Electrolyte And Acid-base Disorders Flashcards
What is hyponatremia
Hyponatraemia (Na <135 mol/L) is a common biochemical abnormality. The causes depend on the associated changes in extracellular volume:
• Hyponatraemia with hypovolaemia (Table 13.7)
• Hyponatraemia with euvolaemia (Table 13.8)
• Hyponatraemia with hypervolaemia (Table 13.9).
Rarely, hyponatraemia may be a ‘pseudo-hyponatraemia’.
This occurs in hyperlipidaemia (either high cholesterol or high triglyceride) or hyperproteinaemia where there is a spuriously low measured sodium concentration, the sodium being confined to the aqueous phase but having its concentration expressed in terms of the total volume of plasma. In this situ-ation, plasma osmolality is normal and therefore treatment of ‘hyponatraemia’ is unnecessary. Note: Artefactual
‘hyponatraemia’, caused by taking blood from the limb into which fluid of low sodium concentration is being infused, should be excluded.
What is hyponatremia with hypovolemia
This is due to salt loss in excess of water loss; the causes are listed in Table 13.7. In this situation, ADH secretion is initially suppressed (via the hypothalamic osmoreceptors); but as fluid volume is lost, volume receptors override the osmoreceptors and stimulate both thirst and the release of ADH. This is an attempt by the body to defend circulating volume at the expense of osmolality.
With extrarenal losses and normal kidneys, the urinary excretion of sodium falls in response to the volume depletion, as does water excretion, leading to concentrated urine containing <10 mmol/L of sodium. However, in salt-wasting kidney disease, renal compensation cannot occur and the only physiological protection is increased water intake in response to thirst.
What are some clinical features of hyponatremia with hypovolemia
With sodium depletion the clinical picture is usually dominated by features of volume depletion (see p. 638). The diagnosis is usually obvious where there is a history of gut losses, diabetes mellitus or diuretic abuse. Examination of the patient is often more helpful than the biochemical inves-tigations, which include plasma and urine electrolytes and osmolality.
What is the treatment for hyponatremia with hypovolemia
This is directed at the primary cause whenever possible.
In a healthy patient:
• Give oral electrolyte-glucose mixtures (see p. 122)
• Increase salt intake with slow sodium 60-80 mmol/day.
In a patient with vomiting or severe volume depletion:
• Give intravenous fluid with potassium supplements, i.e.
1.5-2 L 5% glucose (with 20 mol K*) and 1 L 0.9% saline over 24 h PLUS measurable losses
• Correction of acid-base abnormalities is usually not required.
What is hyponatremia with euvolemia
This results from an intake of water in excess of the kidney’s ability to excrete it (dilutional hyponatraemia) with no change in body sodium content but the plasma osmolality is low.
• With normal kidney function, dilution hyponatraemia is uncommon even if a patient drinks approximately 1 L per hour.
• The most common iatrogenic cause is overgenerous infusion of 5% glucose into postoperative patients; in this situation it is exacerbated by an increased ADH secretion in response to stress.
• Postoperative hyponatraemia is a common clinical problem (almost 1% of patients) with symptomatic hyponatraemia occurring in 20% of these patients.
• Marathon runners drinking excess water and ‘sports drinks’ can become hyponatraemic.
• Premenopausal females are at most risk for developing hyponatraemic encephalopathy postoperatively, with postoperative ADH values in young females being 40 times higher than in young males.
To prevent hyponatraemia, avoid using hypotonic fluids postoperatively and administer 0.9% saline unless otherwise clinically contraindicated. The serum sodium should be measured daily in any patient receiving continuous parenteral fluid.
Some degree of hyponatraemia is usual in acute oliguric kidney injury, while in chronic kidney disease (CKD) it is most often due to ill-given advice to ‘push’ fluids.
What are some clinical features of hyponatremia with euvolemia
Dilutional hyponatraemia symptoms are common when hyponatraemia develops acutely (<48 h, often postopera-tively). Symptoms rarely occur until the serum sodium is less than 120 mol/L and are more usually associated with values around 110 mol/L or lower, particularly when chronic. They are principally neurological and are due to the movement of water into brain cells in response to the fall in extracellular osmolality.
Hyponatraemic encephalopathy symptoms and signs include headache, confusion and restlessness leading to drowsiness, myoclonic jerks, generalized convulsions and eventually coma. MRI scan of the brain reveals cerebral edema but, in the context of electrolyte abnormalities and neurological symptoms, it can help to make a confirmatory diagnosis.
Risk factors for developing hyponatraemic encepha-lopathy. The brain’s adaptation to hyponatraemia initially involves extrusion of blood and CS, as well as sodium, potassium and organic osmolytes, in order to decrease brain osmolality. Various factors can interfere with successful adaptation. These factors rather than the absolute change in serum sodium predict whether a patient will suffer hyponat-raemic encephalopathy.
• Children under 16 ears are at increased risk due to their relatively larger brain-to-intracranial volume ratio compared with adults.
• Premenopausal women are more likely to develop encephalopathy than postmenopausal females and males because of inhibitory effects of sex hormones and the effects of vasopressin on cerebral circulation resulting in vasoconstriction and hypoperfusion of brain.
• Hypoxaemia is a major risk factor for hyponatraemic encephalopathy. Patients with hyponatraemia, who develop hypoxia due to either non-cardiac pulmonary edema or hypercapnic respiratory failure, have a high risk of mortality. Hypoxia is the strongest predictor of mortality in patients with symptomatic hyponatraemia.
What are some investigations to make in hyponatremia
The cause of hyponatraemia with apparently normal extracel-lular volume requires investigation:
• Plasma and urine electrolytes and osmolalities. The plasma concentrations of sodium, chloride and urea are low, giving a low osmolality. The urine sodium concentration is usually high and the urine osmolalit is typically higher than the plasma osmolality.
However, maximal dilution (<50 mosmol/kg) is not always present.
• Further investigations to exclude Addison’s disease, hypothyroidism, ‘syndrome of inappropriate ADH secretion’ (SIADH) and drug-induced water retention, e.g. chlorpropamide.
Remember, potassium and magnesium depletion poten-tiate ADH release and are causes of diuretic-associated hyponatraemia.
The syndrome of inappropriate ADH secretion is often over-diagnosed. Some causes are associated with a lower set-point for ADH release, rather than completely autonomous ADH release - an example is chronic alcohol use.
What is the treatment for hyponatremia
The underlying cause should be corrected where possible.
• Most cases are simply managed by restriction of water intake (to 1000 or even 500 mL/day) with review of diuretic therapy. Magnesium and potassium deficiency must be corrected. In mild sodium deficiency, 0.9% saline given slowly (1 L over 12 hours) is sufficient.
• Acute onset with symptoms. The most common cause of acute hyponatraemia in adults is postoperative iatrogenic hyponatraemia. Excessive water intake associated with psychosis, marathon running and use of Ecstasy (a recreational drug) are other causes. All are acute medical emergencies and should be treated aggressively and immediately. In patients in whom there are severe neurological signs, such as fits or coma or cerebral edema, hypertonic saline (3%, 513 mmol/L) should be used. It must be given very slowly (not more than 70 mmol/h), the aim being to increase the serum sodium by 4-6 mol/L in the first 4 hours, but the absolute change should not exceed 15-20 mol/L over 48 hours.
In general, the plasma sodium should not be corrected to
>125-130 mmol/L. 1 mL/kg of 3% sodium chloride will raise the plasma sodium by 1 mol/L, assuming that total body water comprises 50% of total bodyweight.
• Symptomatic hyponatraemia in patients with intracranial pathology should be managed aggressively and immediately with 3% saline like acute hyponatraemia.
• Chronic/asymptomatic. If hyponatraemia has developed slowly, as it does in the majority of patients, the brain will have adapted by decreasing intracellular osmolality and the hyponatraemia can be corrected slowly (without use of hypertonic saline).
However, clinically it can be difficult to know how long the hyponatraemia has been present and 3% of hypertonic saline is still required.
How do you avoid osmotic demyelination syndrome
A rapid rise in extracellular osmolality, particularly if there is an ‘overshoot’ to high serum sodium and osmolality, will result in the osmotic demyelination, syndrome (ODS), formally known as central pontine demyelination, which is a devastating neurologic complication. Plasma sodium concentration in patients with hyponatraemia should not rise by more than 8 mmol/L per day. The rate of rise of plasma sodium should be even lower in patients at higher risk for ODS, e.g. patients with alcohol excess, cirrhosis, malnutri-tion, or hypokalaemia. Other factors predisposing to demyelination are pre-existing hypoxaemia and CNS radiation (see above). ODS is diagnosed by the appearance of characteristic hypointense lesions on T,-weighted images and hyper-intense on T2-weighted images on MRl; these take up to 2 weeks or longer to appear.
The pathophysiology of ODS is not fully understood. The most plausible explanation is that the brain loses organic osmolytes very quickly in order to adapt to hyponatraemia so that osmolarity is similar between the intracellular and extracellular compartments. However, neurones reclaim organic osmolytes slowly in the phase of rapid correction of hyponatraemia, resulting in an hypo-osmolar intracellular compartment and lead to shrinkage of cerebral vascular endothelial cells. Consequently the blood-brain barrier is functionally impaired, allowing lymphocytes, complement, and cytokines to enter the brain, damage oligodendrocytes, activate microglial cells and cause demyelination.
The most crucial issue in the treatment of hyponatraemia is to prevent rapid correction. A rapid rise in plasma sodium is almost always due to a water diuresis, which happens when vasopressin (ADH) action stops suddenly, for example with volume repletion in patients with intravascular volume depletion, cortisol replacement in patients with Addison disease, resolution of non-osmotic stimuli for vasopressin release such as nausea or pain. However, sometimes chronic hyponatraemia can develop in the absence of vasopressin excess. Even in these cases, water diuresis due to increased distal delivery of filtrate is the main cause of rapid rise in plasma sodium.
In the absence of vasopressin, it is generally assumed that the total urine volume is equal to the volume of filtrate delivered to the distal nephron, which is the GFR minus the volume reabsorbed in the proximal convoluted tubule (PCT).
Approximately 80% of the GR is reabsorbed in PCT under normal circumstance (increases even more in the presence of intravascular volume depletion). However, in real life water excretion will be less than the volume of distal delivery of filtrate, even in the absence of vasopressin, because a significant degree of water is reabsorbed in the inner medullary collecting duct through its residual water permeability, prompted by a very high osmotic force in the interstitium (see Fig. 12.2).
Even a modest water diuresis in the elderly with reduced muscle mass is large enough to cause a rapid rise in plasma sodium. Moreover, there is a higher risk for ODS if hypokalae-mia is present. In such cases if plasma sodium rises too quickly due to anticipated water diuresis, administration of desmopressin to stop the water diuresis is beneficial. If plasma sodium rises regardless then lowering plasma sodium to the maximum limit of correction (<8 mol/L per day) with the administration of 5% glucose solution is the best strategy.
Explain reversible hyponatraemia culminating in hypernatraemia
In many patients, the cause of water retention is reversible (e.g. hypovolaemia, thiazide diuretics). On correction of the cause, vasopressin levels fall and plasma sodium rises b up to 2 mmol/L per hour as a result of excretion of dilute urine.
This excessive water diuresis should be anticipated and prevented by use of desmopressin.
Patients who are chronically hyponatraemic with concomitant hypokalaemia are especially susceptible to overcorrec-tion. Plasma sodium is a function of the ratio of exchangeable body sodium plus potassium to total body water, so potassium administration increases sodium concentration. For example, a mildly symptomatic hyponatraemic patient with a plasma sodium of <120 mol/L and potassium of <2 mmol/L can potentially develop ODS as a result of overcorrection of hyponatraemia simply as a direct result of replacing the large potassium deficit.
Describe antidiuretic hormone antagonists (vasopressin antagonists)
Vasopressin V2 receptor antagonists (see p. 645), which produce a free water diuresis, are being used in clinical trials for the treatment of hyponatraemic encephalopathy. Three oral agents, lixivaptan, tolvaptan and satavaptan, are selective for the V2 (antidiuretic) receptor, while conivaptan blocks both the Via and V2 receptors.
These agents produce a selective water diuresis without affecting sodium and potassium excretion; they raise the plasma sodium concentration in patients with hyponatraemia caused by the SIADH, heart failure and cirrhosis.
The efficacy of oral tolvaptan in ambulatory patients has been demonstrated in patients with hyponatraemia (mean plasma sodium 129 mol/L) caused by the SIADH, heart failure, or cirrhosis who had a sustained rise in plasma sodium to 136 mol/L for 4 weeks. Tolvaptan is now approved for use in patients with euvolaemic hyponatraemia and those with SIADH. In addition, intravenous conivaptan is available and is also approved for the treatment of euvolae-mic hyponatraemia (i.e. SIADH) in some countries. The approved dosing for conivaptan is a 20 mg bolus followed by continuous infusion of 20 mg over 1-4 days. The continuous infusion increases the risk of phlebitis, which requires the use of large veins and changing the infusion site every 24 hours.
What is hyponatremia with hypervolemia
The common causes of hyponatraemia due to water excess are shown in Table 13.9. In all these conditions, there is usually an element of reduced glomerular filtration rate with avid reabsorption of sodium and chloride in the proximal tubule. This leads to reduced delivery of chloride to the ‘dilut-ing’ ascending limb of Henle’s loop and a reduced ability to generate ‘free water’, with a consequent inability to excrete dilute urine. This is commonly compounded by the administration of diuretics that block chloride reabsorption and interfere with the dilution of filtrate either in Henle’s loop (loop diuretics) or distally (thiazides).
What is syndrome of inappropriate
ADH secretion
There is inappropriate secretion of ADH, causing water retention and hyponatraemia.
What is hypernatremia
This is much rarer than hyponatraemia and nearly always indicates a water deficit. Causes are listed in Table 13.11).
Hypernatraemia is alwas associated with increased plasma osmolality, which is a potent stimulus to thirst. None of the above cause hypernatraemia unless thirst sensation is abnormal or access to water limited. For instance, a patient with diabetes insipidus will maintain a normal serum sodium concentration by maintaining a high water intake until an intercurrent illness prevents this. Thirst is frequently deficient in elderly people, making them more prone to water deple-tion. Hypernatraemia may occur in the presence of normal, reduced or expanded extracellular volume, and does not necessarily imply that total body sodium is increased.
What are some clinical features of hypernatremia
Symptoms of hypernatraemia are nonspecific. Nausea, vomiting, fever and confusion may occur. A history of longstanding polyuria, polydipsia and thirst suggests diabetes insipidus. Assessment of extracellular volume status guides resuscitation. Mental state should be assessed. Convulsions occur in severe hypernatraemia.
What are some investigations to make in hypernatremia
Simultaneous urine and plasma osmolality and sodium should be measured. Plasma osmolality is high in hypernat-raemia. Passage of urine with an osmolality lower than that of plasma in this situation is clearly abnormal and indicates diabetes insipidus. In pituitary diabetes insipidus, urine osmolality will increase after administration of desmopressin; the drug (a vasopressin analogue) has no effect in nephro-genic diabetes insipidus. If urine osmolality is high this suggests either an osmotic diuresis due to an unmeasured solute (e.g. in parenteral feeding) or excessive extrarenal loss of water (e.g. heat stroke).
What is the treatment for hypernatremia
Treatment is that of the underlying cause, e.g.
• In ADH deficiency, replace ADH in the form of desmopressin, a stable non-pressor analogue of ADH
• Remember to withdraw nephrotoxic drugs where possible and replace water either orally or, if necessary, intravenously.
In severe (>170 mmol/L) hypernatraemia, 0.9% saline (150 mmol/L) should be used initially. Avoid too rapid a drop in serum sodium concentration; the aim is correction over 48 h, as over-rapid correction may lead to cerebral oedema.
In less severe (e.g. >150 mmol/L) hypernatraemia, the treatment is 5% glucose or 0.45% saline; the latter is obviously preferable in hyperosmolar diabetic coma. Very large volumes - 5 L/day or more - may need to be given in diabetes insipidus.
If there is clinical evidence of volume depletion (see p.
646), this implies that there is a sodium deficit as well as a water deficit.
How is serum potassium regulated
Serum potassium levels are controlled by:
• uptake of K* into cells
• renal excretion
• extrarenal losses (e.g. gastrointestinal).
Uptake of potassium into cells is governed by the activity of the Na/K-ATPase in the cell membrane and by H concentration.
Uptake is stimulated by:
• insulin
• B-adrenergic stimulation
• theophyllines.
Uptake is decreased by:
• a-adrenergic stimulation
• acidosis - K exchanged for H+ across cell membrane
• cell damage or cell death - resulting in massive K* release.
Kidney plays the pivotal role in the maintenance of potassium balance by varying its secretion with changes in dietary intake. Over 90% of the filtered potassium is reabsorbed in the proximal tubule and the loop of Henle and only <10% of the filtered load is delivered to the early distal tubule. Potassium absorption on proximal tubule is entirely passive and follows that of sodium and water, while its reabsorption in the thick ascending limb of the loop of Henle is mediated by the sodium-potassium-2-chloride cotransporter. However, potassium is secreted by the principal cells in the cortical and outer medullary collecting tubule. Secretion in these segments is very tightly regulated in health and can be varied according to individuals needs and is responsible for most of urinary potassium excretion.
Renal excretion of potassium is increased by aldosterone, which stimulates K* and H* secretion in exchange for Na* in the principal cells of the collecting duct (Fig. 13.8). Because H* and K* are interchangeable in the exchange mechanism, acidosis decreases and alkalosis increases the secretion of K*. Aldosterone secretion is stimulated by hyperkalaemia and increased angiotensin II levels, as well as by some drugs, and this acts to protect the body against hyperkalaemia and against extracellular volume depletion. The body adapts to dietary deficiency of potassium by reducing aldosterone secretion. However, because aldosterone is also influenced by volume status, conservation of potassium is relatively inefficient, and significant potassium depletion may therefore result from prolonged dietary deficiency.
A number of drugs affect K* homeostasis by affecting aldosterone release (e.g. heparin, NSAIDs) or by directly affecting renal potassium handling (e.g. diuretics).
Recent evidence has shown that other endogenous proteins and metabolites also affect potassium homeostasis.
Klotho, an anti-ageing protein expressed in the distal tubule (and other organs), increases potassium excretion. CD63, a tetra-spanning protein, inhibits its excretion. Moreover, protein kinase A and C mediated phosphorylation inhibits conductance K channels in the principal cells of the collecting duct but the cytochrome p450-epoxygenase-mediated metabolite of arachidonic acid (11-12-epoxyeicosatrienoic acid activates these channels and plays a role in overall potassium homeostasis.
Normally, only about 10% of daily potassium intake is excreted in the gastrointestinal tract. Vomit contains around
5-10 mol/L of Kt, but prolonged vomiting causes hypoka-laemia by inducing sodium depletion, stimulating aldoster-one, which increases renal potassium excretion. Potassium is secreted by the colon, and diarrhoea contains 10-30 mol/L of K; profuse diarrhoea can therefore induce marked hypokalaemia. Colorectal villous adenomas may rarely produce profuse diarrhoea and K loss.
What are some common causes of hypokalemia
The most common causes of chronic hypokalaemia are diuretic treatment (particularly thiazides) and hyperaldos-teronism. Acute hypokalaemia is often caused by intravenous fluids without potassium and redistribution into cells. The common causes are shown in Table 13.12.
What are some rare causes of hypokalemia
Barter’s syndrome (clinically similar to loop diuretics)
Gitelman’s syndrome (similar to thiazide diuretics)
Liddle’s syndrome
Hypokalaemic periodic paralysis
What is Bartter’s syndrome
This consists of metabolic alkalosis, hypokalaemia, hyper-calciuria, occasionally hypomagnesaemia (see p. 657), normal blood pressure, and an elevated plasma renin and aldosterone. The primary defect in this disorder is an impairment in sodium and chloride reabsorption in the thick ascending limb of the loop of Henle (Fig. 13.6). Mutation in the genes encoding either the sodium-potassium-2-chloride cotrans-porter (NKCC2), the ATP-regulated renal outer medullary potassium channel (ROMK) or kidney-specific basolateral chloride channels (CIC-Kb) - Bartter types I, Il and lil, respectively - causes loss of function of these channels, with consequent impairment of sodium and chloride reabsorption. There is also an increased intrarenal production of prostaglandin Ez which is secondary to sodium and volume depletion, hypoka-lamia and the consequent neurohumoral response rather than a primary defect. PGE2 causes vasodilatation and may explain why the blood pressure remains normal.
Barttin, a B-subunit for CIC-Ka and CIC-Kb chloride chan-nels, is encoded by the BSND (Barter’s syndrome with sensorineural deafness) gene. Loss of function mutations cause type IV Batter’s syndrome associated with sensorineural deafness and renal failure. Barttin co-localizes with a subunit of the chloride channel in basolateral membranes of the renal tubule and inner ear epithelium. It appears to mediate chloride exit in the thick ascending limb (TAL) of the loop of Henle and chloride recycling in potassium-secreting strial marginal cells in the inner ear. A very rare variant of type IV is a disorder with an impairment of both chloride channels (CIC-Ka and CIC-Kb) producing the same phenotypic defects.
A gain of function mutation of the calcium sensing receptor (CaR) which leads to autosomal dominant hypocalcaemia has also been recognized in Barter’s syndrome. In the kidney, the CaR is expressed mainly in the basolateral membrane of cortical TAL. Activation of CaR by high calcium or magnesium or by gain of function mutation triggers intracellular signalling, including release of arachidonic acid and inhibition of adenylate cyclase. Both actions result in inhibition of ROMK activity, which in turn leads to reduction in the lumen-positive electrical potential and transcellular absorption of calcium. This effect of CaR explains why patients with mutations in this receptor may present with both hypocalcaemia, hypercalciuria and renal wasting of NaCI, resulting in a Bartter-like syndrome.
In summary, these defects in sodium chloride transport are thought to initiate the following sequence, which is almost identical to that seen with chronic ingestion of a loop diuretic.
The initial salt loss leads to mild volume depletion, resulting in activation of the renin-angiotensin-aldosterone system.
The combination of hyperaldosteronism and increased distal flow (owing to the reabsorptive detect) enhances potassium and hydrogen secretion at the secretory sites in the collecting tubules, leading to hypokalaemia and metabolic alkalosis.
Diagnostic pointers include high urinary potassium and chloride despite low serum values as well as increased plasma renin (NB: in primary aldosteronism, renin levels are low). Hyperplasia of the juxtaglomerular apparatus is seen on renal biopsy (careful exclusion of diuretic abuse is neces-sary). Hypercalciuria is a common feature but magnesium wasting, though rare, also occurs.
Treatment is with combinations of potassium supple-ments, amiloride and indomethacin.
What is Gitelman’s syndrome
Gitelman’s syndrome is a phenotype variant of Barter’s syndrome characterized by hypokalaemia, metabolic alkalosis, hypocalciuria, hypomagnesaemia, normal blood pressure, and elevated plasma renin and aldosterone. There are striking similarities between the Gitelman’s syndrome and the biochemical abnormalities induced by chronic thiazide diuretic administration. Thiazides act in the distal convoluted tubule to inhibit the function of the apical sodium-chloride cotransporter (NCCT) (Fig. 13.7). Analysis of the gene encoding the NCCT has identified loss of function mutations in Gitelman’s syndrome.
Like Barter’s syndrome, defective NCCT function leads to increased solute delivery to the collecting duct, with resultant solute wasting, volume contraction and an aldosterone-mediated increase in potassium and hydrogen secretion.
Unlike Barter’s syndrome, the degree of volume depletion and hypokalaemia is not sufficient to stimulate prostaglandin Ez production. Impaired function of NCCT is predicted to cause hypocalciuria, as does thiazide administration.
Impaired sodium reabsorption across the apical membrane, coupled with continued intracellular chloride efflux across the basolateral membrane, causes the cell to become hyper-polarized. This in turn stimulates calcium reabsorption via apical, voltage-activated calcium channels. Decreased intra-cellular sodium also facilitates calcium efflux via the basola-teral sodium-calcium exchanger. The mechanism for urinary magnesium losses is described on page 656.
Treatment consists of potassium and magnesium supplementation (MgCh2) and a potassium-sparing diuretic.
Volume resuscitation is usually not necessary, because patients are not dehydrated. Elevated prostaglandin Ez does not occur (see above) and, therefore, NSAIDs are not indicated in this disorder.
What is Liddle’s syndrome
This is characterized by potassium wasting, hypokalaemia and alkalosis, but is associated with low renin and aldosterone production, and high blood pressure. There is a mutation in the gene encoding for the amiloride-sensitive epithelial sodium channel in the distal tubule/collecting duct. This leads to constitutive activation of the epithelial sodium channel, resulting in excessive sodium reabsorption with coupled potassium and hydrogen secretion. Unregulated sodium reabsorption across the collecting tubule results in volume expansion, inhibition of renin and aldosterone secretion and development of low renin hypertension (Fig. 13.8).
Therapy consists of sodium restriction along with amilo-ride or triamterene administration. Both are potassium-sparing diuretics which directly close the sodium channels.
The mineralocorticoid antagonist spironolactone is ineffec-tive, since the increase in sodium-channel activity is not mediated by aldosterone.
What is hypokalemic periodic paralysis
This condition may be precipitated by carbohydrate intake, suggesting that insulin-mediated potassium influx into cells may be responsible. This syndrome also occurs in association with hyperthyroidism (thyrotoxic periodic paralysis) which occurs in Asians.
