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Biomedical subjects

B S Hsieh

Publications and source records attributed to B S Hsieh.

At least 55 records · Page 3Linked to original sources
PubMed1991

Urinary kallikrein excretion in chronic renal disease with respect to salt intake and renal reserve.

In order to investigate the status of urinary kallikrein excretion (UKE) in various chronic renal diseases, we measured the UKE in 56 patients with chronic renal diseases. They ranged in age from 19 to 80 with 26 males and 30 females. Among them were 31 patients with primary glomerulonephritis (GN) without nephrotic syndrome, 8 with nephrotic syndrome, 10 with various renal diseases in the azotemic stage, 3 in the uremic stage and 4 with type I renal tubular acidosis (RTA) due to Sjögren syndrome. The primary GN patients who were on a low salt diet were classified as group II GN, while those who partook freely of salt were classified as group I GN. Thirty-six normal volunteers were enrolled as controls. Kallikrein activity was determined by enzymatic hydrolysis of synthetic chromogenic substrate S-2266. Urinary electrolytes were measured by flame photometry. The results showed that UKE was lower in patients with group I GN, azotemic or uremic patients and in patients with RTA, as compared with normal controls. If UKE was corrected by creatinine clearance (CCr), the UKE/CCr ratio was still lower in group I GN patients, but became higher in patients with azotemia and uremia. The UKE/CCr ratio was not different from that of controls or patients with RTA. In nephrotic patients, the UKE and UKE/CCr ratio were both higher than that for normal controls. However, in group II GN patients, neither UKE nor the UKE/CCr ratio differed from that of controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Plasma renin and kallikrein in parturient women and newborn babies.

There are changes in both the plasma renin system and plasma kallikrein system during parturition. To investigate the interrelationship between plasma inactive renin and plasma kallikrein, we measured plasma active renin, inactive renin, active kallikrein and inactive kallikrein in 21 parturient women just before delivery and on the 5th day after delivery, and also in 30 newborn babies upon birth and on the 5th day after birth. Plasma active renin was measured by radioimmunoassay of angiotensin I generated after the addition of an exogenous substrate. Inactive renin was activated by trypsin. Active kallikrein was measured by kallikrein activity on substrate S-2302. Inactive kallikrein was activated by an activator containing the Hageman factor and kininogen. The results showed a significant decrease in active renin, inactive renin, and a significant increase in active kallikrein, inactive kallikrein and the active/total kallikrein ratio in mothers on the 5th day after delivery. In vaginally delivered babies, a decrease in active renin and in the active/total renin ratio were observed on the 5th day after birth, but inactive renin, active and inactive kallikrein showed no change. In babies delivered by cesarean section, no change in either the renin or kallikrein level was found. The patterns of change in plasma active renin and inactive renin in mothers and babies are in keeping with previous suggestions that plasma inactive renin is prorenin. There was no correlation between the plasma active/total renin ratio or the plasma active kallikrein level in mothers and babies, either before or after delivery.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Comparison between spot urine and overnight urine in the estimation of 24-hour excretion of urine protein, sodium and kallikrein.

To compare the value of spot urine and overnight 9-hour urine in the estimation of 24-hour urinary sodium excretion (UNaV), protein excretion (UpV) and kallikrein excretion (UKaV), we measured the concentration of sodium, protein, kallikrein and creatinine in spot urine, overnight 9-hour urine, and 24-hour urine samples obtained from 21 patients with various renal diseases. They ranged in age from 16 to 75 years with 10 males and 11 females. Urinary protein was measured by the Coomassie Blue dye-binding method. Urinary kallikrein activity was measured by assay of its amidase activity on synthetic substrate S-2266. The results showed that the 9-hour UpV and 9-hour urine P/Cr ratio was better correlated with the 24-hour UpV than the spot urine P/Cr ratio (at 9-11 AM), and the 9-hour UKaV and spot urine Ka/Cr ratio were better correlated with the 24-hour UKaV than the 9-hour Ka/Cr ratio. Only the 9-hour UNaV was correlated with the 24-hour UNaV. We conclude that overnight 9-hour urine, in view of its lower cost, equal effectiveness and convenience, is the best method to substitute for 24-hour urine collection in the evaluation of Na, P and Ka excretion in patients with renal diseases.

Adolescent↗
PubMed1991

Changes in plasma active and inactive renin and prekallikrein during hemodialysis.

To investigate the physiologic role of plasma inactive renin and its relationship to plasma kallikrein, we measured the changes in plasma active renin, inactive renin and prekallikrein levels in 14 uremic patients before and after hemodialysis. Blood was collected before, during and after hemodialysis, and prior to the next dialysis session. Plasma active renin was measured by radioimmunoassay of generated angiotensin I after addition of an exogenous substrate. Plasma inactive renin was activated by trypsin. Plasma prekallikrein was measured by the kallikrein-like activity on synthetic substrate S-2302 after activation of prekallikrein. The results showed that there was no change in blood pressure before, during or after dialysis, whereas the change in body weight after dialysis was significant. There was also no significant difference in the plasma active renin, inactive renin and prekallikrein levels for any of the collection periods. Plasma active renin was significantly correlated with inactive renin. The correlation between the active renin/total renin ratio and the plasma prekallikrein level was also not significant. These results suggest that in uremic patients undergoing chronic hemodialysis, the response of the renin system to acute plasma volume change is blunted. These data only provide evidence that plasma active renin is linked with inactive renin, but provide no evidence to support the idea that plasma inactive renin is a precursor of active renin or that plasma kallikrein is related to activation of inactive renin in vivo.

Adult↗
PubMed1991

Exaggerated natriuresis in primary aldosteronism.

Acute response in blood pressure (BP) and natriuresis to saline infusion was evaluated in 16 patients with primary aldosteronism caused by aldosteronoma (PA) and 12 patients with salt-sensitive essential hypertension (SSEH). Salt-sensitivity was defined by a decrease in mean BP exceeding 5% at the second hour after a 20 mg furosemide injection. Plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urine electrolytes in response to saline infusion were determined. During a 2-liter isotonic saline infusion, a similar degree of natriuresis and change in BP were observed in PA and SSEH patients. A significantly inverse correlation between the increase in mean BP and the degree of natriuresis at the end of the infusion was found in patients with SSEH (r = -0.80, p less than 0.01). No correlation was observed between these parameters in patients with PA (r = 0.28, p greater than 0.05). These results suggest that hypernatriuresis in SSEH may play a protective mechanism against abrupt increases in BP and volume during acute saline loading. This protective mechanism was not evident in patients with PA.

Adrenal Cortex Neoplasms↗
PubMed1991

Sequential changes in plasma renin activity and aldosterone level during pregnancy.

Sequential changes in plasma renin activity (PRA) and the plasma aldosterone (PA) level were studied prospectively in 101 patients at Taipei Municipal Women and Children Hospital from the 20th week of gestation to the 4th week postpartum. Average maternal age was 31.8 years old and average fetal birth weight was 3,235 g. The PRA and PA levels during pregnancy were higher than those of the normal nonpregnant women. PRA decreased gradually from the 20th week of gestation and dropped markedly after delivery. The PA level increased after the 20th week of gestation and peaked at the 32nd gestational week, then returned to the nonpregnancy level after delivery. A dissociation between the PRA and PA levels after the 28th week of gestation was observed. Possible causes for this dissociation are discussed. This study provides reference data on PA and PRA levels during the course of a normal pregnancy for use in further studies on abnormal gestation.

Adult↗
PubMed1990

Exaggerated natriuresis in salt-sensitive essential hypertension.

Acute responses of blood pressure and natriuresis to intravenous injection of furosemide and saline infusion were evaluated in 38 patients with essential hypertension. Twelve patients whose mean arterial blood pressure decreased by more than 5% at two hours after intravenous administration of 20 mg furosemide were classified as salt-sensitive (SS); the remainders as salt-resistant (SR). The extent of natriuresis induced by furosemide was not different between the two subgroups. During 2-liter isotonic saline infusion the SS subjects excreted more sodium than the SR subjects did (108.7 +/- 11.9 vs 55.9 +/- 6.6 mmole, p less than 0.001). There was a significant correlation (r = 0.57, p less than 0.001) between the hypotensive effect of furosemide and the 4-hour sodium excretion during saline infusion. A reverse correlation between the sodium excretion during saline infusion and the increase in mean blood pressure at the end of infusion was shown in the SS subgroup (r = -0.72, p less than 0.01), but not in the SR subgroup (r = 0.045). The results suggest that prompt natriuresis on saline infusion in the SS hypertensives may function as a protective mechanism to prevent abrupt increase in blood volume and blood pressure during acute sodium loading.

Adult↗
PubMed1990

A simulation study on renin and aldosterone secretions in primary aldosteronism.

A system dynamics modeling method was developed to predict changes in plasma renin activity (PRA), plasma aldosterone (PA) and electrolyte concentrations in response to diuretic stimulation in patients with primary aldosteronism. Its clinical validity was evaluated by comparing experimental and simulation results. In a clinical experiment, furosemide 20 mg was given by intravenous injection to 20 patients with primary aldosteronism. PRA, PA and electrolyte concentrations were measured hourly for 3 hours after administration of the drug. The computer simulation outputs were consistent with the experimentally measured values at each corresponding point of time. An analysis of model predictions indicates that the method may predict the changes in PRA, PA and electrolyte concentrations after diuretic administration in accordance with a time interval.

Aldosterone↗
PubMed1990

Diurnal variation in water, sodium and potassium excretion in primary glomerulonephritic patients and its relation to diurnal kallikrein excretion.

In order to investigate whether or not primary glomerulonephritic patients have abnormal diurnal water, sodium, and potassium excretion and its relation to diurnal urinary kallikrein excretion (UKE)., we studied the diurnal patterns of urinary water, sodium, potassium, and kallikrein excretion in 16 primary glomerulonephritic patients and 12 normal persons. Urinary kallikrein activity was measured by the enzymatic hydrolysis of synthetic chromogenic substrate S-2266, and urinary electrolytes were measured by flame photometry. The day, night, and 24-hour urine outputs were significantly higher in glomerulonephritic patients, but urinary sodium, potassium and kallikrein excretion at all periods of collection did not differ between glomerulonephritic patients and normal controls. UKE was positively correlated with urinary potassium excretion in both normal controls (r = 0.5, p less than 0.05) and glomerulonephritic patients (r = 0.66, p less than 0.01), whereas no correlation existed between UKE and urinary water excretion, or UKE and urinary sodium excretion in either group. The day/night output ratio of water, sodium and potassium excretion were not different between glomerulonephritic patients and normal subjects. These results indicate that: (1) there is no abnormal diurnal water, sodium, potassium, and kallikrein excretion in primary glomerulonephritic patients with fair renal function; and (2) urinary kallikrein may play a role in the regulation of urinary potassium excretion.

Adult↗
PubMed1987

Probenecid interferes with the natriuretic action of furosemide.

The interaction between probenecid and furosemide was studied in eight hospital patients (ages 20-65 years) who had been treated with oral furosemide, 40 mg daily, and moderate salt restriction for 10 days or longer. After stabilization of drug therapy and diet for at least 3 days, probenecid, 0.5 g twice a day, was given for 3 days and then discontinued. The 24-h urinary sodium excretion (UNaV) significantly decreased from 56.3 +/- 7.2 to 35.9 +/- 7.1 mmol/day when probenecid was added to the treatment regimen (p less than 0.01), and then significantly increased to 61.7 +/- 10.3 mmol/day after probenecid was discontinued (p less than 0.01). Parallel with the changes in UNaV, there were also significant corresponding changes (p less than 0.01) in urinary excretion of uric acid (392.4 +/- 46.5, 600.9 +/- 102.1, and 345.0 +/- 33.2 mg/day, respectively), renal clearance of uric acid (3.7 +/- 0.3, 14.3 +/- 2.4, and 4.1 +/- 0.3 ml/h/kg, respectively), and serum uric acid concentration (7.7 +/- 0.5, 3.3 +/- 0.2, and 6.3 +/- 0.3 mg/dl, respectively). Before and after discontinuing probenecid therapy, there were no significant differences in these parameters (p greater than 0.05). In conclusion, the natriuretic action of furosemide was attenuated by concurrent probenecid therapy, probably owing to a reduction of furosemide delivery to the luminal side of renal tubules.

Adult↗
PubMed1986

Effect of acetylsalicylic acid on urinary excretion of prostaglandin E in stroke patients.

In 12 of 76 stroke patients complicated by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), a significant increase in urinary prostaglandin E (PGE) (p less than 0.005), and a significant positive relationship between the plasma arginine vasopressin (AVR) level and urinary PGE excretion were observed (r = 0.72, p less than 0.05). The experimental results are consistent with the view that renal PGE acts as a modulator of ADH. Nowadays acetylsalicylic acid (ASA), an inhibitor of prostaglandin biosynthesis, is widely used in ischemic stroke, it was felt necessary to study the effect of this drug on urinary PGE excretion. Therefore various daily doses of ASA were given orally for 3 days to patients with ischemic stroke. PGE values in 24-hour urine samples were measured every day for 3 days before administration of the drug and for 3 days during ASA administration. In 10 patients who took 75 mg of ASA, the decrease in urinary PGE excretion was not statistically significant. On the other hand when ASA was administered 300 mg once in 19 patients or 300 mg 4 times in 11 cases, urinary PGE excretion decreased significantly (p less than 0.05 and p less than 0.05 respectively). In another group of 8 patients who were observed before, during and after the ASA administration, a daily oral dose of 300 mg for 3 days caused a significant decrease in urinary PGE excretion during these 3 days (p less than 0.05). The urinary PGE excretion returned to the control level within 3 days after cessation of the ASA administration.

Arginine Vasopressin↗