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Background: Because hemodiafiltration (HDF) involves large amounts of ultra-filtration and substitution fluid infusion, its effects on serum electrolytes may be different from those of hemodialysis (HD). Serum sodium and blood pressures were compared between patients undergoing online HDF and high-flux HD (HFHD). Methods: Thirty-two of 101 patients on HFHD switched voluntarily to online HDF. Their pre- and postdialysis serum measurements were compared with those of the remaining 69 HFHD patients. Results: Online HDF patients had lower pre- and postdialysis systolic blood pressures (SBPs) than HFHD patients (predialysis, 136±21 vs. 145±19 mmHg, P

In several sections of our review paper, cited in the title, we have found some errors in quotation of sentences from the Dr. Aaron Spital's review article entitled "Diuretic-induced hyponatremia" published in American Journal of Nephrology 19:447-452, 1999. Quotation marks were missed, and we should have specifically acknowledged the source of our statements. In Introduction (p. 51), "The first detailed description of diuretic-induced hyponatremia was published over 35 years ago4). Since that time, numerous additional cases have been reported" 14. Spital A: Diuretic-induced hyponatremia. Am J Nephrol 19:447-452, 1999 In Clinical characteristics of TIH(p. 53), "One of the most remarkable features of TIH is the rapidity with which it can occur. In susceptible individuals, the serum sodium may fall within hours of administration8), and severe hyponatremia can develop within less than 2 days7,14). In most reported cases (50% to 90%) the duration of thiazide use was less than 2 weeks7,8,14,22)" 14. Spital A: Diuretic-induced hyponatremia. Am J Nephrol 19:447-452, 1999 In Pathogenesis of TIH(p. 54), "Friedman et al.8) showed that within 6 h of ingesting a single hydrochlorothiazide-amiloride tablet, previously affected patients had a small rise in urine osmolality and a fall in serum sodium of 5.5mmol/L in association with a small gain in weight; controls had only a slight fall in serum sodium, and their mean weight fell. Although water intake was not measured, the authors suggested that thiazides might cause polydipsia which, when combined with the renal effects, results in expansion of total body water and development of hyponatremia" 14. Spital A: Diuretic-induced hyponatremia. Am J Nephrol 19:447-452, 1999 In Pathogenesis of TIH(p. 54), "While thiazide diuretics do not inhibit concentrating ability, they do impair diluting ability in several ways15,26,34). As mentioned above, they inhibit electrolyte transport at the cortical diluting sites, thereby raising the minimum urinary osmolality34-36). Diuretics may also reduce glomerular filtration rate and enhance reabsorption of Na+ and water in the proximal nephron, diminishing fluid delivery to the distal diluting sites35)." 14. Spital A: Diureticinduced hyponatremia. Am J Nephrol 19:447-452, 1999 In Pathogenesis of TIH(p. 54), "There is much evidence that patients with TIH are electrolyte-deficient. First, virtually all relevant studies have found that during the development of TIH, sodium balance is negative4,6,10) Second, once diuretics are withdrawn, urinary sodium excretion falls to very low levels4,10). Third, many of these patients are hypokalemic4,6,10). Fichman et al.10) emphasized the importance of potassium depletion in TIH. The great majority of their 25 patients were hypokalemic, and hyponatremia was corrected in 4 of them by potassium repletion despite continued diuretic use and sodium restriction. These investigators argued that potassium depletion predisposes the patients to hyponatremia because the serum sodium concentration is dependent upon the ratio of the sum of exchangeable sodium and potassium to total body water. They also speculated that potassium depletion might cause a shift of sodium into the intracellular space, thereby further compromising the extracellular volume and stimulating vasopressin release" 14. Spital A: Diuretic-induced hyponatremia. Am J Nephrol 19: 447-452, 1999

The importance of thiazide-induced hyponatremia (TIH) is reemerging because thiazide diuretic prescription seems to be increasing after the guidelines recommending thiazides as first-line treatment of essential hypertension have been introduced. Thiazide diuretics act by inhibiting reabsorption of Na(+) and Cl(-) from the distal convoluted tubule by blocking the thiazide-sensitive Na(+)/Cl(-) cotransporter. Thus, they inhibit electrolyte transport in the diluting segment and may impair urinary dilution in some vulnerable groups. Risk factors predisposing to TIH are old age, women, reduced body masses, and concurrent use of other medications that impair water excretion. While taking thiazides, the elderly may have a greater defect in water excretion after a water load compared with young subjects. Hyponatremia is usually induced within 2 weeks of starting the thiazide diuretic, but it can occur any time during thiazide therapy when subsequent contributory factors are complicated, such as reduction of renal function with aging, ingestion of other drugs that affect free water clearance, or changes in water or sodium intake. While some patients are volume depleted on presentation, most appear euvolemic. Notably serum levels of uric acid, creatinine and urea nitrogen are usually normal or low, suggestive of syndrome of inappropriate secretion of antidiuretic hormone. Despite numerous studies, the pathophysiological mechanisms underlying TIH are unclear. Although the traditional view is that diuretic-induced sodium or volume loss results in vasopressin-induced water retention, the following 3 main factors are implicated in TIH: stimulation of vasopressin secretion, reduced free-water clearance, and increased water intake. These factors will be discussed in this review.

Lymphocytic interstitial pneumonia (LIP) is a rare disorder characterized by a diffuse infiltration of the alveolar space, interstitium by lymphocytes, plasma cells, and reticuloendothelial cells. Although its etiology is unknown, LIP has been associated with autoimmune disorders and with viral infections. Because it’s clinical and radiographic features are nonspecific, a confirmatory diagnosis is performed by open lung biopsy. A 59-year-old female presented dry cough, which had been present for 1 month. On initial findings of multifocal consolidation at the right middle lobe on both lower lobes in chest radiography, the first diagnosis of cryptogenic organizing pneumonia was suggested. On open lung biopsy, LIP was diagnosed. The patient had no autoimmune disease, viral infection or monoclonal gammopathy. After 3 months of corticosteroid treatment, the patient experienced improved symptoms, reduced abnormalities on chest radiography, and improved pulmonary function testing.Key Words: Lymphocytic interstitial pneumonia, Cryptogenic organizing pneumonia, Interstitial lung disease

Gastrointestinal manifestations are common in systemic lupus erythematosus (SLE). Intestinal pseudo-obstruction (IpO) is a rare, poorly understood and recently recognized gastrointestinal manifestation of SLE. We report a 26-year-old female with SLE for 3 years. 10 months ago, IpO was diagnosed first, and it was responded well to high-dose steroid therapy. After then, oral prednisolone and azathioprine were administered, but the patient had been lost to follow up until recurrence of IpO. She was admitted with diffuse abdominal pain, distension, frequent vomiting, and intermittent dysuria due to recurrent IpO accompanied with bilateral ureterohydronephrosis. Despite of high dose steroid therapy, her symptom and imaging findings were not improved. The patient was treated with pulses of cyclophosphamide, and then the patient's symptoms and signs were gradually subsided. Three weeks following cyclophosphamide therapy, she was able to eat without vomiting and following abdominal CT showed nearly complete resolution of diffuse intestinal distension and bilateral ureterohydronephrosis. High level of awareness of IpO in SLE and appropriate medical treatment is needed to prevent unnecessary surgical treatment. And if this complication is refractory to corticosteroid, active immunosuppressive therapy, such as cyclophosphamide, should be considered.