Nephrol Dial Transplant (1999) 14: 2505-2506
© 1999 European Renal Association-European Dialysis and Transplant Association
Nephroquiz For The Beginner
Hyperkalaemia in a patient with hepatic cirrhosis
Department of Internal Medicine, Medical School University of Ioannina, Greece
A 53-year-old man with cirrhotic ascites due to chronic hepatitis B infection was admitted because of malaise, fatigue and ascites deterioration. The patient was on frusemide 80 mg per o.s. and spironolactone 100 mg per o.s. daily. On physical examination, cachexia, ascites and flapping tremor were evident.
Biochemical parameters and arterial gas determination are shown in Table 1
. Serum aldosterone was 800 pg/ml (normal range 7.5–150 pg/ml), and plasma renin activity was 18 ng/ml/h (normal range 0.2–2.8 ng/ml/h).
- (i) What are the underlying mechanisms of hyperkalaemia in cirrhotic patients?
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(ii) How can we explain the absence of hypokalaemia in view of the marked increase in serum aldosterone levels?
(iii) What is the management of hyperkalaemia in cirrhotic patients?
(iv) What is the preferred serum potassium concentration in cirrhotic patients (i.e. towards low of high serum level)?
Answer to quiz on preceding page
- (i) The most common causes of hyperkalaemia in cirrhotic patients are shown in Table 2
, with potassium-sparing diuretics being the most frequent cause. The administration of these drugs (particularly spironolactone) in patients with concurrent potassium homeostasis disturbances (i.e. increased potassium intake, decreased glomerular filtration rate, decreased distal delivery sodium) might lead to a significant increase of serum potassium levels. Many end-stage cirrhotic patients display progressive azotaemia, hyperkalaemia, and hyponatraemia. Additionally, hyperkalaemia might result from potassium outflow from cells because of acidaemia, hyperglycaemia, or beta-blockage. Finally, severe hyperkalaemia may be the result of rhabdomyolysis (e.g. due to alcohol intoxication) or haemolysis [1–4].
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(ii) Even though secondary aldosteronism, due to congestive heart failure or due to liver cirrhosis with ascites, is considered to be a cause of hypokalaemia because of inappropriate kaliuresis, this is not observed routinely. On the contrary, untreated patients with heart failure or hepatic cirrhosis are typically normokalaemic. These patients present with significant circulating volume depletion. In such hypovolaemic states enhanced secretion of aldosterone and ADH contribute to the retention of sodium and water. However, these patients do not present with kaliuresis and hypokalaemia, since the associated increases in proximal sodium reabsorption and ADH-induced water reabsorption combine to reduce distal flow, thereby counteracting both aldosterone and ADH effects on potassium secretion. In other words, the low distal delivery of sodium allows aldosterone to regulate sodium balance without interfering with potassium balance. On the contrary, our patient developed hyperkalaemia, occasionally reported in patients with effective volume depletion and related to the impaired ability to handle a potassium load, due to reduction in urinary excretion and perhaps to impaired potassium entry into cells. It should be mentioned that in our case spironolactone administration could also have played a prominent role in the development of hyperkalaemia. Low FEK+ and TTKG document that it is diminished potassium secretion which is mainly responsible for the increased potassium levels [5].
(iii) The treatment of hyperkalaemia varies with the severity of the electrolyte disturbance. In the absence of concurrent acid-base and electrolyte abnormalities, symptomatic hyperkalaemia usually when serum potassium levels exceed 7.5 mmol/l. In hyperkalaemic cirrhotic patients discontinuation of potassium-sparing diuretis, decrease of oral potassium intake, and avoidance of massive blood transfusions are significant modifiable factors. In addition, in patients with refractory severe hyperkalaemia, intravenous calcium gluconate is administered in order to antagonize the depolarizing effect of hyperkaemia on membrane potential. Increased potassium entry into cells is induced by intravenous glucose and insulin coadministration, as well as administration of NaHCO3 , and beta-adrenergic agonists (e.g. high doses of aerosolized salbutamol). Finally, potassium excess is removed by loop or thiazide-type diuretics or by cation-exchanging resins (kayexalate). In almost all patients the above-mentioned conservative measures reverse hyperkalaemia, and only very rarely dialysis (haemodialysis) is required. (The latter is usually in the presence of a hypercatabolic state (rhabdomyolysis) or renal function deterioration [1,3].)
Although hyperkalaemia may lead to clinical problems, hypokalaemia is probably more significant as it is a risk factor for the development of hepatic encephalopathy in cirrhotic patients. Hypokalaemia has been shown to increase tubular NH3 synthesis resulting in high serum ammonia levels. Therefore, cirrhotic patients must have their serum potassium levels regularly checked, aiming towards prevention of potassium depletion. In practice, Henle-loop diuretics (e.g. frusemide) in combination with potassium-sparing diuretics (e.g. spironolactone) should be carefully administered in order to maintain normal serum potassium levels [6].
Notes
The readers of our journal are encouraged to submit material suitable for this section. Submissions should be directed to the Section Editor, Dr T. J. Rabelink, University Hospital, Department of Nephrology, PO Box 85500, Fo 3.226, 3508 GA Utrecht, The Netherlands.
References
- Anderson RJ. Electrolyte, water, mineral, and acid-base disorders in liver disease. In: Narins R, ed. Clinical Disorders of Fluid and Electrolyte Metabolism. 5th edition. MacGraw Hill, New York: 1994: 1153–1172
- Gabow PA, Moore S, Schrier RW. Spironolactone-induced hyperchloremic acidosis in cirrhosis. Ann Intern Med 1979; 90: 338–340
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Siamopoulos KC, Elisaf M, Katopodis K. Iatrogenic hyperkalaemia-points to consider in dianosis and management. Nephrol Dial Transplant 1997; 13: 2402–2406
[Free Full Text] - Casey TH, Summerskill WHJ, Orvis AL. Body and serum potassium in liver disease: II. Relationships to arterial ammonia, blood pH, and hepatic coma. Gastroenterology 1965; 48: 198–207[Web of Science][Medline]
- Rose BP. Potassium homeostasis. In: Rose BD, ed. Clinical Physiology of Acid-Base and Electrolyte Disorders. 4th edition. MacGraw-Hill, New York: 1994; 346–376
- Zavagli G, Ricci G, Bader G, Mapelli G, Tomasi F, Maraschin B. The importance of the highest normokalemia in the treatment of early hepatic encephalopathy. Miner Electrolyte Metab 1993; 19: 362–367[Medline]
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