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      Pathogenesis, diagnosis and management of hyperkalemia

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      Author(s): ,
      Publication date (Electronic):
      Journal: Pediatric Nephrology (Berlin, Germany)
      Publisher: Springer-Verlag
      Keywords: Hyperkalemia, Potassium, Renal failure, Salbutamol

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          Abstract

          Hyperkalemia is a potentially life-threatening condition in which serum potassium exceeds 5.5 mmol/l. It can be caused by reduced renal excretion, excessive intake or leakage of potassium from the intracellular space. In addition to acute and chronic renal failure, hypoaldosteronism, and massive tissue breakdown as in rhabdomyolysis, are typical conditions leading to hyperkalemia. Symptoms are non-specific and predominantly related to muscular or cardiac dysfunction. Treatment has to be initiated immediately using different therapeutic strategies to increase potassium shift into the intracellular space or to increase elimination, together with reduction of intake. Knowledge of the physiological mechanisms of potassium handling is essential in understanding the causes of hyperkalemia as well as its treatment. This article reviews the pathomechanisms leading to hyperkalemic states, its symptoms, and different treatment options.

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          Human hypertension caused by mutations in WNK kinases.

          F. Wilson, S Disse-Nicodème, K A Choate … (2001)
          Hypertension is a major public health problem of largely unknown cause. Here, we identify two genes causing pseudohypoaldosteronism type II, a Mendelian trait featuring hypertension, increased renal salt reabsorption, and impaired K+ and H+ excretion. Both genes encode members of the WNK family of serine-threonine kinases. Disease-causing mutations in WNK1 are large intronic deletions that increase WNK1 expression. The mutations in WNK4 are missense, which cluster in a short, highly conserved segment of the encoded protein. Both proteins localize to the distal nephron, a kidney segment involved in salt, K+, and pH homeostasis. WNK1 is cytoplasmic, whereas WNK4 localizes to tight junctions. The WNK kinases and their associated signaling pathway(s) may offer new targets for the development of antihypertensive drugs.
          Article 0 comments Cited 278 times – based on 0 reviews     Review now
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            Potassium homeostasis and renin-angiotensin-aldosterone system inhibitors.

            Mark Rolfe, Jacquelyn Weir (2010)
            Inhibition of the renin-angiotensin-aldosterone system (RAAS) is a key strategy in treating hypertension and cardiovascular and renal diseases. However, RAAS inhibitors (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone receptor antagonists, and direct renin inhibitors) increase the risk of hyperkalemia (serum potassium >5.5 mmol/L). This review evaluates the effects on serum potassium levels of RAAS inhibitors. Using PubMed, we searched for clinical trials published up to December 2008 assessing the effects on serum potassium levels of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone receptor antagonists, and direct renin inhibitors, alone and in combination, in patients with hypertension, heart failure (HF), or chronic kidney disease (CKD); 39 studies were identified. In patients with hypertension without risk factors for hyperkalemia, the incidence of hyperkalemia with RAAS inhibitor monotherapy is low (< or =2%), whereas rates are higher with dual RAAS inhibition ( approximately 5%). The incidence of hyperkalemia is also increased in patients with HF or CKD (5% to 10%). However, increases in serum potassium levels are small ( approximately 0.1 to 0.3 mmol/L), and rates of study discontinuation due to hyperkalemia are low, even in high-risk patient groups (1% to 5%). Patients with HF or CKD are at greater risk of hyperkalemia with RAAS inhibitors than those without these conditions. However, the absolute changes in serum potassium are generally small and unlikely to be clinically significant. Moreover, these patients are likely to derive benefit from RAAS inhibition. Rather than denying them an effective treatment, electrolyte levels should be closely monitored in these patients.
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              Sodium channelopathies of skeletal muscle result from gain or loss of function

              Karin Jurkat-Rott, Boris Holzherr, Michael Fauler … (2010)
              Five hereditary sodium channelopathies of skeletal muscle have been identified. Prominent symptoms are either myotonia or weakness caused by an increase or decrease of muscle fiber excitability. The voltage-gated sodium channel NaV1.4, initiator of the muscle action potential, is mutated in all five disorders. Pathogenetically, both loss and gain of function mutations have been described, the latter being the more frequent mechanism and involving not just the ion-conducting pore, but aberrant pores as well. The type of channel malfunction is decisive for therapy which consists either of exerting a direct effect on the sodium channel, i.e., by blocking the pore, or of restoring skeletal muscle membrane potential to reduce the fraction of inactivated channels.
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                Author and article information

                Contributors
                : +49-40-741051200 , +49-40-741051299 , kemper@uke.de
                Journal
                Journal ID (nlm-ta): Pediatr Nephrol
                Title: Pediatric Nephrology (Berlin, Germany)
                Publisher: Springer-Verlag (Berlin/Heidelberg )
                ISSN (Print): 0931-041X
                ISSN (Electronic): 1432-198X
                Publication date (Electronic): 22 December 2010
                Publication date PMC-release: 22 December 2010
                Publication date (Print): March 2011
                Volume: 26
                Issue: 3
                Pages: 377-384
                Affiliations
                Department of Pediatric Nephrology, University Medical Center Hamburg-Eppendorf, Martinistr. 5, 20246 Hamburg, Germany
                Article
                Publisher ID: 1699
                DOI: 10.1007/s00467-010-1699-3
                PMC ID: 3061004
                PubMed ID: 21181208
                SO-VID: edd8171a-a04e-4dbf-af33-7e28f790b4c4
                Copyright © © IPNA 2010
                History
                Date received : 8 July 2010
                Date revision received : 1 October 2010
                Date accepted : 4 October 2010
                Categories
                Subject: Educational Review
                Custom metadata
                issue-copyright-statement © IPNA 2011

                ScienceOpen disciplines: Nephrology
                Keywords: renal failure,potassium,hyperkalemia,salbutamol
                Data availability:
                ScienceOpen disciplines: Nephrology
                Keywords: renal failure, potassium, hyperkalemia, salbutamol

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