Chapter 046. Sodium and Water (Part 17)

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Decreased aldosterone synthesis may be due to primary adrenal insufficiency (Addison's disease) or congenital adrenal enzyme deficiency (Chap. 336). Heparin (including low-molecular-weight heparin) inhibits production of aldosterone by the cells of the zona glomerulosa and can lead to severe hyperkalemia in a subset of patients with underlying renal disease, diabetes mellitus, or those receiving K+-sparing diuretics, ACE inhibitors, or NSAIDs. Pseudohypoaldosteronism is a rare familial disorder characterized by hyperkalemia, metabolic acidosis, renal Na+ wasting, hypotension, high renin and aldosterone levels, and end-organ resistance to aldosterone. ...

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Chapter 046. Sodium and Water (Part 17) Decreased aldosterone synthesis may be due to primary adrenal insufficiency (Addison's disease) or congenital adrenal enzyme deficiency (Chap. 336). Heparin (including low-molecular-weight heparin) inhibits production of aldosterone by the cells of the zona glomerulosa and can lead to severe hyperkalemia in a subset of patients with underlying renal disease, diabetes mellitus, or those receiving K+-sparing diuretics, ACE inhibitors, or NSAIDs. Pseudohypoaldosteronism is a rare familial disorder characterized by hyperkalemia, metabolic acidosis, renal Na+ wasting, hypotension, high renin and aldosterone levels, and end-organ resistance to aldosterone. The gene encoding the mineralocorticoid receptor is normal in these patients, and the electrolyte abnormalities can be reversed with suprapharmacologic doses of an exogenous mineralocorticoid (e.g., 9α-fludrocortisone) or an inhibitor of 11β-HSDH (e.g., carbenoxolone). The kaliuretic response to aldosterone is impaired by K+-sparing
diuretics. Spironolactone is a competitive mineralocorticoid antagonist, whereas amiloride and triamterene block the apical Na + channel of the principal cell. Two other drugs that impair K+ secretion by blocking distal nephron Na+ reabsorption are trimethoprim and pentamidine. These antimicrobial agents may contribute to the hyperkalemia often seen in patients infected with HIV who are being treated for Pneumocystis carinii pneumonia. Hyperkalemia frequently complicates acute oliguric renal failure due to increased K+ release from cells (acidosis, catabolism) and decreased excretion. Increased distal flow rate and K+ secretion per nephron compensate for decreased renal mass in chronic renal insufficiency. However, these adaptive mechanisms eventually fail to maintain K+ balance when the GFR falls below 10–15 mL/min or oliguria ensues. Otherwise asymptomatic urinary tract obstruction is an often overlooked cause of hyperkalemia. Other nephropathies associated with impaired K+ excretion include drug-induced interstitial nephritis, lupus nephritis, sickle cell disease, and diabetic nephropathy. Gordon's syndrome is a rare condition characterized by hyperkalemia, metabolic acidosis, and a normal GFR. These patients are usually volume- expanded with suppressed renin and aldosterone levels as well as refractory to the kaliuretic effect of exogenous mineralocorticoids. It has been suggested that these findings could all be accounted for by increased distal Cl – reabsorption (electroneutral Na+ reabsorption), also referred to as a Cl–shunt. A similar
mechanism may be partially responsible for the hyperkalemia associated with cyclosporine nephrotoxicity. Hyperkalemic distal (type 4)RTA may be due to either hypoaldosteronism or a Cl– shunt (aldosterone-resistant). Clinical Features Since the resting membrane potential is related to the ratio of the ICF to ECF K+ concentration, hyperkalemia partially depolarizes the cell membrane. Prolonged depolarization impairs membrane excitability and is manifest as weakness, which may progress to flaccid paralysis and hypoventilation if the respiratory muscles are involved. Hyperkalemia also inhibits renal ammoniagenesis and reabsorption of NH4+ in the TALH. Thus, net acid excretion is impaired and results in metabolic acidosis, which may further exacerbate the hyperkalemia due to K+ movement out of cells. The most serious effect of hyperkalemia is cardiac toxicity, which does not correlate well with the plasma K+ concentration. The earliest electrocardiographic changes include increased T-wave amplitude, or peaked T waves. More severe degrees of hyperkalemia result in a prolonged PR interval and QRS duration, atrioventricular conduction delay, and loss of P waves. Progressive widening of the QRS complex and merging with the T wave produces a sine wave pattern. The terminal event is usually ventricular fibrillation or asystole. Diagnosis
(Fig. 46-4) With rare exceptions, chronic hyperkalemia is always due to impaired K+ excretion. If the etiology is not readily apparent and the patient is asymptomatic, pseudohyperkalemia should be excluded, as described above. Oliguric acute renal failure and severe chronic renal insufficiency should also be ruled out. The history should focus on medications that impair K + handling and potential sources of K+ intake. Evaluation of the ECF compartment, effective circulating volume, and urine output are essential components of the physical examination. The severity of hyperkalemia is determined by the symptoms, plasma K+ concentration, and electrocardiographic abnormalities. Figure 46-4