Chapter 048. Acidosis and Alkalosis (Part 9)

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Approach to the Patient: Hyperchloremic Metabolic Acidoses In diarrhea, stools contain a higher [HCO3–] and decomposed HCO3– than plasma so that metabolic acidosis develops along with volume depletion. Instead of an acid urine pH (as anticipated with systemic acidosis), urine pH is usually around 6 because metabolic acidosis and hypokalemia increase renal synthesis and excretion of NH4+, thus providing a urinary buffer that increases urine pH. Metabolic acidosis due to gastrointestinal losses with a high urine pH can be differentiated from RTA (Chap. 278) because urinary NH 4+ excretion is typically low in RTA and high with diarrhea. Urinary...

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Chapter 048. Acidosis and Alkalosis (Part 9) Approach to the Patient: Hyperchloremic Metabolic Acidoses In diarrhea, stools contain a higher [HCO3–] and decomposed HCO3– than plasma so that metabolic acidosis develops along with volume depletion. Instead of an acid urine pH (as anticipated with systemic acidosis), urine pH is usually around 6 because metabolic acidosis and hypokalemia increase renal synthesis and excretion of NH4+, thus providing a urinary buffer that increases urine pH. Metabolic acidosis due to gastrointestinal losses with a high urine pH can be differentiated from RTA (Chap. 278) because urinary NH 4+ excretion is typically low in RTA and high with diarrhea. Urinary NH4+ levels can be estimated by calculating the urine anion gap (UAG): UAG = [Na+ + K+]u – [Cl–]u. When [Cl–]u
> [Na+ + K+], the urine gap is negative by definition. This indicates that the urine ammonium level is appropriately increased, suggesting an extrarenal cause of the acidosis. Conversely, when the urine anion gap is positive, the urine ammonium level is low, suggesting a renal cause of the acidosis. Loss of functioning renal parenchyma by progressive renal disease leads to hyperchloremic acidosis when the glomerular filtration rate (GFR) is between 20 and 50 mL/min and to uremic acidosis with a high AG when the GFR falls to 20 mmol/L. Since HCO3– is not reabsorbed normally in the proximal tubule, therapy with NaHCO 3 will enhance renal potassium wasting and hypokalemia.
The typical findings in acquired or inherited forms of classic distal RTA (type 1 RTA) include hypokalemia, hyperchloremic acidosis, low urinary NH 4+ excretion (positive UAG, low urine [NH4+]), and inappropriately high urine pH (pH > 5.5). Such patients are unable to acidify the urine below a pH of 5.5. Most patients have hypocitraturia and hypercalciuria, so nephrolithiasis, nephrocalcinosis, and bone disease are common. In generalized distal nephron dysfunction (type 4 RTA), hyperkalemia is disproportionate to the reduction in GFR because of coexisting dysfunction of potassium and acid secretion. Urinary ammonium excretion is invariably depressed, and renal function may be compromised, for example, due to diabetic nephropathy, amyloidosis, or tubulointerstitial disease. Hyporeninemic hypoaldosteronism typically causes hyperchloremic metabolic acidosis, most commonly in older adults with diabetes mellitus or tubulointerstitial disease and renal insufficiency. Patients usually have mild to moderate renal insufficiency (GRF, 20–50 mL/min) and acidosis, with elevation in serum [K+] (5.2–6.0 mmol/L), concurrent hypertension, and congestive heart failure. Both the metabolic acidosis and the hyperkalemia are out of proportion to impairment in GFR. Nonsteroidal anti-inflammatory drugs, trimethoprim, pentamidine, and angiotensin-converting enzyme (ACE) inhibitors can also cause hyperkalemia with hyperchloremic metabolic acidosis in patients with renal
insufficiency (Table 48-5). See Chap. 278 for the pathophysiology, diagnosis, and treatment of RTA. Metabolic Alkalosis Metabolic alkalosis is manifested by an elevated arterial pH, an increase in the serum [HCO3–], and an increase in PaCO2 as a result of compensatory alveolar hypoventilation (Table 48-1). It is often accompanied by hypochloremia and hypokalemia. The arterial pH establishes the diagnosis, since it is increased in metabolic alkalosis and decreased or normal in respiratory acidosis. Metabolic alkalosis frequently occurs in association with other disorders such as respiratory acidosis or alkalosis or metabolic acidosis. Pathogenesis Metabolic alkalosis occurs as a result of net gain of [HCO 3–] or loss of nonvolatile acid (usually HCl by vomiting) from the extracellular fluid. Since it is unusual for alkali to be added to the body, the disorder involves a generative stage, in which the loss of acid usually causes alkalosis, and a maintenance stage, in which the kidneys fail to compensate by excreting HCO 3–. Under normal circumstances, the kidneys have an impressive capacity to excrete HCO3–. Continuation of metabolic alkalosis represents a failure of the kidneys to eliminate HCO3– in the usual manner. For HCO3– to be added to the
extracellular fluid, it must be administered exogenously or synthesized endogenously, in part or entirely by the kidneys. The kidneys will retain, rather than excrete, the excess alkali and maintain the alkalosis if (1) volume deficiency, chloride deficiency, and K+ deficiency exist in combination with a reduced GFR, which augments distal tubule H+ secretion; or (2) hypokalemia exists because of autonomous hyperaldosteronism. In the first example, alkalosis is corrected by administration of NaCl and KCl, whereas in the latter it is necessary to repair the alkalosis by pharmacologic or surgical intervention, not with saline administration.