eMedicine Specialties > Nephrology > Acid-Base, Fluid, and Electrolyte Disorders

Hyporeninemic Hypoaldosteronism: Treatment & Medication

Author: James H Sondheimer, MD, Director of Hemodialysis Unit, Harper Hospital; Associate Professor, Department of Internal Medicine, Division of Nephrology, Wayne State University School of Medicine
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Updated: Oct 7, 2009

Treatment

Medical Care

If the patient has severe hyperkalemia and/or ECG abnormalities are present, emergency measures for hyperkalemia are necessary (see Hyperkalemia). The need for dialysis in patients with hyperkalemia and mild CKD is uncommon, because medical measures usually suffice.

Reduce or eliminate, if at all possible, medications that cause or may exacerbate potassium retention. The long-term approach is to utilize measures that increase net potassium excretion by the renal or intestinal routes:

• Diuretics, loop and/or thiazide
  • These agents are well known for their kaliuretic and chloruretic effects. While usually viewed as adverse effects, in RTA type IV these effects are exploited as a way to remove potassium and to treat the acidosis.
  • Diuretics are the first-line therapy for patients with signs of volume overload on examination.
  • Caution these patients to ignore the label that pharmacists may put on the diuretic bottle instructing them to take with a glass of orange juice.
  • The main adverse effects of diuretics are overdiuresis with volume depletion and alkalosis.
• Sodium bicarbonate (ie, NaHCO₃)
  • This adjunctive agent is administered in 10 grain (650 mg) tablets.
  • This agent usually corrects the acidosis and, by increasing distal delivery of bicarbonate anion, increases UK excretion.
  • The consumption of NaHCO₃ may cause the patient to belch and may also lead to volume overload.
  • NaHCO₃ tablets may be used as a first-line agent in patients with more severe acidosis (eg, 14-16 mEq/L) or in volume-depleted patients who should not be given diuretics.
• Fludrocortisone (ie, Florinef)
  • This is the third-line agent for patients with RTA type IV.
  • This synthetic corticosteroid is unique because its mineralocorticoid activity significantly exceeds its glucocorticoid activity.
  • Florinef is used as an aldosterone analogue; note, however, that the dosage needed to achieve effective kaliuresis is generally 0.1-0.3 mg/d, which is higher than the dosage used as replacement in patients with adrenal insufficiency and therefore indicates the importance of tubular hyporesponsiveness to aldosterone in most patients with RTA type IV.
  • Also, note that Florinef has some glucocorticoid activity with the resultant metabolic and long-term side effects.
  • Florinef can exacerbate hypertension and fluid overload, and patients taking this drug need close follow-up care.
  • Reports regarding the adverse effects of endogenous aldosterone on cardiac remodeling in patients with CHF raise serious concerns about the long-term use of Florinef, unless all other methods are exhausted.
• Sodium polystyrene sulfonate (ie, Kayexalate)
  • This agent is an exchange resin that is useful in achieving potassium removal via the colon, thereby bypassing the impaired renal excretory mechanisms.
  • Kayexalate now is available in premixed doses in a sorbitol solution (to provide laxation, which is necessary for Kayexalate to be effective).
  • Effectiveness is variable; however, on average, Kayexalate removes 1 mEq of potassium for each gram ingested, at the cost of about 1 mEq of absorbed sodium. This sodium retention may be problematic for patients with CHF or impaired renal function
  • Compliance is an issue for long-term use because this agent is not very palatable.
  • If the patient develops constipation, this agent is ineffective.
  • Intestinal complications of oral or rectal use are well known.
  • Kayexalate clearly has a role in the long-term treatment of patients for whom the above kaliuretic approaches have failed, patients who are intolerant to them, or patients who are noncompliant with dietary restrictions.
  • Kayexalate cannot be used in patients with ileostomy (absence of colon), ileus, or obstruction or in patients who have undergone recent intestinal surgery.

Surgical Care

If the patient presents with hyperkalemia as a complication of urinary tract obstruction, institute appropriate urologic measures.

Consultations

• Consult a dietitian for assistance in teaching the patient about a potassium-restricted diet.
• Consultation with a urologist will be necessary if urinary tract obstruction is discovered.
• Because many cardiac medications (eg, ACE inhibitors, angiotensin receptor blockers [ARBs], beta-blockers, aldosterone inhibitors) produce hyperkalemia, a cardiologic consultation may be indicated to design a cardiac regimen that is compatible with the patient's intolerance of these medication classes.

Diet

Recommend a dietary review, preferably by a renal dietitian, to uncover sources of dietary potassium excess. Salt substitutes commonly are overlooked, which often contain large amounts of potassium chloride (KCl). Dietary teaching also is an important part of long-term therapy.

• Two-gram potassium restriction, including complete avoidance of KCl-containing salt substitutes.
• Sodium intake is variable because most patients are hypertensive and/or retain salt from CKD, but some patients waste salt.
• Counsel patients against the use of OTC nonsteroidal agents.
• Caution patients on the use of herbal remedies and dietary supplements unless known to be safe.

Activity

Although no published data exist regarding whether to limit patient activity with this condition, a theoretical concern exists that these patients might be ill equipped to handle the transient hyperkalemia that strenuous exercise produces; accordingly, instruct the patient to approach strenuous exercise with caution and only if stable control of potassium is demonstrated.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Loop diuretics

Diuretics increase sodium and potassium loss in the urine. The latter usually is considered an adverse effect but is the desired effect in treating patients with RTA type IV.

Furosemide (Lasix)

Inhibits reabsorption of chloride, predominantly in the thick ascending limb of loop of Henle. The high efficacy of this drug is largely due to the large amount of sodium usually reabsorbed in this site.

Mineralocorticoids

Provide pharmacologic amounts of mineralocorticoid activity, so the patient can overcome tubular resistance to physiologic amounts of aldosterone.

Fludrocortisone (Florinef)

Used as a third-line agent in patients for whom treatment with diuretics, sodium bicarbonate, and dietary measures has failed. Promotes increased reabsorption of sodium and loss of potassium from renal distal tubules.

Ion-exchange resins

By increasing gut excretion of potassium, these agents bypass renal impairment of potassium excretion. Difficult to take on a regular basis, limiting its use in long-term therapy.

Sodium polystyrene sulfonate (Kayexalate)

Exchanges sodium for potassium and binds in the gut, primarily in the large intestine. Also decreases total body potassium. Onset of action after PO administration ranges from 2-12 hours and is longer when administered rectally.

Alkalinizing agents

Provide bicarbonate anion to replete patients with metabolic acidosis. Alkalinizes urine, enhancing kaliuresis.

Sodium bicarbonate (Neut)

Used IV in emergency treatment of hyperkalemia. Used PO in patients with metabolic acidosis and hyperkalemia.

Thiazide diuretics

Useful in the treatment of RTA type IV because of kaliuretic effects. Less likely to produce marked volume depletion than loop diuretics and may be better antihypertensive agents.

Hydrochlorothiazide (HydroDIURIL, Esidrix)

Inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium, water, potassium, and hydrogen ions.

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