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In both respiratory and metabolic imbalances,acid gain (acidosis) or loss (alkalosis) is compensated for by the renal excretion of acid or HCO3−, respectively. When blood pH is outside of the physiologic window (less than 7.35 or above 7.45), there is alsorespiratory compensation by hyperventilation or hypoventilation.major cation, Na+, and the major plasma anions, Cl− andHCO3−. When Cl− and HCO3− concentrations are subtractedfrom the Na+ concentration, the “anion gap” is normally ∼8to 12 mEq/L.
The anion gap represents the sum of the concentrations of about 10 anions present in the plasma andincludes proteins, lactate, citrate, phosphates, sulfates, etc.:AG = Na+ − (Cl− + HCO3−)As illustrated in Figure 20.4, middle panel, when acidosisresults from acid loading, the anion gap increases, as a resultof the lower plasma bicarbonate (used to buffer the acid). Incontrast, when HCO3− is lost, it is replaced by Cl−, and theanion gap is normal (see Fig.
20.4, right panel). Thus, theanion gap can help determine the cause of the metabolic acidosis, with the specific cause of the acid load or base lossremaining to be determined.Regulation of Acid–Base Balance by the Kidneys237Anion GapAcidosis from Acid LoadAG increasesNormalAG 10AG 8AG 17HCO3 24Na14Cl108Acidosis from Base LossAG normalHCO3 12HCO3 15Cl108Na140Na140Cl118Figure 20.4 Plasma Anion Gap In cases of metabolic acidosis, measurement of the anion gap willreveal whether the disruption in pH was from acid loading or base loss.AlkalosisWhy don’t the renal HCO3−/Cl− exchangers always workduring alkalosis? It is important to recall that undernormal conditions the HCO3−/Cl− exchangers in the β-intercalated cells are not active, because HCO3− is being retained, notexcreted.
However, these exchangers are expressed during alkalosis and depend on the lumenal concentration of Cl− to effectively transport the HCO3− into the tubule. The importance ofdistal lumenal Cl− is illustrated in contraction alkalosis, as seenwith chronic vomiting and volume depletion.In response to the alkalosis caused by loss of H+ during vomiting, the renal HCO3−/Cl− exchangers are expressed but areunable to function because of the low level of Cl− in the collecting duct fluid.
The low Cl− is a result of fluid- and sodiumretaining mechanisms (e.g., sympathetic nervous system [SNS],renin-angiotensin system, aldosterone, antidiuretic hormone[ADH]) stimulated in response to volume depletion. Chlorideis avidly reabsorbed with the sodium and water, leaving little inthe distal areas of the nephron. The problem can be correctedby isotonic fluid replacement, which will decrease SNS andrenin-angiotensin system activation and aldosterone and ADHrelease, and increase Na+ and Cl− delivery to the collecting ducts.The HCO3−/Cl− exchanger will then be able to function, andexcess HCO3− will be excreted, correcting the alkalosis.Alkalosis results from the loss of fixed acid or gain of HCO3−.Chronic hyperventilation (for example, at high altitude) willcause the loss of CO2 and result in respiratory alkalosis.
Metabolic alkalosis can result from:■■■Vomiting, which results in the loss of significant amountsof H+ in the form of HCl and volume contraction.Sodium bicarbonate overdose.Chronic diuretic usage, which can cause hypokalemia,volume contraction, aldosterone excess, and chloridedepletion, all of which are associated with alkalosis.During alkalosis, HCO3−/Cl− exchange by transporters in βintercalated cells of the renal collecting ducts is activated,allowing secretion and excretion of bicarbonate until normalpH is attained.238Renal PhysiologyCLINICAL CORRELATEMetabolic KetoacidosisA common cause of ketoacidosis is poorly controlled diabetes.When glucose is not able to efficiently enter cells there aretwo immediate consequences: elevated blood glucose, andincreased cellular β-oxidation of fatty acids to provide an alternateenergy source in the absence of intracellular glucose. If the rate ofoxidation is high, metabolites including ketoacids (or ketonebodies) enter the blood, decreasing the pH.
Several problemsensue:■Acidosis: The ketoacids are filtered at the glomeruli and eliminated in the urine, but the production overwhelms excretion.Plasma bicarbonate may not be sufficient to buffer the acid load,and in severe cases the free bicarbonate will be heavily consumed, and blood pH will be dangerously reduced (i.e., below7.2). Contributing to this problem, ketone bodies interfere withthe production of ammonia from glutamine in the nephron,and thus decrease new bicarbonate generation (further decreasing plasma bicarbonate levels).■■■Glucosuria: Glucose is excreted in the urine, because the elevation in filtered glucose load overwhelms the renal sodiumglucose transporters.
The glucose pulls water with it, creatingpolyuria (high urine volume).Volume expansion and cellular contraction: When glucoseincreases in the blood, it exerts additional osmotic force,keeping water in the vascular space. This expands the ECF,while the ICF decreases. Blood pressure may increase, and theconcentration of other plasma constituents, including electrolytes and proteins, will be diluted. Ultimately, diabetic ketoacidosis may actually result in dehydration due to osmotic diuresisand vomiting.Toxicity: The keto acids in the blood are toxic and ultimatelymay cause coma and death if blood glucose level is not corrected. The most severe consequences are seen primarily in type1 (insulin-dependent) diabetes, and death from ketoacidoticcoma is rarely seen in people with type 2 (insulin-resistant)diabetes. With insulin treatment, β-oxidation of fatty acids andtherefore ketoacid production are reduced, and urinary excretion is able to eliminate the excess acid.Review Questions239Review QuestionsCHAPTER 16: OVERVIEW, GLOMERULARFILTRATION, AND RENAL CLEARANCE1.
If the clearance of a freely filtered substance is less than theclearance of inulin, then the substance:A.B.C.D.E.is filtered and completely reabsorbed.is filtered and completely secreted.underwent net reabsorption.underwent net secretion.was neither secreted nor reabsorbed.2. Diabetic nephropathy is associated with thickened glomerular capillary basement membranes. The decrease in glomerular filtration rate results from:A.
a reduction in renal blood flow.B. a reduction in glomerular capillary hydrostatic pressure.C. a reduction in the permeability of the glomerular filtrationbarrier.D. an increase in the glomerular capillary hydrostaticpressure.E. an increase in the permeability of the glomerular filtrationbarrier.C. thick ascending limb of Henle.D. distal tubule.E. collecting duct.6. Potassium handling by the kidneys is affected by all of thefollowing EXCEPT:A.B.C.D.E.dietary potassium.plasma potassium concentration.plasma aldosterone.plasma antidiuretic hormone.acidosis.7.
“Loop” diuretics such as furosemide or bumetanideproduce a diuresis by targeting which of the followingtransporters?A.B.C.D.E.Na+-glucose cotransportersNa+/H+ antiportersNa+/K+ ATPaseNa+-K+-2Cl− cotransportersNa+-HCO3− cotransporters3. The kidneys perform all the following functionsEXCEPT:CHAPTER 18: URINE CONCENTRATION ANDDILUTION MECHANISMSA.B.C.D.E.8. Antidiuretic hormone (ADH)–sensitive water channels(aquaporins) are located in the:production of aldosterone.excretion of excess body acid.regulation of fluid and electrolyte homeostasis.activation of vitamin D.ammoniagenesis.4.
Renal blood flow (RBF) in a young man was determinedto be 1 L/min. If his inulin clearance is 125 mL/min, andhematocrit is 0.4, what is his renal filtration fraction?A.B.C.D.E.15%20%25%30%35%CHAPTER 17: RENAL TRANSPORT PROCESSES5. Reabsorption of glucose occurs in the:A. proximal tubule.B. thin descending limb of Henle.A.B.C.D.E.proximal tubule.thin descending limb of Henle.thick ascending limb of Henle.distal tubule.collecting duct.9. All of the following factors contribute to establishing ormaintaining the medullary interstitial concentration gradientEXCEPT:A. distal tubule sodium reabsorption.B.
Na+-K+-2Cl− cotransporters on the thick ascending limbof Henle.C. solute-free water reabsorption in the descending limb ofHenle.D. the counter-current multiplier effect.E. urea recycling.240Renal Physiology10. A patient with chronic pyelonephritis has the followinglaboratory values:CHAPTER 20: REGULATION OF ACID–BASEBALANCE BY THE KIDNEYSUrine flow = 3 mL/min Posm = 300 mosm/LUosm = 200 mosm/L14. Renal tubular hydrogen secretion increases:The free water clearance in this person is:A.B.C.D.E.−3.−1.0.+1.+3.A. when ECF volume is increased.B.
when arterial PCO2 is decreased.C. when plasma bicarbonate concentration is low due tometabolic acidosis.D. when plasma aldosterone is low.E. when plasma antidiuretic hormone is low.15. Net acid excretion (NAE) is dependent on all of the following factors EXCEPT:CHAPTER 19: REGULATION OFEXTRACELLULAR FLUID VOLUMEAND OSMOLARITY11. Select the TRUE statement regarding the reninangiotensin-aldosterone system.A. Renin secretion is stimulated by high tubular fluid sodiumconcentration.B. Angiotensin I is converted to angiotensin II exclusively inthe pulmonary circulation.C. Angiotensin II directly stimulates proximal tubular sodiumreabsorption.D.
High tubular fluid flow rate in the distal tubule will stimulate renin secretion.E. Aldosterone stimulates proximal tubule sodiumreabsorption.12. A severely dehydrated patient is admitted to the Emergency Department. Which of the following would NOT beelevated in this patient?A.B.C.D.E.Plasma atrial natriuretic peptide (ANP)Plasma reninPlasma antidiuretic hormone (ADH)Sympathetic nervous system activityPlasma aldosterone13.
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