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S Eiam-Ong

Publications and source records attributed to S Eiam-Ong.

At least 19 recordsLinked to original sources
PubMed2006

Measurement of urinary chemokine and growth factor messenger RNAs: a noninvasive monitoring in lupus nephritis.

Noninvasive molecular tests of urine cells have been developed to monitor the activity of kidney diseases. We evaluate whether measurement of urinary messenger RNA (mRNA) levels of chemokine and growth factor genes could distinguish between diffuse proliferative lupus nephritis (class IV LN) and others and whether it is able to predict the response to therapy. Prebiopsy urine samples were collected from 26 LN patients. Urine specimens were serially collected over a period of 6 months from class IV LN patients who were receiving standard immunosuppressive treatments. Urinary interferon-producing protein 10 and its CXC chemokine receptor (CXCR)3, transforming growth factor-beta (TGF-beta), and vascular endothelial growth factor (VEGF) mRNA levels were analyzed by quantitative real-time polymerase chain reactions. Levels of chemokine or growth factor mRNAs in urine could distinguish class IV LN from others, with a sensitivity of 85% and a specificity of 94%. The receiver-operative characteristic curve demonstrated that urine mRNA levels of these genes could identify active class IV LN with an accuracy greater than the current available clinical markers, namely systemic lupus erythematosus (SLE) disease activity index, proteinuria, renal function, or urinalysis. A significant reduction of interferon-producing protein 10 (IP-10), CXCR3, TGF-beta, and VEGF mRNA levels from baselines was observed in patients who responded to therapy, whereas the levels tended to increase in those who resisted to treatment. Measurement of urinary chemokine and growth factor mRNAs can precisely distinguish class IV LN from others. Temporal association between these markers and therapeutic response is demonstrated. This noninvasive approach serves as a practical tool in diagnosis and management of LN.

Adult↗
PubMed2004

Monitoring of T-cell subsets in patients treated with anti-CD 25 antibody.

Daclizumab and basiliximab, the antibodies to the interleukin-2 receptor (anti-IL-2R), decrease the incidence of acute rejection in renal transplantation. However, prolonged blockade of IL-2 receptor (IL-2R:CD25) may hamper apoptosis of reactive T-cell clones and thus may obstruct tolerance induction. We determined the effect of varying doses of anti-IL-2R on the number of CD3+CD25+ cells as an index of CD 25 blockade. The number of CD3+CD25+ cells was determined in four groups of induction therapies: no antibody induction; two doses of 50 or 25 mg daclizumab on day 0 and day 14; and two doses of 20 mg basiliximab at day 0 and day 4 (n=10, 24, 10, and 10, respectively). The number of CD3+CD25+ cells were monitored in whole blood before antibody infusion as well as 24 hours thereafter and weekly after transplantation. With two doses of 50 mg daclizumab, two doses of 25 mg daclizumab, and two doses of 20 mg basiliximab, the expression of CD3+CD25+ cells was completely suppressed for 12, 10, and 12 weeks posttransplantation, respectively. The reappearance of CD3+CD25+ cells above the baseline for each induction regimen was: 17 weeks for two doses of 50 mg daclizumab, 11 weeks for two doses of 25 mg daclizumab, and 13 weeks for two doses of 20 mg basiliximab. Monitoring of CD3+CD25+ cells may be utilized to tailor anti-IL-2R administration at a minimal dosage, yet retaining adequate IL-2R blockade for at least 3 months posttransplantation.

Adult↗
PubMed2004

Convective-controlled double high flux hemodiafiltration: a novel blood purification modality.

Convective-controlled double high flux hemodiafiltration (CC-DHF) was set-up using two high flux dialyzers. The convection occurred in the first while the fluid replacement took place in the second dialyzer. The system of CC-DHF basically resembled that of hemodiafiltration. CC-DHF was performed in 9 chronic hemodialysis Thai patients who had been treated with high flux hemodialysis for at least 6 months. When compared with high flux hemodialysis, CC-DHF could provide higher Kt/Vurea (2.4+/-0.4 vs. 2.0+/-0.4, p<0.05) and beta2-microglobulin clearance (106.2+/-15.4 vs. 48.9+/-6.1 ml/min, p<0.01). Following 6-month therapy of CC-HDF, the predialysis beta2-microglobulin levels were reduced by 12.7% while the values of Kt/Vurea were consistently higher than 2.7. The quality of life consistently improved during the 6 months of CC-DHF treatment. There were no differences in clinical and technical complications between CC-DHF and high flux hemodialysis. In conclusion, CC-DHF could provide performance comparable to hemodiafiltration without the need for expensive hemodiafiltration machines.

Hemodiafiltration↗
PubMed2001

Exchange transfusion in severe falciparum malaria: a simple method modified from hemodialysis circuit.

We set up a simple extracorporeal circuit, modified from the extracorporeal method generally used in conventional hemodialysis, for exchange transfusion. Temporary vascular access was used in exchange transfusion for both draining the infected blood and infusion of the freshly non-infected blood. This method of exchange transfusion was performed in 3 severe complicated falciparum malaria patients who had a percentage of parasitemia of 80, 40, and 35. The magnitude of parasitemia decreased immediately to less than one per cent and this value persisted twenty-four hours after the procedure. No complications of exchange transfusion were detected in all patients. Erythrocyte morphology determined by scanning electron microscopy was unaltered by exchange transfusion. Because of the simplicity, the effectiveness, and the safety of the procedure, this extracorporeal circuit modified from hemodialysis circuit would be a more beneficial exchange transfusion method in the treatment of severe complicated falciparum malaria than the manually-performed one.

Adult↗
PubMed2001

Life-long food restriction prevents renal membrane lipid deposition and lowers renal work in rats.

Renal cortical brush-border (BBM), basolateral membrane (BLM), and medullary plasma membrane (mPM) preparations were analyzed to assess the effects of life-long food restriction in aged rats on membrane lipid content. Young male Fischer 344 x Brown-Norway F1 rats consumed food ad libitum (young AL) or were food-restricted (FR, 60% of AL consumption) for either 6 weeks (young FR) or until the age of 30 months old (old FR). Senescent FR rats had 50 per cent decreases in fractional excretion of Na and K (p < 0.001) as compared with the young AL rats. Long-term FR reduced phosphate and titratable acid excretion by 80 per cent (p < 0.001). These values were not significantly different from those observed in young rats during 6 weeks of FR. Food restriction decreased renal Na, K-ATPase activity by 50 per cent (p < 0.001) in both old and young FR animals. Reduction of food intake, in old and young rats, decreased all BBM phospholipid concentrations (phosphatidylserine, phosphatidylcholine, phosphatidylethanolamine, and sphingomyelin) by 50 per cent than in the AL rats (p < 0.001). In BLM, chronic FR resulted only in lower phosphatidylcholine concentration (by 21%, p < 0.05) while phosphatidylethanolamine was increased approximately 80 per cent (p < 0.001). Total phospholipid content in mPM was progressively decreased by 23 per cent (p < 0.05) in the young FR group to be 55 per cent (p < 0.001) in the old FR rats. Cholesterol content was reduced in BBM and mPM by 38 per cent and 25 per cent (p < 0.05), respectively, during long-term FR. Both total phospholipid and cholesterol contents detected in mPM of the old FR rats were significantly lower than those obtained from the young FR animals (by 42%, p < 0.001 and 12%, p < 0.05, respectively). Plasma glucose, blood urea nitrogen, and body weight maintained at significantly lower levels during chronic FR. That life-long FR could prevent renal membrane lipid deposition and could lower renal work may explain the mechanisms that FR can delay the onset and diminish the severity of age-associated renal diseases.

Aging↗
PubMed2001

Necrotizing ileitis caused by cytomegalovirus in patient with systemic lupus erythematosus: case report.

We report a systemic lupus erythematosus (SLE) patient with necrotizing ileitis diagnosed at a tertially care centre in Thailand. The patient was surgically explored because peritonitis was suspected and segmental gangrenous and perforation of the terminal iliem were found. The pathological finding was necrotizing ileitis with appearance of cytomegalic intranuclear inclusion body. The presence of cytomegalovirus (CMV) infection in tissue was confirmed by CMV-DNA detection using polymerase chain reaction and ELISA probe hybridization method. The hemoculture and peritoneal fluid culture results revealed no pathogenic organisms. Postoperatively, the clinical course of the patient deteriorated and she developed hypotension. Vasopressive drugs were administered without clinical improvement. She expired on day 5 postoperation. Regarding CMV infection, the organism involves the small bowel in only 4.3 per cent of all CMV infections of the gastrointestinal tract. Isolated cases of ileal perforation due to CMV infection have never been reported in a SLE patient. Thus, chronic right lower abdominal pain, fever with or without diarrhea in immunocompromised patients should cause clinicians to consider CMV ileitis in the differential diagnosis. Immediate surgical resection and prompt antiviral therapy lead to successful treatment.

Cytomegalovirus↗
PubMed2000

Pharmacokinetic studies of cyclosporin in Thai kidney transplantation patients.

Pharmacokinetic studies were performed in 10 Thai patients with kidney transplantation who received microemulsion formulation (Neoral) of cyclosporin A (CsA) twice daily. No agents having pharmacokinetic effect on CsA had been used in these patients. The mean values of 12-h AUC (area under the concentration-blood curve) were 4603.63 +/- 344.61 ng x h/ml. CsA concentrations at 2 hours after dosing had the best value of correlation coefficient with the 12-h AUC. Abbreviated AUC could be calculated by stepwise multiple linear regression analysis and linear trapezoidal rule. The latter is more simple and superior to the former one.

Adult↗
PubMed1999

Environmental distal renal tubular acidosis in Thailand: an enigma.

Distal renal tubular acidosis is a common health problem in northeastern Thailand, with the population background of the low potassium intake, low urine citrate, and decreased red blood cell Na-K adenosine triphosphatase (ATPase) activity and the environment of the high soil vanadium. The disease is usually seen in the people with low socioeconomic status in summer. The patients have decreased gastric acidity and low urine potassium. There are varying degrees of renal function from normal to impairment. Gastric hypoacidity is an important clue. Defects in H-K ATPase and anion exchange (AE2) mechanism are considered. The urine vanadium is higher in the patients than that of normal rural northeastern villagers. Inhibition of H-K ATPase by vanadium seems possible and requires more supporting evidence. AE1 gene mutation is noted in few patients. The cause of dRTA is not apparent. The AE2 gene and H-K ATPase gene remain to be studied. Both environmental and genetic factors could contribute to the pathogenesis of the disease.

Acidosis, Renal Tubular↗
PubMed1999

Potassium depletion: renal membrane lipid metabolism and Na/H exchanger abundance in aged F344 x BNF1 rats.

Potassium depletion (-K) is a common electrolyte abnormality in elderly humans, occurring after diuretic use or poor oral intake. We hypothesized that aging would result in an increase in renal membrane lipid metabolism in both control and -K, and that the Na/H exchanger's protein abundance to -K would be blunted. Young and senescent non-obese male Fisher 344 x Brown-Norway F1 rats (F344 x BNF1) were fed either a normal or a K-deficient diet for 7 days. At 24-h, 32P incorporation was measured for renal cortical brush-border (BBM) and basolateral membrane (BLM) lipid metabolism. All -K animals showed a reduction in total body potassium stores, a fall in plasma aldosterone, a urinary concentrating defect, and an increase in plasma cholesterol and urine ammonium excretion (p < .001). In BBM of both age groups, -K increased phosphatidylserine, sphingomyelin, phosphatidylcholine, and phosphatidylethanolamine concentrations, but 32P incorporation fell. In BLM of young K-depleted rats, however, only phosphatidylcholine concentration increased. In the hypokalemic aged rats, the concentration of all BLM phospholipids rose, whereas 32P incorporation fell. In both membranes, cholesterol concentration and the molar ratio of cholesterol to total phospholipid increased with -K (p < .05). Potassium depletion caused brush-border membrane NHE-3 protein abundance to rise, but only in the young rats. Neither NHE-3 nor basolateral NHE-1 protein abundance was affected in aged animals with -K. These results provide the first evidence, in non-obese aged rats, that selective age-associated modifications occur in membrane lipid metabolism and membrane transporter protein abundance during -K. That aging causes a maladaptive response in brush-border NHE-3 protein expression may have important implications for elderly humans, particularly if they are given diuretics and become potassium depleted.

Aging↗
PubMed1999

Food restriction beneficially affects renal transport and cortical membrane lipid content in rats.

Food restriction (FR) exerts a variety of beneficial effects and may prolong life in both humans and animals. However, studies of its effects on the cortical brush border membrane (BBM) and basolateral membrane (BLM) lipid concentration, which may be pertinent to renal function, have not been reported in detail. We hypothesized that FR would decrease renal work and lower renal membrane lipid concentration. The changes in lipid concentration would be most dramatic in BBM because this membrane is the entry site for the recovery of filtered ions and nutrients. Young male Fischer 344 x Brown-Norway F1 rats consumed food ad libitum (AL) or were food-restricted (FR, 60% of AL consumption) for 6 wk. AL rats had higher fractional excretions of Na(+), K(+), and Cl(-) than did the FR group (P < 0.001). Renal Na,K-ATPase activity in AL rats was 100% higher than in FR rats (P < 0.001), reflecting greater renal work. The work required for renal proton secretion was lower in FR than in the AL rats. In FR rats, all BBM phospholipid concentrations (phosphatidylserine, phosphatidylcholine, phosphatidylethanolamine, and sphingomyelin) were approximately 50% lower than in the AL rats (P < 0.001). In the BLM, food restriction resulted only in lower phosphatidylcholine concentration, while the other phospholipids were unaffected. Plasma and renal membrane (BBM and BLM) cholesterol concentrations were significantly lower in FR than in AL rats. These results show that a nutritionally complete, but energy restricted, diet improves renal function. It also prevents renal membrane lipid deposition and decreases plasma cholesterol. Prolonged food restriction might attenuate the renal injury that occurs in obese humans as a consequence of insulin resistance and atherosclerosis.

Animals↗
PubMed1998

Falciparum malaria and the kidney: a model of inflammation.

Renal and renal-related disorders commonly occur in infection with Plasmodium falciparum, which can cause fluid and electrolyte disorders, glomerulonephritis, and acute renal failure (ARF). It appears that ARF and other life-threatening complications in falciparum malaria are not directly caused by the parasite itself but are the result of interaction of mechanical, immunologic, and humoral components. P. falciparum-infected erythrocytes impair microcirculation and cause hemolysis. Glycosylphosphatidylinositol moieties covalently linked to the surface antigens of falciparum malarial parasites appear to act like endotoxin. Glycosylphosphatidylinositol, via CD14, which is a receptor on monocytes, stimulates monocytes to release tumor necrosis factor, which in turn enhances synthesis of various cytokine cascades and mediators. Besides contributing to ARF, these mediators also cause changes in blood volume status. The degree of vasodilatation caused by vasodilating mediators varies with the severity of infection. Increased vascular permeability by the mediators occurs in severe infection, which results in hypovolemia and contributes to ARF. Although the cornerstone of treatment of malaria still is antimalarial drugs, several new modalities of treatment targeting toxin, signal transduction, mediators, and cytokines have great potential.

Acute Kidney Injury↗
PubMed1996

Studies on the mechanism of trimethoprim-induced hyperkalemia.

We examined the effects of trimethoprim (TMP) on metabolic parameters and renal ATPases in rats after a 90 minute infusion (9.6 mg/hr/kg body wt, i.v.) and after 14 days (20 mg/kg body wt/day, i.p.). After one dose of TMP, plasma electrolytes, arterial pH and aldosterone levels were normal, but a natriuresis, bicarbonaturia, and decreased urinary potassium excretion occurred. Na-K-ATPase activity in microdissected segments from these animals was decreased by 36 +/- 0.9% in proximal convoluted tubule (PCT) (P < 0.005); decreases of 50 +/- 2.1% and 40 +/- 1.1% were seen in cortical and medullary collecting tubules (CCT and MCT), respectively (P < 0.005). Na-K-ATPase activity was unaffected in medullary thick ascending limb (MTAL). H-ATPase (in PCT and collecting duct) and H-K-ATPase (in CCT and MCT)-activities were not changed. Following chronic TMP administration, plasma potassium increased as compared to control (5.16 +/- 0.05 mEq/liter vs. 3.97 +/- 0.05 mEq/liter, P < 0.05), however, acid-base status and plasma aldosterone levels were normal. Na-K-ATPase activity was decreased by 45 +/- 2.6% in PCT (P < 0.005), 73 +/- 2.0% in CCT (P < 0.001), and 53 +/- 2.5% in MCT (P < 0.005). Na-K-ATPase, activity in MTAL and H-K-ATPase activity in CCT and MCT were unchanged. H-ATPase activity in PCT and MTAL was normal, but in the collecting tubule (CCT and MCT) it was decreased by approximately 25% (P < 0.05). TMP inhibited Na-K-ATPase activity in a dose-dependent fashion in PCT, CCT, and MCT when tubules from normal animals were incubated in vitro with the drug; TMP in vitro did not affect H-ATPase or H-K-ATPase activity. These results suggest that TMP-induced hyperkalemia may result from decreased urinary potassium excretion caused by inhibition of distal Na-K-ATPase, in the face of intact H-K-ATPase activity.

Adenosine Triphosphatases↗
PubMed1996

Biochemical mechanisms and regulation of hydrogen transport in renal tubules.

In normal humans, blood pH and bicarbonate concentration are maintained within a very narrow range despite wide variations in dietary intake. The mechanisms involved in the chronic regulation of acid-base homeostasis relate to the kidney in general, and specifically to changes in membrane-bound ATPases and exchangers. This review summarizes some of the data regarding the Na/H exchanger, the H-ATPase and its interaction with Na,K-ATPase and the Ca-ATPase and Ca/H exchanger in renal tissue. While there remain gaps in our knowledge, the significant advances in molecular biology along with the development of selective ligands and dyes for localization have allowed an important picture to emerge regarding transport in the kidney. These data, when integrated with biochemical information and clinical observation, provide a clearer understanding of physiology and the pathophysiology of disease. Some information, particularly involving the Ca-ATPase and Ca/H exchanger, comes primarily from other tissues; however, these important observations provide a framework which adds to our body of work in the kidney.

Acid-Base Imbalance↗
PubMed1996

Hepatitis virus and kidney.

Hepatitis A, B and C viruses are major causes of viral hepatitis in human. These infectious agents not only damage liver parenchyma but can also affect renal parenchyma. Hepatitis A virus could produce acute renal failure in a similar fashion to hepatorenal syndrome. Several lines of evidence have shown that chronic hepatitis B virus-infected patients could develop immune complex glomerulopathy. There are convincing data which incriminate hepatitis C virus as the proximate aetiology of certain forms of glomerulonephritis. In post-renal transplanted patients, hepatitis B and C virus could cause increased morbidity and mortality from chronic viral hepatitis. Whether renal transplantation should be performed, either as a donor or as a recipient, in subjects infected with hepatitis B or C virus, is still an issue of controversy.

Hepatitis A↗
PubMed1995

Diseases of renal adenosine triphosphatase.

Most renal transport is a primary or secondary result of the action of one of three membrane bound ion translocating ATPase pumps. The proximal tubule mechanisms for the reabsorption of salt, volume, organic compounds, phosphate, and most bicarbonate reabsorption depend upon the generation and maintenance of a low intracellular sodium concentration by the basolateral membrane Na-K-ATPase pump. The reabsorption of fluid and salt in the loop of Henle is similarly dependent on the energy provided by Na-K-ATPase activity. Some proximal tubule bicarbonate reabsorption and all distal nephron proton excretion is a product of one of two proton translocating ATPase pumps, either an electrogenic H-ATPase or an electroneutral H-K-ATPase. In this article, the authors review the biochemistry and physiology of pump activity and consider the pathophysiology of proximal and distal renal tubular acidosis, the Fanconi syndrome, and Bartter's syndrome as disorders of ATPase pump function.

Acidosis, Renal Tubular↗
PubMed1993

Effect of furosemide-induced hypokalemic metabolic alkalosis on renal transport enzymes.

Hypokalemic metabolic alkalosis is one of the most common complications of chronic furosemide administration. In this study we examined acid-base composition and ATPase enzyme activities in medullary thick ascending limb of Henle's loop (MTAL) and collecting tubule (CCT and MCT) after seven days of chronic furosemide therapy. All of the studies were conducted in adrenal intact (AI) rats or in adrenalectomized (ADX) glucocorticoid replete rats replaced with a physiological dose of aldosterone (Aldo). Furosemide (F) was administered to each rat by mini-osmotic pump. In the AI+F group, plasma Aldo was high and obvious metabolic alkalosis occurred (HCO3- = 37 +/- 2 mEq/liter vs. 22 +/- 2 mEq/liter in controls, P < 0.005); activities of H-K-ATPase, H-ATPase, and Na-K-ATPase were increased approximately twofold in both CCT and MCT. In the ADX+F group (HCO3- = 28 +/- 2 mEq/liter, P < 0.05 from control), H-ATPase activity was normal in CCT and it was slightly increased in MCT. CCT and MCT H-K-ATPase activities were markedly increased (approximately twofold). Na-K-ATPase activity was the same as control in CCT but it was increased in MCT. In ADX+F+Vanadate (V) group which also had normal Aldo levels, acid-base changes were modest (20 +/- 2 mEq/liter, NS from control); in CCT and MCT H-K-ATPase and Na-K-ATPase activities were markedly reduced, but H-ATPase activity in MCT was increased. In all three experimental groups Na-K-ATPase activity in MTAL was reduced fivefold. Hypokalemia developed in both intact and ADX animals receiving furosemide.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗