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...
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Chapter 048. Acidosis and Alkalosis (Part 9) Chapter 048. Acidosis and Alkalosis (Part 9) Approach to the Patient: Hyperchloremic Metabolic Acidoses In diarrhea, stools contain a higher [HCO3–] and decomposed HCO3– thanplasma so that metabolic acidosis develops along with volume depletion. Insteadof an acid urine pH (as anticipated with systemic acidosis), urine pH is usuallyaround 6 because metabolic acidosis and hypokalemia increase renal synthesis andexcretion of NH4+, thus providing a urinary buffer that increases urine pH.Metabolic acidosis due to gastrointestinal losses with a high urine pH can bedifferentiated from RTA (Chap. 278) because urinary NH 4+ excretion is typicallylow in RTA and high with diarrhea. Urinary NH4+ levels can be estimated bycalculating 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 urineammonium level is appropriately increased, suggesting an extrarenal cause of theacidosis. Conversely, when the urine anion gap is positive, the urine ammoniumlevel is low, suggesting a renal cause of the acidosis. Loss of functioning renal parenchyma by progressive renal disease leads tohyperchloremic acidosis when the glomerular filtration rate (GFR) is between 20and 50 mL/min and to uremic acidosis with a high AG when the GFR falls to 20 mmol/L. Since HCO3– is not reabsorbednormally in the proximal tubule, therapy with NaHCO 3 will enhance renalpotassium 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. Mostpatients have hypocitraturia and hypercalciuria, so nephrolithiasis,nephrocalcinosis, and bone disease are common. In generalized distal nephrondysfunction (type 4 RTA), hyperkalemia is disproportionate to the reduction inGFR because of coexisting dysfunction of potassium and acid secretion. Urinaryammonium excretion is invariably depressed, and renal function may becompromised, for example, due to diabetic nephropathy, amyloidosis, ortubulointerstitial disease. Hyporeninemic hypoaldosteronism typically causes hyperchloremicmetabolic acidosis, most commonly in older adults with diabetes mellitus ortubulointerstitial disease and renal insufficiency. Patients usually have mild tomoderate renal insufficiency (GRF, 20–50 mL/min) and acidosis, with elevation inserum [K+] (5.2–6.0 mmol/L), concurrent hypertension, and congestive heartfailure. Both the metabolic acidosis and the hyperkalemia are out of proportion toimpairment in GFR. Nonsteroidal anti-inflammatory drugs, trimethoprim,pentamidine, and angiotensin-converting enzyme (ACE) inhibitors can also causehyperkalemia with hyperchloremic metabolic acidosis in patients with renalinsufficiency (Table 48-5). See Chap. 278 for the pathophysiology, diagnosis, andtreatment of RTA. Metabolic Alkalosis Metabolic alkalosis is manifested by an elevated arterial pH, an increase inthe serum [HCO3–], and an increase in PaCO2 as a result of compensatory alveolarhypoventilation (Table 48-1). It is often accompanied by hypochloremia andhypokalemia. The arterial pH establishes the diagnosis, since it is increased inmetabolic alkalosis and decreased or normal in respiratory acidosis. Metabolicalkalosis frequently occurs in association with other disorders such as respiratoryacidosis or alkalosis or metabolic acidosis. Pathogenesis Metabolic alkalosis occurs as a result of net gain of [HCO 3–] or loss ofnonvolatile acid (usually HCl by vomiting) from the extracellular fluid. Since it isunusual 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, inwhich the kidneys fail to compensate by excreting HCO 3–. Under normal circumstances, the kidneys have an impressive capacity toexcrete HCO3–. Continuation of metabolic alkalosis represents a failure of thekidneys to eliminate HCO3– in the usual manner. For HCO3– to be added to theextracellular fluid, it must be administered exogenously or synthesizedendogenously, in part or entirely by the kidneys. The kidneys will retain, ratherthan 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 ofautonomous hyperaldosteronism. In the f ...