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Objective: The objective of this study was to examine the effects of angiotensin II receptor blocker (ARB), used as an antihypertensive medication, on peritoneal membrane transporters in continuous ambulatory peritoneal dialysis (CAPD) patients., Material and Method: Prospective and cross-over experimental study of peritoneal membrane transporters was conducted in 7 CAPD patients with hypertension. All previous antihypertensive drugs had been replaced by candesartan at the dose of 8-16 mg/day to control blood pressure below 140/90 mmHg. Hydralazine, which has no effect on peritoneal membrane transports, was added if the target blood pressure was not achieved. All patients had received candesartan for 12 weeks, then, were retreated with the previous antihypertensive drugs for another 6-week period. The modified peritoneal function tests assessing peritoneal membrane transports were performed at 1) baseline, 2) 6 weeks, 3) 12 weeks following candesartan treatment, and 4) 6 weeks after candesartan withdrawal., Results: The blood pressure target was achieved in all patients and was not different among the 4 periods. The albumin clearance and 4-hour albumin loss were significantly decreased following candesartan treatment (p < 0.05). Both values returned to the high baseline levels after 6 weeks of candesartan withdrawal. There were no significant changes in net ultrafiltration and various small and large solute transports. No adverse effects, including hyperkalemia or increased erythropoietin dosage, had been observed., Conclusion: In hypertensive CAPD patients, candesartan could provide nutritional benefit by attenuating peritoneal loss of albumin and provides an effective antihypertensive action. Furthermore, candesartan does not impair other solute transports and net ultrafiltration.

Objectives: To determine the interval of intravenous iron administration during maintenance iron therapy in erythropoietin-treated hemodialysis patients., Material and Method: The method of maintenance intravenous iron therapy has been studied in 20 stable erythropoietin-treated hemodialysis patients who have iron deficiency anemia diagnosed by transferring saturation (TSAT) below 20%., Results: After receiving 1000 mg of intravenous iron as the first loading dose, the TSAT was increased from 16.4 +/- 0.5 to 29.3 +/- 2.6% (p < 0.05). After 155.6 +/- 7.3 days, such values was reduced to 16.3 +/- 1.4% (p < 0.05). The second loading dose was administered and could raise the TSAT to 33.7 +/- 3.9% (p < 0.05). The patients, then, received 100 mg of intravenous iron for every 15.6 +/- 2.9 days, one-tenth of the duration between the two loading doses. The values of TSAT at 1, 2, 3, 4, 5 and 6 months after the second loading dose were 38.5 +/- 2.4, 37.1 +/- 0.2, 34.2 +/- 3.6, 34.1 +/- 3.3, 35.3 +/- 4.1, and 36.5 +/- 3.1% (NS)., Conclusion: As such, in erythropoietin-treated hemodialysis patients, after loading with 1000 mg, prescription of 100 mg of intravenous iron for every 2 weeks could maintain the TSAT levels above 20%.

Objective: To determine whether 4-hour urine protein value correlates with 24-hour urine protein value in women with hypertensive disorders in pregnancy., Study Design: Cross-sectional study was performed in 38 in-patient pregnant women who were initially diagnosed as having hypertensive disorders in pregnancy. Urine samples were collected within 24 hours in 2 successive periods: the first 4-hour and the next 20-hour urine, in separate containers. The urine volume, urine protein and creatinine concentrations were thus separately measured. The 4- and 24-hour urine proteins were calculated and the correlation between both groups was determined by simple linear regression analysis., Results: A total of 38 patients were recruited into the study, 26 had mild preeclampsia, 5 had severe preeclampsia, and 7 had superimposed preeclampsia. The result of the 4-hour urine protein was found to correlate with those of the 24-hour urine protein for patients with hypertensive disorders in pregnancy (p < 0.001)., Conclusion: Total protein values of 4-hour samples positively correlated with values of 24-hour samples of patients with hypertensive disorders in pregnancy. This might be modified and used for urine protein collection in outpatients to improve the compliance.

Sudden Unexplained Death Syndrome (SUDS) is a major health problem in rural residents of Northeast Thailand. The cause of death in SUDS is suspected to be cardiovascular abnormalities. As magnesium (Mg) and zinc (Zn) deficiency contribute significantly to several cardiovascular diseases, we investigated the Mg- and Zn-status of patients with sudden respiratory distress and cardiac arrest who had survived resuscitation attempts or a near-SUDS episode (N-SUDS). The following subjects were enrolled: 12 N-SUDS inhabitants of rural Northeast Thailand (rural group 1, R1), 13 rural villagers with no past history of N-SUDS (rural group 2, R2), 15 urban Northeasterners (urban group 1, U1); 13 Bangkokians (urban group 2, U2). All subjects were free of structural heart disease. Magnesium and zinc were assessed by atomic absorption spectrophotometry of samples of plasma, red blood cells (RBC), white blood cells (WBC), and 24-hour urine. The mean levels of magnesium in the RBC, WBC, and 24-hour urine of N-SUDS patients (R1) were significantly lower than those of the urban groups (U1 and U2), while the plasma levels did not show any differences. When comparing the Zn-status of R1 with that of the urban groups (U1 and U2), the plasma, RBC, and WBC levels were found to be significantly lower in R1 (except for the RBC-Zn of the U1 group), while the 24-hour urine levels was higher. Although the magnesium and zinc parameters were not significantly different between the rural groups R1 and R2, the prevalence of hypomagnesuria (<2.2 mmol/day), hypozincemia (<9.7 micromol/l), and hyperzincuria (>10.7 micromol/day) was higher in the R1 group. These findings suggest that the homeostasis of both magnesium and zinc is altered in N-SUDS patients. Similar alterations, to a lesser degree, were observed in those people living in the same rural environment (R2).

Healthy northeastern Thais have a higher erythrocyte sodium concentration and a lower erythrocyte membrane Na,K-adenosine triphosphatase (ATPase) activity than central Thais. To elucidate whether the defect is hereditary or acquired, we studied plasma sodium and potassium and erythrocyte sodium, potassium, Na,K-ATPase activity, and ouabain-binding sites (OBS) in the following groups: healthy newborns of ethnic central Thais (group 1), healthy newborns of ethnic northeast Thais (group 2), healthy adults of central Thailand ethnicity who lived in the rural central region (group 3) or in Bangkok (group 4), healthy adults of northeast Thailand ethnicity who lived in the rural northeast region (group 5) or who migrated to work in Bangkok for at least 1 year (group 6). Erythrocyte Na was higher in group 2 than in group 1. Group 3 had lower erythrocyte Na,K-ATPase activity than group 4, and it was lower in group 5 than in group 6. Among all groups, group 5 had the highest erythrocyte Na (11.6 mmol/L,F < 0.0001) and the lowest Na,K-ATPase activity (63 mmol Pi/mg x h, F < 0.0001) and erythrocyte OBS (397 sites per cell, F < 0.05) than the other adult groups. There was a positive correlation between erythrocyte Na,K-ATPase and erythrocyte OBS (r = .416, P < .0001). Multiple regression analysis demonstrated a correlation between erythrocyte Na as a dependent variable and erythrocyte OBS, plasma potassium, erythrocyte potassium, and erythrocyte Na,K-ATPase (r = .517, P < .0001). The erythrocyte Na,K-ATPase/OBS ratio, an expression of Na,K-ATPase activity equalized for the number of Na,K-pump units, was lowest among rural adults of the central region (group 3) and the northeast region (group 5) (F < 0.0002). Our data suggest that rural dwellers in Thailand tend to have lower erythrocyte Na,K-ATPase activity than urban dwellers and that this is probably acquired after birth. It was more severe among those from the northeast versus the central region, and was less severe among those who migrated to an urban area. This defect in northeast rural dwellers was probably associated with low numbers of Na,K-pump units and a defect of the pump to express activity, whereas in central rural dwellers it was probably associated with the latter condition. We postulate that there might be circulating Na,K-pump inhibitors and metabolic disturbances that cause attenuation of Na,K-ATPase function and synthesis in the northeast Thailand rural population, and that such substances may have an environmental origin. There may be a relationship between these abnormalities and sudden unexpected deaths.

A Thai female patient developed muscular weakness, hypouricemia, hypokalemia and hyperchloremic metabolic acidosis after taking outdated tetracycline. A pathophysiologic study shows a proximal tubular defect for reabsorption of urate and bicarbonate and a distal tubular acidification defect, probably caused by outdated tetracycline.

We studied the cellular membrane enzyme responsible for potassium transport in different Thai populations. We measured plasma and intraerythrocytic concentrations of sodium and potassium, activities of erythrocytic membrane Na, K-activated adenosine triphosphatase (Na, K-ATPase), ouabain-insensitive ATPase, total ATPase and the activity ratio of Na, K-ATPase/total ATPase in 25 healthy blood donors at Khon Kaen University Hospital, Khon Kaen (group 1), and in 32 donors at the National Blood Center, Thai Red Cross Society, Bangkok (group 2). Group 1 subjects had significantly higher concentrations of erythrocyte sodium (p < 0.001) and lower activity of Na, K-ATPase (p < 0.001) than group 2. When data of these 2 groups were combined, erythrocyte Na+ correlated inversely with Na, K-ATPase and the activity ratio of Na, K-ATPase/total ATPase. Our study suggests that there is a defect in membrane transport enzymes for sodium/potassium in certain northeast Thai populations.

1H-NMR spectra of 60 human urine specimens were recorded without pretreatment by a JEOL FX 90 Q spectrometer operating at 89.55 MHz. The signals of the methyl protons of creatinine (3.04 +/- 0.02 ppm) were observed in all spot fasting morning urine samples collected from 7 healthy persons, 10 patients with nephrotic syndrome and 43 patients with diabetes mellitus. The concentrations of creatinine measured by NMR spectroscopy (Y) and the chemical assay based on the Jaffe reaction (X), over the range of 19-190 mg/dl, were compared by the least-squares linear regression analysis (Y = 6.7799 + 0.6717 X). The mean urinary creatinine concentration by NMR spectroscopy appeared to be lower than that obtained by the Jaffe reaction at the normal and high normal levels. In the urine of 20 diabetic patients with an average blood glucose of 251.30 +/- 50.26 (SD) mg/dl typical spectra of the multiple large signals of glucose protons at position from 3.13 +/- 0.04 to 4.04 +/- 0.12 (SD) ppm were shown. Moreover, some urinary metabolites and amino acids spectra were occasionally detected at one time.