Hyperkalemia can result from increased potassium intake, decreased potassium excretion, or a shift of potassium from the intracellular to the extracellular space. The most common causes involve decreased excretion. Alone, excessive intake or an extracellular shift is distinctly uncommon. Often, several disorders are present simultaneously. Alone, increased intake of potassium is a rare cause of hyperkalemia, because the mechanisms for renal excretion and intracellular disposition are very efficient. In general, a relatively high potassium intake contributes to hyperkalemia in individuals who have impaired renal excretion or intracellular-to-extracellular shift. Increased intake may result from the following:
Almost all patients who present with persistent hyperkalemia have impaired renal excretion of potassium. Mild degrees of renal failure generally do not result in resting hyperkalemia, because of compensation by adaptive mechanisms in the kidneys and GI tract. However, once the GFR falls below 15-20 mL/min, significant hyperkalemia can occur, even in the absence of an abnormally large potassium load. The simple lack of nephron mass prevents normal potassium homeostasis. Other mechanisms, such as drug effects or renal tubular acidosis, can decrease renal potassium excretion and cause hyperkalemia even in individuals with normal or only mildly decreased kidney function. Two other causes of decreased excretion of potassium are reduced distal sodium delivery and reduced tubular fluid flow rate. Medications that can decrease potassium excretion include the following:
In a study of 396 consecutive patients with heart failure who were taking renin-angiotensin-aldosterone system inhibitors (RAASi), 26% developed hyperkalemia of 5.5 mmol/L or greater and 12% developed hyperkalemia of 6.0 mmol/L or greater, over mean follow-up of 6.9 years. Independent risk factors for hyperkalemia included diabetes mellitus (odds ratio [OR] = 1.80, 95% CI = 1.03-3.19) and elevated baseline creatinine (OR = 2.37, 95% CI = 2.37-3.85). [30] Initial analysis of data on 9222 outpatients in a European heart failure registry showed that hyperkalemia was independently associated with higher mortality. After adjusting for RAASi discontinuation, however, hyperkalemia was no longer associated with mortality, suggesting that hyperkalemia may be a risk marker for RAASi discontinuation rather than a risk factor for worse outcomes. [31] Disorders that can cause type IV renal tubular acidosis, resulting in hyperkalemia, include the following:
Like increased intake, this is rarely the sole cause of hyperkalemia, because the mechanisms for renal excretion are very efficient. However, the inability to transport potassium intracellularly exacerbates hyperkalemia in individuals who have impaired renal excretion. Factors that can shift potassium into the extracellular space include the following:
Hypertonicity may lead to hyperkalemia by the following 2 mechanisms:
The most common cause of hyperosmolality is hyperglycemia in uncontrolled diabetes mellitus. Other conditions with hypertonicity are hypernatremia, hypertonic mannitol, and high-osmolarity contrast media.. Aldosterone deficiency is somewhat controversial as a cause of hyperkalemia. There is some evidence that long-term aldosterone deficiency impairs cell potassium uptake. Toad venom, which is used in traditional Chinese medicine and in folk medicine in southeastern Asia, contains cardiac glycosides whose structure and biochemical activity are similar to those of digitalis. These cause hyperkalemia by binding to the alpha subunit of Na+ -K+ -ATPase and thus inhibiting reuptake of potassium from the extracellular space. [37] Toad venom is prepared from dried secretions, typically from the Asiatic toad (Bufo gargarizans). In addition being an ingredient in Chinese medications (eg, Chan Su, Lu-Shen Wan), toad venom has also turned up in purported aphrodisiacs. Digoxin Fab fragments have been used to treat toad venom poisoning. [38] Genetic disorders that can result in hyperkalemia include the following:
Glomerulopathy with fibronectin deposits GFND is a genetically heterogeneous autosomal dominant disorder which manifests as proteinuria, hypertension, type IV renal tubular acidosis. It eventually leads to end-stage renal failure, in the second to fifth decade of life. Type 1 GFND maps to chromosome 1q32, but the gene is unknown at this time. Type 2 GFND is caused by mutations in the FN1 gene located on chromosome 2q34. Disorders of steroid metabolism and mineralocorticoid receptors 21-hydroxylase deficiency in its classic form and aldosterone synthase deficiency result in hyperkalemia due to low aldosterone levels. 11-Beta hydroxylase deficiency, 3-beta hydroxysteroid dehydrogenase deficiency, and 17 alpha-hydroxylase/17,20-lyase deficiency are generally not characterized by the development of hyperkalemia. Congenital hypoaldosteronism Congenital hypoaldosteronism is caused by mutations in the CYP11B2 gene, which encodes the type II corticosterone methyloxidase enzyme. It is inherited in an autosomal recessive manner. Patients with this disorder have decreased aldosterone and salt wasting. They will have an increased serum ratio of 18-hydroxycorticosterone to aldosterone. Pseudohypoaldosteronism Type I pseudohypoaldosteronism (PHAI) can be caused by an inactivating mutation of 1 of 3 encoding subunits of the epithelial sodium channel (SCNN1A, SCNN1G, or SCNN1B). PHAI is inherited in an autosomal recessive manner. These mutations result in impaired potassium secretion due to impaired sodium reabsorption in the distal tubule. [40] PHAI tends to be most severe in the neonatal period, causing renal salt wasting and respiratory tract infections. Sweat, stool, and saliva have high sodium concentrations. Sometimes this disorder can be mistaken for cystic fibrosis. Another form of PHAI is caused by mutations in the NR3C2 gene and is inherited in an autosomal dominant manner. Patients with this disorder may present in the neonatal period with renal salt wasting and hyperkalemic acidosis similar to those seen in the autosomal recessive form. Patients with this form of PHAI generally improve with age and are typically asymptomatic in adulthood. [41] Gordon syndrome, or pseudohypoaldosteronism type II (PHAII), characterized by hyperkalemia and hypertension, is caused by mutations in several genes. The following 5 loci are known to be associated with PHAII:
The genes causing this disorder code for protein kinases that are localized to the distal tubule and that regulate ion transport in this nephron segment. WNK4 appears to have several roles in regulating sodium, potassium, and chloride transport through transcellular and paracellular pathways. [42] Interestingly, PHAII from mutations in WNK1 is significantly less severe than PHAII from mutations in WNK4 or KLHL3, whereas PHAII from mutations in CUL3 is more severe. [43] All forms of PHII generally respond to treatment with thiazide diuretics. Disorders of chloride homeostasis Disorders of chloride homeostasis can also result in hyperkalemia. Isolated hyperchlorhidrosis is caused by mutations in the CA12 gene, and is inherited in an autosomal recessive manner. This disorder can cause excessive salt wasting in sweat, which can result in severe hyponatremic dehydration and hyperkalemia. [44] Nephronophthisis Nephronophthisis is characterized by enlargement of the kidneys, inflammatory portal fibrosis of the liver, and variable development of end-stage renal disease (ESRD). Patients with the infantile form of this disease generally reach ESRD before the age of 2 years. Patients with the juvenile form reach ESRD at a median age of 13 years. Patients with other forms of the disease have variable natural history. Ultimately, this disorder causes a progressive interstitial fibrosis and tubulopathy. Routine laboratory evaluation will show increased creatinine and potassium. Hyperkalemic periodic paralysis HYPP is caused by mutations in the SCN4A gene and is inherited in an autosomal dominant manner. During attacks (which can be precipitated by administration of potassium), individuals with HYPP have flaccid generalized weakness and increased serum potassium levels. In addition, patients with HYPP can also have myotonia, which is not typically a feature of hypokalemic periodic paralysis (HOKPP). A number of similar disorders involving myotonia or muscular weakness are allelic to HYPP. [45] Patients with diabetes constitute a unique high-risk group for hyperkalemia, in that they develop defects in all aspects of potassium metabolism. [16, 17] The typical healthy diabetic diet often is high in potassium and low in sodium. Diabetic persons frequently have underlying kidneyl disease and often develop hyporeninemic hypoaldosteronism (ie, decreased aldosterone secondary to suppressed renin levels), impairing renal excretion of potassium. [20, 21] Many patients with diabetes are placed on ACE inhibitor or ARB therapy for treatment of hypertension or diabetic nephropathy, exacerbating the defect in potassium excretion. Finally, persons with diabetes have insulin deficiency or resistance to insulin action, limiting their ability to shift potassium intracellularly. |
A nurse is reviewing the laboratory report for a client who has been taking sodium polystyrene
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