Metabolic alkalosis in patients with renal failure

Sir,

In the Teaching Point section of the November 2003 issue of NDT, Ostermann et al. described, in an instructive manner (in three patients), features of the underlying pathophysiology as well as common diagnostic and therapeutic errors in the management of alkalosis in patients with renal failure [1]. However, some issues warrant special attention.

Hypokalaemia. Hypokalaemia is not due to secondary hyperaldosteronism but most probably due to a voltage-mediated potassium secretion owing to increased bicarbonate concentrations. Secondary hyperaldosteronism does not usually lead to urinary potassium wasting, as the stimulatory effect of aldosterone is counterbalanced by the hypovolaemia-induced increase in proximal sodium and water re-absorption and consequent decrease in distal tubular flow [2]. For example, in Cases 1 and 2, urine potassium concentrations were not increased at the time measured. In these settings, markers of urinary potassium excretion, such as transtubular potassium gradient, should be calculated.

Hyponatraemia. Hyponatraemia cannot be attributed to nausea-induced ADH release coupled with continued ingestion of water (?) but most probably resulted from hypovolaemia-induced ADH hypersecretion [3]. In all cases, NaCl 0.9% was administered, followed by an increase in serum sodium levels. In fact, urine sodium was <20 mmol/l despite the presence of renal failure, which is associated with some degree of tubular dysfunction.

Mild elevations of anion gap have been described in metabolic alkalosis [4]. Contributing factors include (i) a rise in plasma albumin concentration due to volume depletion, (ii) an increase in the number of negative charges per albumin molecule and (iii) alkalaemia-induced increased lactate production in order to lower pH towards normal [5]. Furthermore, it was presumed that restlessness, agitation and pain impaired the patients’ ability to hypoventilate, thus leading to lower than expected pCO2 values [1]. However, this fall in pCO2 levels could possibly be due to a superimposed respiratory alkalosis caused by acute alcohol intoxication (Case 1), pain (Case 2), presumably hypoxaemia or co-existing disease and Grand mal seizures (Case 3) or alcohol withdrawal (Case 3) [6].

Conflict of interest statement. None declared.

Haralampos J. Milionis and Moses S. Elisaf

Department of Internal Medicine Medical School University of Ioannina Greece Email: hmilioni{at}cc.uoi.gr

References

  1. Ostermann ME, Girgis-Hanna Y, Nelson SR, Eastwood JB. Metabolic alkalosis in patients with renal failure. Nephrol Dial Transplant 2003; 18: 2442–2448[Free Full Text]
  2. Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders. 5th Edn, McGraw-Hill, New York, NY 2001; 383–396
  3. Milionis HJ, Liamis G, Elisaf MS. The hyponatraemic patient: a systematic diagnostic approach. Can Med Assoc J 2002; 166: 1056–1062[Abstract/Free Full Text]
  4. Madia NE, Ayus JC, Adrogue HJ. Increased anion gap in metabolic alkalosis: the role of plasma-protein equivalency. N Engl J Med 1979; 300: 1421–1423[ISI][Medline]
  5. Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders. 5th Edn, McGraw-Hill, New York, NY 2001; 583–592
  6. Elisaf M, Merkouropoulos M, Tsianos EV, Siamopoulos KC. Acid-base and electrolyte abnormalities in alcoholic patients. Miner Electrolyte Metab 1994; 20: 274–281[ISI][Medline]




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