Chapter 048. Acidosis and Alkalosis (Part 10)

Differential DiagnosisTo establish the cause of metabolic alkalosis (Table 48-6), it is necessary to assess the status of the extracellular fluid volume (ECFV), the recumbent and upright blood pressure, the serum [K+], and the renin-aldosterone system. For example, the presence of chronic hypertension and chronic hypokalemia in an alkalotic patient suggests either mineralocorticoid excess or that the hypertensive patient is receiving diuretics. Low plasma renin activity and normal urine [Na+] and [Cl–] in a patient who is not taking diuretics indicate a primary mineralocorticoid excess syndrome. The combination of hypokalemia and alkalosis in a normotensive, nonedematous patient can be...
Nội dung trích xuất từ tài liệu:
Chapter 048. Acidosis and Alkalosis (Part 10) Chapter 048. Acidosis and Alkalosis (Part 10) Differential Diagnosis To establish the cause of metabolic alkalosis (Table 48-6), it is necessary toassess the status of the extracellular fluid volume (ECFV), the recumbent andupright blood pressure, the serum [K+], and the renin-aldosterone system. Forexample, the presence of chronic hypertension and chronic hypokalemia in analkalotic patient suggests either mineralocorticoid excess or that the hypertensivepatient is receiving diuretics. Low plasma renin activity and normal urine [Na+]and [Cl–] in a patient who is not taking diuretics indicate a primarymineralocorticoid excess syndrome. The combination of hypokalemia andalkalosis in a normotensive, nonedematous patient can be due to Bartters orGitelmans syndrome, magnesium deficiency, vomiting, exogenous alkali, ordiuretic ingestion. Determination of urine electrolytes (especially the urine [Cl –])and screening of the urine for diuretics may be helpful. If the urine is alkaline,with an elevated [Na+] and [K+] but low [Cl–], the diagnosis is usually eithervomiting (overt or surreptitious) or alkali ingestion. If the urine is relatively acidand has low concentrations of Na+, K+, and Cl–, the most likely possibilities areprior vomiting, the posthypercapnic state, or prior diuretic ingestion. If, on theother hand, neither the urine sodium, potassium, nor chloride concentrations aredepressed, magnesium deficiency, Bartters or Gitelmans syndrome, or currentdiuretic ingestion should be considered. Bartters syndrome is distinguished fromGitelmans syndrome because of hypocalciuria and hypomagnesemia in the latterdisorder. The genetic and molecular basis of these two disorders has beenelucidated recently (Chap. 278). Table 48-6 Causes of Metabolic Alkalosis I. Exogenous HCO3- loads A. Acute alkali administration B. Milk-alkali syndrome II. Effective ECFV contraction, normotension, K+ deficiency, andsecondary hyperreninemic hyperaldosteronism A. Gastrointestinal origin 1. Vomiting 2. Gastric aspiration 3. Congenital chloridorrhea 4. Villous adenoma B. Renal origin 1. Diuretics 2. Posthypercapnic state 3. Hypercalcemia/hypoparathyroidism 4. Recovery from lactic acidosis or ketoacidosis 5. Nonreabsorbable anions including penicillin, carbenicillin 6. Mg2+ deficiency 7. K+ depletion 8. Bartters syndrome (loss of function mutations in TALH) 9. Gitelmans syndrome (loss of function mutation in Na+-Cl- cotransporter in DCT) III. ECFV expansion, hypertension, K+ deficiency, andmineralocorticoid excess A. High renin 1. Renal artery stenosis 2. Accelerated hypertension 3. Renin-secreting tumor 4. Estrogen therapyB. Low renin 1. Primary aldosteronism a. Adenoma b. Hyperplasia c. Carcinoma 2. Adrenal enzyme defects a. 11 α-Hydroxylase deficiency b. 17 α-Hydroxylase deficiency 3. Cushings syndrome or disease 4. Other a. Licorice b. Carbenoxolone c. Chewers tobacco IV. Gain-of-function mutation of renal sodium channel with ECFV expansion, hypertension, K+ deficiency, and hyporeninemic- hypoaldosteronism A. Liddles syndrome Note: ECFV, extracellular fluid volume; TALH, thick ascending limb ofHenles loop; DCT, distal convoluted tubule.