] Thus, by manipulating firstly the concentration of the weak acid, and secondly the weak base, the pH of the extracellular fluid (ECF) can be adjusted very accurately to the correct Continue reading >>

Acid-base Homeostasis

Acid-base Homeostasis

Abstract Acid-base homeostasis and pH regulation are critical for both normal physiology and cell metabolism and function. The importance of this regulation is evidenced by a variety of physiologic derangements that occur when plasma pH is either high or low. The kidneys have the predominant role in regulating the systemic bicarbonate concentration and hence, the metabolic component of acid-base balance. This function of the kidneys has two components: reabsorption of virtually all of the filtered HCO3− and production of new bicarbonate to replace that consumed by normal or pathologic acids. This production or generation of new HCO3− is done by net acid excretion. Under normal conditions, approximately one-third to one-half of net acid excretion by the kidneys is in the form of titratable acid. The other one-half to two-thirds is the excretion of ammonium. The capacity to excrete ammonium under conditions of acid loads is quantitatively much greater than the capacity to increase titratable acid. Multiple, often redundant pathways and processes exist to regulate these renal functions. Derangements in acid-base homeostasis, however, are common in clinical medicine and can often be related to the systems involved in acid-base transport in the kidneys. Basic Concepts Intracellular and extracellular buffers are the most immediate mechanism of defense against changes in systemic pH. Bone and proteins constitute a substantial proportion of these buffers. However, the most important buffer system is the HCO3−/CO2 buffer system. The Henderson–Hasselbach equation (Equation 1) describes the relationship of pH, bicarbonate (HCO3−), and PCO2:where HCO3− is in milliequivalents per liter and PCO2 is in millimeters of mercury. Equation 2 represents the reaction (water [H2O] Continue reading >>

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