Hyponatremia thiazide diuretics causing

Thiazide diuretic-induced hyponatremia is much more common in older than in younger patients, probably due to thiazide-mediated impairment in renal diluting capacity superimposed on the already present age-related decrease in capacity to dilute urine. Older studies indicated this was an extremely common cause... 

Treatment with thiazide diuretics is one of the most common causes of hyponatremia (92). Patients can present with variable hypovolemia or apparent euvolemia,... 

Like all diuretics, the thiazides can cause electrolyte abnormalities, such as hypokalemia and hyponatremia, and dehydration. These complications are uncommon in patients with uncomplicated hypertension, but are more common in patients with heart failure or decompensated hepatic cirrhosis with secondary hyperaldosteronism. Until a patient is accustomed to the effect of a diuretic, dizziness may be experienced. Serum lipid concentrations are slightly raised acutely and hyperglycemia can occur during long-term therapy. Rare effects are thrombocytopenia, rashes, drug fever, cholestatic jaundice, pancreatitis, and precipitation of hepatic... 

Diuretic drugs often cause a mild reduction of the plasma potassium concentration hyponatremia may be observed. Hypercalcemia may occur with hemoconcentration, but occasionally the free-ionized and the protein-bound fraction is increased. Thiazides cause hyperglycemia and reduce glucose tolerance, especially in diabetics. Thiazides may cause prerenal azotemia with hyperuricemia as a result of decreased renal blood flow and GFR as a result of reduced blood volume. Thiazides, like other diuretics, by causing hemoconcentration increase the plasma concentration of lipids. Many thiazides induce microsomal enzymes and thus affect lipoprotein concentrations. 

Diuretic-induced hyponatremia occurs more frequently in patients treated with thiazide diuretics than in patients who are receiving loop diuretics. In addition to causing extracellular volume depletion and nonosmotic stimulation of ADH, thiazides interfere with urinary dilution and water excretion by blocking tubular sodium and potassium reabsorption in the distal tubule. Water is then retained in excess of sodium by virtue of nonosmotic release of ADH and excretion of urine with a concentration of sodium and potassium that exceeds that of the plasma. 

Diuretics are used widely for the treatment of hypertension see Chapter 32), and loop diuretics appear to lower blood pressure as effectively as Na+-CL symporter inhibitors e.g., thiazides and thiazide-hke diuretics) while causing smaller perturbations in the Upid profile. However, the short elimination half-lives of loop diuretics render them less useful for hypertension than thiazide-type diuretics. The edema of nephrotic syndrome often is refractory to other classes of diuretics, and loop diuretics often are the only drugs capable of reducing the massive edema associated with this disease. Loop diuretics also are employed in the treatment of edema and ascites of hepatic cirrhosis however, care must be taken not to induce encephalopathy or hepatorenal syndrome. In patients with a drug overdose, loop diuretics can be used to induce a forced diuresis to facilitate more rapid renal elimination of the offending drug. Loop diuretics, combined with isotonic saline administration to prevent volume depletion, are used to treat hypercalcemia. Loop diuretics interfere with the kidney s capacity to produce a concentrated urine. Consequently, loop diuretics combined with hypertonic saline are useful for the treatment of hfe-threatening hyponatremia. Loop diuretics also are used to treat edema associated with chronic renal insufficiency. Most patients with ARE receive... 

ADVERSE EFFECTS AND PRECAUTIONS Adverse effects of diuretics see Chapter 28) determine tolerance and adherence. Erectile dysfunction is a troublesome adverse effect of thiazide diuretics physicians should inquire specifically regarding its occurrence. Albeit uncommon, gout may be a consequence of the hyperuricemia induced by these diuretics. Either of these adverse effects is reason to consider alternative therapies. Hydrochlorothiazide may cause rapidly developing, severe hyponatremia in some patients. Thiazides inhibit renal Ca " excretion, occasionally leading to hypercalcemia although generally mUd, this can be more severe in patients subject to hypercalcemia, such as those with primary hyperparathyroidism. The thiazide-induced decreased Ca excretion may be used therapeutically in patients with osteoporosis or hypercalciuiia. 

Because Henle s loop is indirectly responsible for water reabsorption by the downstream collecting duct, loop diuretics can cause severe dehydration. Hyponatremia is less common than with the thiazides (see below), but patients who increase water intake in response to hypovolemia-induced thirst can become severely hyponatremic with loop agents. Loop agents are sometimes used for their calciuric effect, but hypercalcemia can occur in volume-depleted patients who have another—previously occult—cause for... 

Like other diuretics, thiazides can induce hypokalemia, hyponatremia, hypochloiemia. hypomagnesemia. hypercalcemia, hyperuricemia, glucose intolerance, dehydration, and changes in the lipid profile. Thiazides may also cause photosensitivity reactions. 

B. Effects In full doses, thiazides produce moderate but sustained sodium and chloride diuresis. Hypokalemic metabolic alkalosis may occur (Table 15-2). Reduction in the transport of sodium into the tubular cell reduces intracellular sodium and promotes sodium-calcium exchange. As a result, reabsorption of calcium from the urine is increased and urine calcium content is decreased— the opposite of the effect of loop diuretics. Because they act in a diluting segment of the nephron, thiazides may interfere with excretion of water and cause dHutional hyponatremia. 

Other causes of euvolemic hyponatremia include hypothyroidism, postoperative state, and idiosyncratic reactions to diuretics (generally thiazides). 

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