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Biomedical subjects

P Futrakul

Publications and source records attributed to P Futrakul.

At least 19 recordsLinked to original sources
PubMed1999

Tubular function and tubulointerstitial disease.

Tubular transport determined by the fractional excretion (FE) of filtered solutes was studied in 129 nephrotic patients; 72 patients with mesangial proliferation (MesP-NS) and intact tubulointerstitium (group 1), 13 patients with MesP-NS and superimposed tubulointerstitial fibrosis (TIF; group 2), 27 patients with mild focal segmental glomerulosclerosis (FSGS; group 3), and 17 patients with severe FSGS (group 4). In the 72 nephrotic patients with MesP-NS and normal tubulointerstitium (no TIF), tubular transport was intact (FE of sodium [FENa], 0.5 +/- 0.5; FE of calcium [FECa], 0.3 +/- 0.3; FE of phosphate [FEPO4], 14 +/- 13; FE of uric acid [FEUA], 9.8 +/- 5; FE of magnesium [FEMg], 1.3 +/- 0.5). In the 13 nephrotic patients with MesP-NS and superimposed TIF (4.9% +/- 2%), there was no difference in FE solutes from those in group 1 except for FEMg (3.3 +/- 0.9; P < 0.001). In the 27 nephrotic patients with mild FSGS (TIF, 28% +/- 9%), four of five variables of FE solutes (FENa, 1.2 +/- 0.7; P < 0.001; FECa, 0.9 +/- 0.8; P < 0.001; FEPO4, 17 +/- 12; P, not significant; FEUA, 16.5 +/- 8; P < 0.001; FEMg, 4. 1 +/-1; P < 0.001) were significantly different from those of patients with MesP-NS without TIF, and two of five variables (FECa, FEMg) were statistically different from those of patients with MesP-NS with TIF. In the severe category of FSGS (TIF, 69% +/-19%), all FE solutes were statistically different from the other groups (FENa, 4.8 +/- 3; FECa, 2 +/- 1; FEPO4, 47 +/- 24; FEUA, 37 +/- 18; FEMg, 12 +/- 6). Thus, the results imply that (1) normal tubular transport reflects an underlying intact tubulointerstitial structure, whereas tubular dysfunction indicates an underlying tubulointerstitial disease, and (2) FEMg is the most sensitive index to detect an early abnormality of tubular structure and function.

Adolescent↗
PubMed1997

Glomerular endothelial dysfunction determines disease progression: a hypothesis.

A glomerular endothelial function with its hemodynamic impact is proposed to determine disease progression. In the clinical settings associated with an intact endothelial function, such as minimal-change steroid-sensitive nephrosis, the early phase of diabetes mellitus and the early stage of an experimental model of renal ablation in animals, it was observed that adequate renal perfusion correlates with the intact structure and function of the nephron with no evidence of disease progression. In contrast, the clinical settings associated with endothelial dysfunction, such as chronic glomerulonephropathy, the late stage of diabetes mellitus and a renal ablation model in animals, are usually associated with a reduction in renal perfusion. The magnitude of renal hypoperfusion observed in all forms of chronic glomerulonephropathies is proportional to the degree of clinical severity. A progressive pattern of renal hypoperfusion is uniquely observed when disease severity progresses. In this context, a new therapeutic maneuver aiming to improve renal perfusion is proposed for treating glomerulonephropathy with disease progression and preventing it from developing to end-stage renal disease.

Animals↗
PubMed1997

Renal dysfunction in glomerulonephropathy associated with rapid onset renal failure.

Eight patients between the ages of 5 and 26 years developed a rapid decline of renal function with a period of oliguria or anuria which ranged between 1 and 21 days. The initial assessment of renal function revealed a severe degree of glomerular, tubular, and vascular abnormalities. The magnitude of the renal dysfunction was quantified and expressed in terms of a clinical score. The degree of glomerular and tubular dysfunction was inversely proportional to the renal plasma flow and peritubular capillary blood flow, respectively. Similar findings have been observed in a variety of other glomerulonephropathies where a relationship exists between the reduction of peritubular capillary blood flow and the severity of the tubulointerstitial disease. Evidence to support the position that the reduction of peritubular capillary blood flow plays a primary role in inducing tubulointerstitial disease is as follows: (i) A reduction of peritubular capillary blood flow has been documented in mesangial proliferative nephrosis with steroid resistance prior to the detection of tubulointerstitial disease. (ii) Ischemic insults are capable of inducing tubulointerstitial disease in the experimental setting of renal artery occlusion in animals. (iii) As demonstrated in the present report, an improvement of tubular function can be achieved following an increase in peritubular capillary blood flow with therapy designed to enhance renal perfusion.

Acute Kidney Injury↗
PubMed1996

Renal dysfunctions in glomerulonephropathy with rapidly declined renal failure.

Eight patients aged between 5 and 26 years developed rapid deterioration of renal function and became oliguric/anuric with duration ranging from 1 to 21 days. The initial functional assessment revealed severe degree of glomerular, tubular, and vascular dysfunctions. The magnitude of renal dysfunction was quantified and expressed in terms of a clinical score. The degree of glomerular and tubular dysfunctions were inversely proportional to the renal plasma flow and peritubular capillary blood flow (PTCB), respectively. Similar findings have been observed in a variety of severe glomerulonephropathies. In this aspect, it is likely that the reduction of peritubular capillary blood flow and tubulointerstitial disease are interrelated. Further evidence to support the primary role of reduction of PTCB in inducing tubulointerstitial disease is provided by the following: (a) Reduction of PTCB is documented in mesangial proliferative nephrosis with steroid resistance prior to the detection of tubulointerstitial disease. (b) Ischemic insult can induce tubulointerstitial disease in experimental setting of renal artery occlusion in animal, (c) Improved tubular function can be achieved following the increase in PTCB with the enhanced renal perfusion therapy.

Adolescent↗
PubMed1992

Intrarenal hemodynamic abnormality in severe form of glomerulonephritis: therapeutic benefit with vasodilators.

Intrarenal hemodynamic and tubular function has been assessed in 16 patients who presented clinically with hypertension, hematuria and severe renal functional impairment. Twelve of these 16 patients had histopathologic classification as DPGN (3 cases), MPGN (3 cases) and FSGS (6 cases). The initial assessment of intrarenal hemodynamics in 11 patients revealed strikingly increased afferent (RA) and efferent arterioles (RE), filtration fraction (FF), intraglomerular capillary hydrostatic pressure (PG), whereas, there was marked reduction in renal plasma flow (RPF), in ultrafiltration coefficient (KFG) and in glomerular filtration rate (GFR). Tubular transporting defect as being reflected by enhanced fractional excretions of solutes was also observed. Both enhanced TXB2 production and diminished PGI2 may be in part responsible for the marked reduction of RPF and elevated intrarenal resistance. In light of the preceding intrarenal hemodynamics alteration, therapeutic intervention with vasodilators consisting of dipyridamole, calcium channel blocker and angiotensin convertase inhibitor has been accomplished with clinical improvement in glomerular and tubular functions following the improvement in intrarenal hemodynamics. Thus, this abnormal intrarenal hemodynamics renders a supportive view of the hemodynamically mediated glomerulo-tubulo-interstitial injury to be central to the pathogenetic mechanism.

Adolescent↗
PubMed1987

Hemodynamic response to high-dose methyl prednisolone and mannitol in severe dengue-shock patients unresponsive to fluid replacement.

Nine children; 4 males and 5 females, aged ranging from 2 1/2 to 13 years presented with signs and symptoms of poor tissue perfusion associated with dengue shock syndrome. All these 9 patients were subjected to the therapeutic trial of high dose methyl prednisolone (MP; 9/9) and mannitol (M; 6/9) after their failure to the saline and plasma replacement. Following the high dose MP and M, a significant increment in the effective circulatory blood volume as reflected by the sustained increment in CVP, widening of PP and declining in PR as well as improvement in clinical tissue perfusion were established in 7 of these nine patients so treated.

Child↗
PubMed1985

Precipitating antibodies to non-treated dengue type 2 viral antigens in sera of Thai hemorrhagic fever patients by crossed immunoelectrophoresis.

Crossed immunoelectrophoresis of dengue type 2 virus revealed at least two precipitating antigens which shared some antigenic determinants. Glycoprotein components of both antigens were detected by binding to concanavalin A. Sera from dengue hemorrhagic fever patients showed precipitating antibodies to both antigens which could be quantitated according to the precipitate patterns formed in the intermediate gel of crossed immunoelectrophoresis. All secondary dengue hemorrhagic fever patients demonstrated an increase in precipitin titers in convalescence sera. Most patients with mild illness contained precipitating antibodies in acute phase sera whereas severe cases did not. Convalescent sera from severe cases showed only low titers. These precipitating antibodies may be associated with protection since they were produced early only in those with mild form of illness.

Adolescent↗
PubMed1984

Clinical features of neurotoxic snake bite and response to antivenom in 47 children.

Among 47 children admitted to the Chulalongkorn Medical School Hospital for neurotoxic snake bite, the attackers were identified in 15; the cobra (Naja naja) was the snake involved in all cases. Clinical manifestations in all 47 children appeared to follow a similar pattern. Drowsiness heralded the systemic effects in most of the patients. The characteristic systemic signs were those resulting from the neuromuscular effects of the venom and included ptosis, frothy saliva, slurred speech, respiratory failure, and paralysis of the skeletal muscles. These episodes occurred within 8 hours in 94% of the cases, and at the latest 19 hours following the bite. In some cases unconsciousness accompanied respiratory failure. Necrosis in the region of the bite, the prominent local sign, developed in 40% of the cases at the end of the 1st week after the bite. Infusion of specific antivenom was an effective therapeutic measure for the neuromuscular changes. Respiratory assistance was mandatory in cases of respiratory failure. Edrophonium chloride demonstrated a supportive role as a countermeasure against the neuromuscular effects.

Antivenins↗
PubMed1983

Crossed immunoelectrophoresis for the detection of split products of the third complement in dengue hemorrhagic fever. I. Observations in patients' plasma.

Crossed immunoelectrophoresis was applied to detect the products of the third component of complement (C3) activation in plasma of patients suffering from dengue hemorrhagic fever (DHF), using inulin-treated normal human sera as positive control. In DHF, C3 split products were demonstrated in severely ill patients classified as having Grade III and Grade IV disease. These split products rapidly disappeared during the convalescent phase. The appearance of C3 activation products in DHF correlated well with signs of shock. This electropherogram of C3 activation could be used as a parameter reflecting immunologic activity in dengue hemorrhagic fever.

Adolescent↗