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Biomedical subjects

K Tokuyama

Publications and source records attributed to K Tokuyama.

At least 55 records · Page 3Linked to original sources
PubMed1999

Difference in airway reactivity in children with atopic vs nonatopic asthma.

STUDY OBJECTIVE: To examine the difference in the mechanisms of bronchial hyperresponsiveness (BHR) in nonatopic asthma and in atopic asthma, we studied bronchial reactivity against nonspecific stimuli in children with atopic asthma and nonatopic asthma. DESIGN AND PARTICIPANTS: Fourteen children with nonatopic asthma, 24 children with atopic asthma, and 20 age-matched controls participated in this study. MEASUREMENTS: Inhalation challenge was performed by administering progressively doubling doses of methacholine with a continuous inhalation provocation method. The speed of bronchoconstriction to methacholine (Sm) and the speed of reversal of bronchoconstriction to methacholine after inhalation of a beta2-agonist (r-Sm), which was considered to represent the effect of the beta2-agonist, were calculated from the dose-response curve. RESULTS: The value of Sm was higher in the nonatopic asthma group than in the atopic asthma group and the control group. The value of r-Sm was also higher in the nonatopic asthma group than in the atopic asthma group, but did not differ from that in the control group. CONCLUSION: These results indicate that bronchial reactivity against methacholine and the beta2-agonist was greater in nonatopic asthma than in atopic asthma, and that the mechanism of BHR in children with nonatopic asthma may differ from that in children with atopic asthma.

Adolescent↗
PubMed1999

Endogenous glucose production and glucose effectiveness in type 2 diabetic subjects derived from stable-labeled minimal model approach.

Insulin sensitivity, glucose effectiveness, and endogenous glucose production (EGP) during stable-labeled, frequently sampled insulin-modified intravenous glucose tolerance test (FSIGT) were evaluated by a single-and two-compartment minimal model combined with nonparametric deconvolution in eleven nonobese Japanese type 2 diabetic patients. Four patients were treated with sulfonylureas, and the remaining seven with diet therapy alone. None had diabetic retinopathy and microalbuminuria. Their fasting glucose level was 117+/-7 mg/dl (mean +/- SE), and HbA1c was 6.6+/-0.3%. Age-, sex-, and BMI-matched subjects with normal glucose tolerance served as control subjects. Plasma insulin response to the stimuli and insulin sensitivity indexes (S(I), S(I)*, and S(I)2* were derived from a minimal model and single- and two-compartment-labeled minimal models) were impaired in the type 2 diabetic patients. The combined ability of glucose, per se, to increase its own uptake and suppress EGP (glucose effectiveness [SG]), which was derived from kinetic analysis of plasma glucose by a minimal model, was significantly lower in the type 2 diabetic patients (0.0132+/-0.0015 vs. 0.0203+/-0.0022; P<0.05). However, the ability of glucose, per se, to stimulate glucose uptake, assessed as S(G)* and S(G)2* from the kinetic analysis of labeled glucose by single- and two-compartment minimal model, was not impaired in those patients. EGP of the type 2 diabetic patients as a whole was suppressed to the level similar to that of the control subjects despite a higher plasma glucose level throughout FSIGT. When EGP in the diabetic subjects was analyzed, considering their recent glycemic control, the initial suppression was blunted in the patients with higher HbA1c levels. In conclusion, glucose mass action to stimulate glucose uptake remains near-normal in the lean Japanese type 2 diabetic patients of this study, whereas ability of glucose to suppress EGP is impaired in the patients with recent hyperglycemia. This blunted suppression of EGP might be one of the conspirators for decreased S(G) in subjects with type 2 diabetes.

Adult↗
PubMed1999

[A case of Goodpasture's syndrome with massive pulmonary hemorrhage ameliorated by cyclophosphamide pulse therapy].

A 22-year-old woman was admitted to our hospital for evaluation of fever, renal dysfunction, and a 3-month-history of macrohematuria. Laboratory evaluation revealed proteinuria (1.8 g/day), hypoproteinemia, microcytic microchromic anemia, renal failure (blood urea nitrogen 30.3 mg/dl, serum creatinine 4.0 mg/dl), and positive serum antiglomerular basement membrane (anti-GBM) antibody. Renal biopsy revealed cellular crescents in all 8 glomeruli and partial rupture of the GBM. The interstitium showed severe inflammatory cell infiltration. Immunofluorescent examination revealed linear deposits of IgG and C3 along the GBM. Pulmonary biopsy revealed linear deposits of IgG along the alveolar basement membrane in the immunofluorescent examination. A diagnosis of Goodpasture's syndrome was made because all of the diagnostic criteria were fulfilled. After admission, the patient's renal function deteriorated rapidly. Hemodialysis was started, and the patient was treated with methylprednisolone pulse therapy and oral prednisolone with double filtration plasma pheresis (DFPP). However, her renal function did not improve. On the 30th hospital day, she showed hemoptysis, and a chest X-ray and CT revealed massive bilateral pulmonary hemorrhage. Despite treatment with pulsed methylprednisolone, oral prednisolone (80 mg/day), and DFPP, the pulmonary hemorrhage improved only transiently, worsening again 5 days later. Cyclophosphamide pulse therapy was administered. After this treatment, the patient's pulmonary manifestations and pulmonary hemorrhage improved. At the present time she is on maintenance dialysis therapy without pulmonary manifestations. These findings suggest that cyclophosphamide pulse therapy is effective against Goodpasture's syndrome with massive pulmonary hemorrhage showing resistance to other conventional therapy.

Adult↗
PubMed1998

Effects of a single bout of resistance exercise on calcium and bone metabolism in untrained young males.

Although resistance exercise training appears to increase bone mineral density in the long term, a single bout of resistance exercise could paradoxically induce bone homeostasis disturbance, secondary to metabolic acidosis. To examine this, we obtained fasting blood and 24-hour urine samples from untrained male subjects for 5 subsequent days (control day, exercise day, and three post-exercise days), and investigated the effects of a single bout of resistance exercise on urinary calcium excretion and bone metabolism as indicated by sensitive biomarkers of bone formation and resorption. After an intense bout of resistance exercise, blood and urine became more acidic and renal net acid excretion significantly increased by 44% on the exercise day. Urinary calcium excretion significantly increased by 48% on the exercise day. Plasma procollagen type-I C-terminal concentration significantly decreased by 12% on the next day of the exercise and serum bone-specific alkaline phosphatase activity also significantly decreased by 13% and 9% on days 2 and 3, respectively, after the exercise. There was no significant change in serum osteocalcin concentration. Serum tartrate-resistant acid phosphatase activity significantly decreased by 15% on the day after the exercise and urinary deoxypyridinoline excretion decreased by 22% and 27% on days 1 and 3, respectively, after the exercise. These results suggest that the early response of bone to a bout of resistance exercise in untrained individuals was transient decreases in bone formation and resorption, whereas urinary calcium excretion increased.

Acid Phosphatase↗
PubMed1998

Intravenous glucose tolerance test-derived glucose effectiveness in strength-trained humans.

The effect of long-term strenuous resistance training on glucose effectiveness (SG) was examined by comparing 11 strength-trained and 20 sedentary males by a minimal model approach. Lean body mass (LBM) was measured by hydrostatic weighing. The LBM in strength-trained subjects (65.7 +/- 3.1 kg) was significantly larger than in sedentary subjects (56.6 +/- 1.2 kg, P < .01). The glucose disappearance constant ([KG] 3.07% +/- 0.45% min(-1)) and insulin sensitivity ([SI] 17.5 +/- 2.0 x 10(-5) x min(-1) x pmol/L(-1)) in strength-trained subjects were significantly higher than in sedentary subjects (2.06% +/- 0.14% x min(-1) and 10.3 +/- 1.2 x 10(-5) x min(-1) x pmol/L(-1), P < .05). SG in strength-trained subjects (0.024 +/- 0.003 min(-1)) was significantly higher than in sedentary subjects (0.018 +/- 0.001 min(-1), P < .05). These results thus suggest that the improved glucose tolerance in strength-trained subjects was due to increased SG and SI.

Adult↗
PubMed1998

Intravenous glucose tolerance test-derived glucose effectiveness in endurance-trained rats.

Glucose tolerance is determined by complex interaction among several physiological processes, including insulin secretion, insulin sensitivity (S[I]), and the action of glucose itself to enhance glucose uptake and suppress its release by the liver. The combined effect of glucose to enhance glucose uptake and suppress endogenous glucose production at basal insulin has been defined as glucose effectiveness (S[G]) and is at least equal to insulin itself in the determination of glucose tolerance. The present study was undertaken to examine the effects of endurance training on S(G) in young rats. Female Sprague-Dawley rats (7 weeks old) were randomly assigned to sedentary and trained groups, and rats in the trained group had access to a running wheel for 3 weeks. Intravenous glucose tolerance tests ([IVGTTs] 500 mg/kg body weight) were performed 30 hours after the rats stopped wheel-running. The glucose disappearance constant (KG) and minimal model-derived S(I) and S(G) for trained rats were higher than for sedentary animals. Increases in S(G) were positively correlated with the relative heart weight, an index of endurance capacity. Our results confirm the previous observation in a cross-sectional study that an improved glucose tolerance in endurance-trained athletes was due to an increase in S(G) and S(I), suggesting that physical exercise is a unique physiological condition that enhances both S(G) and S(I).

Animals↗
PubMed1998

Inhaled procaterol inhibits histamine-induced airflow obstruction and microvascular leakage in guinea-pig airways with allergic inflammation.

BACKGROUND: Beta2-adrenoceptor agonists (beta2-agonists) are shown to inhibit airway microvascular leakage in experimental animals. This effect may change in animals with chronic airway inflammation. OBJECTIVE: We examined whether inhaled beta2-agonists inhibit microvascular leakage in guinea-pig airways with chronic allergic inflammation. METHODS: Three weeks after the sensitization with ovalbumin (OA; 6 mg/mL), each guinea pig was challenged with inhaled OA once a day for 1 or 3 weeks. Control animals without sensitization with OA also inhaled vehicle for OA (saline) for 3 weeks. One day after the last challenge, different doses of inhaled procaterol (1, 3 or 10 microg/mL) or vehicle was given to animals for 10 min after an anaesthesia. Fifteen minutes after the end of inhalation, the animals were given i.v. Evans blue dye (EB dye; 20 mg/kg), a marker of microvascular leakage, and then i.v. histamine (3 or 30 microg/kg) or vehicle. Lung resistance, a parameter of airflow obstruction, was measured for 6 min and the lungs were removed to calculate the amount of extravasated EB dye into the airways. RESULTS: A significant increase in eosinophil infiltration into the airways was seen in sensitized and challenged animals compared with control animals without sensitization. Among animals receiving antigenic exposure for either 0 (control), 1 or 3 weeks, 10 microg/mL procaterol significantly inhibited 30 microg/kg histamine-induced increase in EB dye extravasation to a similar degree (ranged from 28.7 to 69.8% inhibition) as well as that in lung resistance (more than 90% inhibition in all groups). The minimal dose of procaterol to inhibit 3 microg/kg histamine-induced microvascular leakage was not different between nonsensitized control animals and those sensitized and challenged for 3 weeks at all airway levels. CONCLUSION: Inhaled beta2-adrenoceptor agonists may be also potent in attenuating microvascular leakage even in the airways with chronic allergic inflammation.

Administration, Inhalation↗
PubMed1998

Role of cyclic adenosine monophosphate in reducing superoxide anion generation in guinea pig alveolar macrophages.

Aveolar macrophages (AM) may contribute to airway inflammation via release of superoxide anion (O2-). Elevation of intracellular cyclic adenosine monophosphate (cAMP) levels has been shown to suppress O2- generation, although the exact mechanism is uncertain. To examine the inhibitory effect of cAMP against different stimuli for O2- generation, we compared the effect of cAMP on O2- generation caused by phorbol myristate acetate (PMA), a direct protein kinase C activator, and N-formyl-methionyl-leucyl-phenylalanine (FMLP), which couples its membrane receptor and stimulates guanosine triphosphate binding protein, in guinea pig AM. Cyclic nucleotide phosphodiesterase (PDE) isoenzyme inhibitors or CPT-cAMP, a cAMP analogue, were used in order to increase intracellular cAMP levels. The O2- generation caused by either PMA or FMLP was reduced by cilostazol (PDE 3 inhibitor) and Ro20-1724 (PDE 4 inhibitor), but not by zaprinast (PDE 5 inhibitor). The degree of reduction in O2- generation was not different between PMA and FMLP. Furthermore, CPT-cAMP also reduced PMA- or FMLP-induced O2- generation to a similar degree, although only high concentrations (10(-5) or 10(-4) mol/l) of this agent were effective in producing significant inhibition. A remarkable elevation of the cAMP level is required to produce the inhibitory effect on O2- generation in guinea pig AM. An elevation of cAMP may suppress O2- generation by inhibiting plural sites of the intracellular signaling pathways.

Animals↗
PubMed1998

Signal transduction in activation of human eosinophils: G protein-dependent and -independent pathways.

Degranulation of eosinophils and subsequent release of toxic granule proteins play a key role in allergic diseases such as bronchial asthma. We have previously shown that stimulation of eosinophils with immobilized secretory immunoglobulin A (sIgA) induced the phosphorylation of several proteins including 51-, 65-, 73-, 78-, 100-, 105- and 113-kD proteins. Pervanadate, a protein tyrosine phosphatase inhibitor, also induced at least 7 tyrosine phosphorylated proteins including those observed with immobilized sIgA. Pervanadate also induced inositol phosphate (IP) production and degranulation of eosinophils in a concentration-dependent manner. Eosinophil production of IP and degranulation as well as tyrosine phosphorylation of proteins induced by sIgA were completely inhibited by a tyrosine kinase inhibitor, genistein, and pertussis toxin (PTX), suggesting the involvement of both the PTX-sensitive guanine nucleotide-binding (G) protein and protein tyrosine kinases (PTK) in sIgA-induced activation of eosinophils. In contrast, PTX did not affect tyrosine phosphorylation induced by sIgA or pervanadate. Furthermore, pervanadate-induced IP production was partially inhibited by PTX. Finally, a phospholipase C-gamma2 isoform was tyrosine phosphorylated by pervanadate, but not by sIgA. These findings suggest that at least two different pathways, i.e. PTK-mediated G protein-dependent or -independent PLC activation, are involved in the activation of human eosinophils.

Asthma↗
PubMed1998

Cross-linking of the beta2 integrin, CD11b/CD18, on human eosinophils induces protein tyrosine phosphorylation and cellular degranulation.

Adhesion molecules, including integrins, play an important role in the selective recruitment of eosinophils. It has recently been shown that integrins also modulate the functions of eosinophils. Here, we tested the hypothesis that cross-linking of the beta2 integrin, alphaMbeta2Mac-/, leads to intracellular signaling events such as activation of protein tyrosine kinases leading to eosinophil degranulation. Cross-of cell surface CD11b/with anti-tibody and goat anti-G immobilized onto the plate triggered tyrosine phosphorylation of several intracellular proteins, including the one with a 115-kD mass (pp115). The same stimulus also provoked degranulation of eosinophils. These findings suggest that engagement of beta2 integrin on eosinophils triggers the activation of intracellular signaling cascade which leads to cellular degranulation.

Antibodies↗
PubMed1998

Diurnal variation of peak expiratory flow in children with cough variant asthma.

Cough variant asthma (CVA) is thought to be a variant form of asthma in which cough is the sole clinical manifestation of airways hyperresponsiveness, a characteristic feature of asthma. Another characteristic feature of asthma includes an increased diurnal variation of peak expiratory flow (PEF) compared to normal subjects. To examine whether diurnal variation of PEF might also increase in children with CVA, we have examined the degree of diurnal variation of PEF in these children (n = 7) by measuring peak flow serially for a week, and compared it with those in mild to moderate asthma (n = 17) and in control children without cough (n = 8). In control children without cough, the average value of the mean diurnal variation of PEF was 10.4 +/- 0.8%. In both groups of children with asthma and with CVA, there was a significant increase in the value (20.5 +/- 1.3% and 23.6 +/- 3.6%, respectively) compared to that in control children (p < 0.01 in both groups), although there was no significant difference between these 2 groups. These results show that mild, but significant airway obstruction is occurring in children with CVA, although clinical wheezing is not recognized. Serial measurements of diurnal variation of PEF may be helpful for the diagnosis of CVA in children.

Asthma↗
PubMed1998

[A female case of Fournier's gangrene in a patient with lupus nephritis].

Infection is one of the common causes of death in patients with systemic lupus erythematosus (SLE). It is associated with the use of immunosuppressive agents, renal failure, and increased disease activity. Fournier's gangrene is a necrotizing fasciitis occurring in the genital region. It is rare, but can be crucial if surgical drainage is delayed. We report a female case of Fournier's gangrene occurring in a patient with lupus nephritis and chronic renal failure. The patient was a 21-year-old female with chronic renal failure due to lupus nephritis. She had suffered from watery diarrhea one month before admission. It improved after increasing the dose of prednisolone, but, she was complicated with Bartholin abscess. The vaginal pain rapidly spread to the left lower quadrant abdomen despite treatment with oral cephalosporin. Focal incision was performed and black fluid emerged with a foul smell. Pelvic computed tomography (CT) revealed many bubbles in that region. She was found to have septic shock on transfer to our hospital. Thereafter, emergency debridement was performed, followed by antibiotic therapy and hyperbaric oxygen therapy. Organisms were found to be 5 anerobes, such as Bacteroides species, and 3 aerobics, such as Morganella morganii. Fournier's gangrene was improved via these treatments, but she needed maintenance hemodialysis. Fournier's gangrene complication should be considered in SLE with urogenital infection.

Adult↗
PubMed1998

[Potential role of primary hypercoagulability and antiphospholipid antibody as a risk factor of acute pulmonary thromboembolism].

To examine whether primary hypercoagulable states, such as protein C and protein S deficiencies and antiphospholipid antibody, are associated with an increased risk, severity and recurrence of acute pulmonary thromboembolism, the blood levels of antithrombin III, protein C, protein S, lupus anticoagulant, anticardiolipin antibodies were measured in 23 patients with acute pulmonary thromboembolism, 7 men and 16 women (mean age +/- SD, 52 +/- 5 years), admitted to Nippon Medical School Hospital from January, 1990 through December, 1997. Four patients (17.4%) had protein C deficiency, one had protein S deficiency (4.3%), 10 had lupus anticoagulant (43.5%), and 2 had anticardiolipin antibodies (8.7%). Hemodynamic evaluation by Swan-Ganz catheter and venography of the lower extremity to detect deep venous thrombi were carried out in 20 and 21 patients, respectively. There were no differences between the patients with and without primary hypercoagulable states in age (52 +/- 14 vs 52 +/- 19 years), gender, or percentage of patients with deep venous thrombi in the lower extremity (91.7% vs 88.9%). Mean pulmonary arterial pressure (38 +/- 9 vs 26 +/- 4 mmHg, p < 0.05) and total pulmonary vascular resistance (10 +/- 5 vs 6 +/- 2 Wood unit, p < 0.1) were higher in the 13 patients with primary hypercoagulable states compared with the 10 patients without primary hypercoagulable states. Recurrence of pulmonary thromboembolism tended to be higher in the 13 patients with primary hypercoagulable states compared with the 10 patients without primary hypercoagulable states (46.2% vs 10.0%, p < 0.1). These findings suggest that primary hypercoagulable states, such as protein C and S deficiencies and antiphospholipid antibody, are associated with the severity and increased risk and recurrence of acute pulmonary thromboembolism.

Acute Disease↗
PubMed1997

Decreased glucose effectiveness but not insulin resistance in glucose-tolerant offspring of Japanese non-insulin-dependent diabetic patients: a minimal-model analysis.

The aim of the study was to estimate insulin sensitivity (SI), insulin secretion, and glucose effectiveness (SG) in 10 subjects with normal glucose tolerance (eight men and two women) with a family history of non-insulin-dependent diabetes mellitus (NIDDM offspring). Ten glucose-tolerant subjects (eight men and two women) without a family history of NIDDM served as control subjects. All subjects were Japanese. They underwent a modified frequently sampled intravenous glucose tolerance test (FSIGT): glucose (300 mg/kg body weight) was administered, and insulin (20 mU/kg over 5 minutes) was infused from 20 to 25 minutes after glucose. SI and SG were estimated by Bergman's minimal-model method. No significant difference was observed in body mass index (22.6 +/- 1.5 v 21.5 +/- 0.6 kg/m2) and fasting glucose (5.1 +/- 0.1 v 5.2 +/- 0.1 mol/L) and insulin (40.7 +/- 6.3 v 42.6 +/- 6.7 pmol/L). SI was not different between the two groups (0.83 +/- 0.11 v 0.94 +/- 0.15 x 10(-1).min-1.pmol/ L-1, P > .05). The acute insulin response to glucose (AIRglucose) estimated by intravenous glucose tolerance testing was significantly lower in the offspring than in the normal controls (2,139 +/- 265 v 3,438 +/- 318 pmol/L.min, P < .05). The glucose disappearance rate (KG) and SG were significantly diminished in the offspring versus normal controls (KG, 1.50 +/- 0.22 v 2.10 +/- 0.15 min-1, P < .05; SG, 0.016 +/- 0.003 v 0.023 +/- 0.002 min-1, P < .05). Thus, glucose-tolerant Japanese NIDDM offspring with normal insulin sensitivity are characterized by a reduced AIRglucose and diminished SG. This is the first report that glucose resistance but not insulin resistance already exists in glucose-tolerant Japanese NIDDM offspring.

Blood Glucose↗
PubMed1997

Intravenous glucose tolerance test-derived glucose effectiveness in bulimia nervosa.

The aim of the present study was to estimate insulin secretion, insulin sensitivity (SI), and glucose effectiveness at basal insulin (SG) in subjects with bulimia nervosa. Eight bulimic patients and eight age-, body mass index-, and sex-matched healthy control subjects without a family history of diabetes were studied. The subjects all had normal glucose tolerance. They underwent a modified frequently sampled intravenous glucose tolerance test; glucose (300 mg/kg body weight) was administered, and insulin (4 mU/kg body weight/min) was infused from 20 to 25 minutes after administration of glucose. SI and SG were estimated by Bergman's minimal model method. Basal insulin (27 +/- 3 v 45 +/- 3 pmol/L) was significantly lower in bulimic patients than in normal controls (P < .05), but basal glucose was similar between the two groups (4.5 +/- 0.1 v 4.9 +/- 0.1 mmol/L, P > .05). The glucose disappearance rate (KG) and acute insulin response to glucose estimated by the intravenous glucose tolerance test (AIR(glucose)) were similar between the two groups (KG, 1.35 +/- 0.29 v 2.20 +/- 0.21 min(-1), P > .05; AIR(glucose), 2,920 +/- 547 v 2,368 +/- 367 pmol/L x min, P > .05). No significant difference was observed in SI between the two groups (1.34 +/- 0.18 v 1.25 +/- 0.20 x 10(-4) x min(-1) x pmol/L(-1), P > .05). On the other hand, glucose effectiveness at basal (SG) and zero (GEZI) insulin was significantly diminished in comparison to normal controls (SG, 0.011 +/- 0.002 v 0.024 +/- 0.002 min(-1), P < .01; GEZI, 0.008 +/- 0.002 v 0.017 +/- 0.003 min(-1), P < .01). Thus, bulimic patients with normal glucose tolerance without a family history of diabetes were characterized by normal insulin secretion, normal SI, and reduced SG and GEZI.

Adult↗
PubMed1997

Low diastolic blood pressure, hypoalbuminemia, and risk of death in a cohort of chronic hemodialysis patients.

In a previous report, we showed that nutritional status and especially serum albumin had great predictive value for death in chronic hemodialysis patients, whereas blood pressure did not. In the present study, we analyzed the causes of death in consideration of the relationship between serum albumin and blood pressure. A total of 1,243 Okinawan patients (719 males, 524 females) undergoing hemodialysis in January 1991 were followed up through the end of 1995. Three hundred forty-two of the patients died, 45 received transplants, and 12 were transferred by the end of the follow-up period. The total duration of observation was 5,110.3 patient-years. Blood pressure as well as clinical and laboratory variables were determined immediately prior to the first dialysis session in January 1991. The crude death rate was 40.0% when the diastolic blood pressure (DBP) <70 mm Hg, 35.0% at 70 to 79 mm Hg, 25.0% at 80 to 89 mm Hg, 25.0% at 90 to 99 mm Hg, and 13.0% at >100 mm Hg. The death rate showed an inverse correlation with DBP. DBP showed a significant positive correlation with serum albumin (r = 0.137, P < 0.001) and age (r = -0.325, P < 0.0001). The adjusted odds ratio (95% confidence interval) of death was 0.84 (0.71 to 0.99) with 10 mm Hg increments in DBP when the reference DBP was less than 69 mm Hg. Low DBP may be a manifestation of malnutrition and/or cardiovascular disease in chronic hemodialysis patients. Target DBP levels may be higher levels in chronic hemodialysis patients than the general population.

Blood Pressure↗