Augmentation of antiproteinuric effect by combined therapy with angiotensin II receptor blocker plus calcium channel blocker in a hypertensive patient with IgA glomerulonephritis.
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Adult↗
Biomedical subjects
H Tomonari
Publications and source records attributed to H Tomonari.
Corticosteroid therapy in encapsulating peritoneal sclerosis.
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Adrenal Cortex Hormones↗
Association of angiotensinogen gene polymorphism with erythropoietin-induced hypertension: a preliminary report.
The association of the angiotensinogen (AGT) gene variation at codon 235, the T235 variant, with hypertension induced by erythropoietin (Epo) was investigated in patients with progressive renal disease requiring treatment for renal anemia with Epo. The subjects for the study were patients with renal diseases with serum creatinine concentration exceeding 2 mg/dl and a hematocrit (Ht) of less than 30%. During the run-in period, blood pressure was well controlled with an appropriate salt restricted diet and/or antihypertensive treatment. The patients were then given 6,000 IU of Epo once a week until the Ht rose by 5%. For the overall patient group, AGT gene polymorphism analysis revealed T235T (T/T) in 31 cases (61%), M235T (M/T) in 19 cases (37%), and M235M (M/M) in 1 case (2%). In response to treatment with Epo, hypertension (defined as an increase in mean blood pressure greater than 10 mmHg) was found in 11 cases (22%), all of who carried the homozygous T allele (T/T). On the other hand, the frequency of T/T in patients who did not develop hypertension was 50% (T/T:T/M=20:19 cases), indicating a significant difference (p=0.003 by Chi-square). Variables estimated to be associated with Epo-induced hypertension were the T allele, gender (male), and the degree of increase in Ht, in descending order. Our preliminary research indicates that individuals who carry two copies of the T allele, i.e., who are homozygous for T, are highly susceptible to development of hypertension when subjected to Epo. These results suggest that the AGT T235 variant may be the primary gene responsible for the development of Epo-induced hypertension.
Adult↗
Beneficial effect of combination therapy with an angiotensin II receptor antagonist and angiotensin-converting enzyme inhibitor on overt proteinuria in a patient with type 1 diabetic nephropathy.
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Adult↗
Circulating adrenomedullin in erythrocopietin-induced hypertension.
Levels of adrenomedullin (AM) have been shown to be elevated in hypertension and chronic renal failure, suggesting that AM plays a role in the pathogenesis of these diseases. The objective of the present study was to investigate whether circulating AM is involved in erythropoietin (Epo)-induced hypertension in patients with renal anemia due to progressive renal disease. Following treatment with 6,000 IU of Epo once a week, the hematocrit (Ht) rose significantly from 25.9+/-4.0 to 33.4+/-3.3% (n=54, p<0.001) with an overall rate of increase in Ht of 0.43+/-0.04%/week. In response to treatment with Epo, a rise in mean blood pressure of >10 mmHg (Epo-induced hypertension) was found in 22% (12/54 cases) of the patients enrolled. There was no difference in the rate of Ht increase between patients with and without Epo-induced hypertension. There was a significant positive correlation between mature AM and serum creatinine (Cr) concentration before treatment with Epo. However, no correlation was found between the plasma concentration of total AM and serum Cr concentration. Long-term treatment with Epo did not influence plasma concentration of either mature AM or total AM in patients developing hypertension during the study period. These results suggest that circulating AM may play a role in the progression of renal disease. However, the present study does not support the notion that circulating AM is associated with the pathogenesis of Epo-induced hypertension. It is too early yet to claim that there is no AM-mediated mechanism in Epo-induced hypertension.
Adrenomedullin↗
[Ambulatory blood pressure monitoring in hypertensive CAPD patients].
The periodic structure of 24-hour blood pressure variation(circadian rhythm of blood pressure by ambulatory blood pressure monitoring(ABPM) in hypertensive CAPD patients was investigated by a new method of analysis based upon the maximum entropy method(MEM). In addition, this method allows the adequacy of antihypertensive therapies to be evaluated in such patients. The results were as follows; 1) The frequency of non-dipper type hypertension was 88%(36/41 cases), and the remaining 12% (5/41) were dipper type hypertension patients. The rise in morning blood pressure(morning surge: MS) was noted in 64% of the former. 2) Night time systolic blood pressure(182 +/- 22 mmHg, n = 36) was higher in patients with non-dipper type hypertension than in those with the dipper type(151 +/- 17 mmHg, n = 5, p < 0.01). 3) The standardized level of systolic blood pressure(SLSBP) calculated by MEM analysis in patients with non-dipper type hypertension(177 +/- 7 mmHg) was comparable with that in those with dipper type hypertension(168 +/- 13 mmHg, ns). 4) Treatment with long-acting Ca antagonist alone significantly reduced both SLSBP and the area over the SLSBP from 188 +/- 18 mmHg to 160 +/- 7 mmHg(p < 0.01, n = 8), and area over the SLSBP from 2,735 +/- 340 mmHg.hr to 1,945 +/- 298 mmHg.hr(p < 0.01, n = 8). 5) In addition to long-acting Ca antagonist, administration of alpha 1-blocker given at bed time was significantly efficacious in reducing the rise in morning blood pressure, MS. The present study using MEM analysis of ABPM suggests that the blood pressure profile of hypertensive CAPD patients is characterized by a non-dipper type dominance and a frequent morning surge. Furthermore, the combined therapy with long-acting Ca antagonist and alpha 1-blocker was substantially effective both in reducing the overall blood pressure level, and in inhibiting the MS. This combined antihypertensive therapy may be potentially useful to prevent CAPD patients from the future development of cardiovascular complications.
Adrenergic alpha-Antagonists↗
Granulocyte colony-stimulating factor-producing primary pericardial mesothelioma.
A 54-year-old male patient presented with a granulocyte colony-stimulating factor (G-CSF)-producing primary pericardial mesothelioma, while showing symptoms of congestive heart failure, a fever of 38 to 39 degrees C, and marked leucocytosis of 52.7 x 10(3) cells/mm3. The histopathologic diagnosis was established after autopsy. G-CSF production was confirmed by the expression of G-CSF mRNA in the tumor extract and the patient's high serum G-CSF concentration. The expression of G-CSF by benign and malignant mesothelial cells has already been reported. However, this is the first case report of G-CSF production in a pericardial mesothelioma.
Fatal Outcome↗
Antiplatelet therapy decreases the incidence of erythropoietin-induced hypertension in predialysis patients.
The observation that antiplatelet therapy may decrease the incidence of Epo-induced hypertension in dialysis patients remains a subject of particular interest. The aim of the present study was to test this hypothesis in patients at the predialysis stage. Predialysis patients with renal anemia were treated with EPO (6000 IU/week) for 6-12 months. Patients were divided into two groups, one of which received antiplatelet therapy and the other did not, and a comparison was made between them with respect to the incidence of EPO-induced hypertension. Logistic regression analysis was used to determine the risk factors for developing hypertension during the EPO therapy. Such predictors included age, gender, antecedent of hypertension, antiplatelet drugs and diabetes mellitus. Overall, 66 patients were enrolled in the study and 18 developed hypertension (27%). Out of the 35 patients not receiving antiplatelet therapy, 15 developed hypertension (43%). In contrast, out of the 31 patients receiving antiplatelet therapy, only 3 (10%) developed hypertension (p=0.003 by Chi square test). Multiple regression analysis showed that the best predictive variables for the development of hypertension were antecedent of hypertension (odds ratio: 0.064, p=0.0118), and use of antiplatelet drugs (odds ratio: 5.081, p=0.0295). The present data provide evidence that antiplatelet therapy may prevent EPO-induced hypertension in predialysis patients. However, the mechanism to explain such an effect still remains to be elucidated.
Adult↗
[Clinical characteristics of renal damage in patients with accidental hypothermia].
We have investigated the clinical characteristics of renal damage and associated complications of 79 patients with accidental hypothermia whom we encountered over the last 5 years. All patients were male, with an average age of 58.9 +/- 9.2 years. Most of these patients were homeless. Body temperature on admission was 29.3 +/- 3.0 degrees C. The most common clinical manifestations on admission were consciousness disturbance and severe hypotension. Complications, including increase in serum transaminase, alcoholism, pneumonia, liver cirrhosis, sepsis, diabetes mellitus, hypoglycemia, acidosis, and an increased level of serum CPK and amylase were found frequently on admission. Death within 48 hours after admission occurred in 23 cases (the death rate; 23/79 = 29%). Renal damage was found in 36 cases (36/79 = 46%), consisting of acute renal failure (ARF) in 27, and acute on chronic in 6. Urinary diagnostic indices suggested that the etiological factor for ARF was pre-renal, which responded well to passive rewarming and an appropriate fluid replacement therapy, resulting in full recovery in most of the cases (the recovery rate; 25/27 = 93%). Among patients with renal damage, there were no cases requiring dialysis. The present data suggest that accidental hypothermia is a fatal condition with an extremely high death rate. It also is associated with multiple complications including ARF. The main cause for ARF is pre-renal, possibly caused by cold diuresis or dehydration superimposed on the underlying diseases such as alcoholism, diabetes mellitus, liver cirrhosis. Such complications, independent of renal damage, determine the patient's prognosis.
Acute Kidney Injury↗
Successful treatment of tumoral calcinosis using CAPD combined with hemodialysis with low-calcium dialysate.
Successful treatment of tumoral calcinosis using continuous ambulatory peritoneal dialysis (CAPD) combined with hemodialysis is described. A 32-year-old male patient with a 2-year history of CAPD rapidly developed multiple metastatic calcification (tumoral calcinosis) adjacent to his fingers, elbows, and knee joints. Tests showed severe hyperphosphatemia, moderate hypercalcemia, and increased Ca-P product without elevation of intact parathyroid hormone. An enlarged parathyroid gland was not found by echography. In order to rapidly lower the excessive Ca and P levels, a combined therapy with CAPD and vigorous transient hemodialysis using a low-Ca dialysate was performed. In parallel, the patient was given calcitonin, bisphosphonate, and short-term Al to ameliorate the metastatic calcifications more effectively. The result was dramatic with disappearance of the tumoral calcinosis as well as improvement in subjective symptoms within a few months. The present case suggests that combined therapy with hemodialysis and CAPD using a low-Ca dialysate, together with Ca-modulating agents, can be effective in ameliorating tumoral calcinosis in patients on CAPD.
Adult↗
Malignant insulinoma with extensive liver metastases presenting as disturbance of consciousness.
A 56-year-old man was referred to our hospital for evaluation of episodic disturbance of consciousness. Hypoglycemic symptoms were noted and Whipple's triad was satisfied. The 75 g OGTT and the glucagon test revealed a high baseline insulin level and hyperreactivity to glucagon. A pancreatic tumor and liver metastases were found by abdominal computed tomography (CT). Based on the finding of liver biopsy, the final diagnosis was malignant insulinoma with liver metastasis. He selected conservative treatment and no hypoglycemic crisis has occurred for one year since discharge. Early diagnosis and long-term follow-up is necessary since this tumor is slow growing.
Blood Glucose↗
Partial deficiency of hypoxanthine-guanine phosphoribosyltransferase manifesting as acute renal damage.
A 32-year-old man who had had frequent gouty arthritis over the past 17 years, was admitted for acute renal failure. Acute renal failure was improved rapidly after medication was resumed and the patient was sufficiently hydrated. The hypoxanthine-guanine phosphoribosyltransferase (HPRT) activity in the patient had been reduced to about 30% of the normal control. Therefore we considered that this patient suffered from a partial deficiency of HPRT. A point mutation of HPRT gene 68G (guanine) to T (thymine) was detected. This is a mutation that has not been previously reported. Familial analysis indicated that his mother and sister were heterozygotes.
Acute Kidney Injury↗
[Renal damage in a chronic active hepatitis C patient receiving interferon-alpha therapy].
A 68-year-old male patient with chronic active hepatitis C was treated with interferon-alpha (IFN-alpha) for a period of 5 months. The patient responded well to the IFN therapy showing substantial improvement in liver function and disappearance of HCV-RNA. However, one year after the treatment he was found to have developed proteinuria and showed a reduction in Ccr. Renal biopsy findings were as follows: Light microscopy showed diffuse expansion of mesangial cells with a focal/local increase in cellularity accompanied by capillary loop thickening. Splitting of the basement membrane was also present. An immunofluorescent study showed that IgA was localized predominantly in the peripheral capillary wall. Electron microscopy showed that there was mesangial cell interposition between the peripheral capillary wall and endothelial cells. Furthermore, endothelial cells were expanded and numerous platelets were seen in the capillary lumen. These findings were compatible with focal MPGN accompanied by activation of endothelial cells. These histological data suggest two clinical disease entities: late-onset renal damage induced by IFN-alpha alone, and HCV-induced renal damage possibly modified by the direct effect of IFN-alpha on the endothelium. The present case suggests that IFN therapy for HCV may produce a particular type of renal damage, under the influence of either IFN or HCV infection, and/or both.
Aged↗
[Aldehyde dehydrogenase 2(ALDH2) gene polymorphism in NIDDM patients with chronic renal failure].
In order to investigate the influence of aldehyde dehydrogenase 2(ALDH2) genotype in the pathogenesis of nephropathy due to non-insulin dependent diabetes mellitus (NIDDM), genotyping of ALDH2 was measured using the PCR-RFLP method in patients with NIDDM on chronic hemodialysis (HD). The results were as follows; 1) The frequency of active ALDH2 was 63% and that of inactive ALDH2 was 37%. 2) The percentage of active ALDH2 was significantly higher in patients with alcohol tolerance than that in those without it (38%). 3) The estimated amount of alcohol consumption in the past was 506 +/- 720 g/week in the active ALDH2 group, and 156 +/- 288 g/week in the inactive ALDH2 group, showing a significant difference between the two groups. 4) Interdialytic body weight gain was larger in patients with active ALDH2 than in those with inactive ALDH2. Since the frequency of active ALDH2 was similar to that in patients without nephropathy, these results do not support the hypothesis that ALDH2 gene polymorphism is involved in the development and persistence of chronic renal failure due to NIDDM. However, salt and water craving in dialysis patients may be influenced partially by an active ALDH2 gene.
Aged↗
Reversal of anemia by erythropoietin therapy retards the progression of chronic renal failure, especially in nondiabetic patients.
Therapy with human recombinant erythropoietin (EPO) has been accepted as effective for renal anemia in dialysis patients. However, studies in rats have shown that correcting anemia with EPO may affect the progression of renal dysfunction. In humans, however, the effect of EPO on residual renal function is a matter of controversy. We, therefore, investigated whether the long-term administration of EPO to predialysis patients influences residual renal function. Anemic patients at the predialysis stage with a serum creatinine (Cr) concentration ranging from 2 to 4 (average 2.9) mg/dl and a hematocrit (Ht) of less than 30% were randomly assigned to two groups which consisted of anemic patients not treated with EPO (group I, untreated anemic controls, n = 31) and anemic patients treated with EPO (group II, treated anemics, n = 42). Patients with nonsevere or moderate anemia (Ht > 30%) with a Cr ranging from 2 to 4 (average 2.6) mg/dl were also recruited as nonanemic controls (group III, untreated nonanemic controls, n = 35). Blood pressure was controlled to the same degree among the three groups by combined treatment with calcium antagonists and angiotensin-converting enzyme inhibitors. All patients were kept strictly on a low-protein (0.6 g/kg/day) and a low-salt (7 g/day) diet. The degree of control of dietary protein and blood pressure and the frequency of angiotensin-converting enzyme inhibitor administration were comparable among the three groups. The primary end point for each patient was a doubling of the baseline Cr which yielded cumulative renal survival rates which were plotted against time. Ht rose significantly from 27.0+/-2.3 to 32.1+/-3.2% in group II (n = 42, p < 0.001) with a rate of increase of 0.4+/-0.06%/week. However, it declined from 27.9+/-1.8 to 25.3+/-1.9% in group I (n = 31, p < 0.001) and from 35.9+/-3.5 to 32.2+/-3.9% in group III (n = 35, p < 0.001). Cr doubled in 26 patients (84%) in group I as compared with 22 (52%) in group II and 21 (60%) in group III. The cumulative renal survival rates in groups II and III were significantly better than that in group I: p = 0.0003 (group I vs. group II) and p = 0.0024 (group I vs. group III). However, there was no difference in the renal survival rate between groups II and III (p = 0.3111). The better survival rate obtained in group II was attributable to the better survival rate for the nondiabetic patients in this group. The present study suggests that anemia, per se, is a factor in the progression of end-stage renal failure and that reversal of anemia by EPO can retard the progression of renal failure, especially in nondiabetic patients, provided that blood pressure control, rate of increase in Ht, and dietary protein restriction are appropriate.
Adult↗
Acute renal failure after binge drinking of alcohol and nonsteroidal antiinflammatory drug ingestion.
A case of reversible acute renal failure (ARF) following binge drinking together with the transient use of a nonsteroidal antiinflammatory drug (NSAID) is described. After binge drinking. the patient experienced hyperdipsia, and the volume of his urine decreased. Subsequently, he took an NSAID to relieve systemic joint pain associated with low grade fever, and then he had complete anuria. One day after taking the NSAID, he visited our hospital, and was found to have severe renal dysfunction accompanied by severe liver damage (blood urea nitrogen and creatinine concentrations were 57 and 5.4 mg/dl, respectively). The impaired renal function progressed over the first three hospital days, as reflected by an elevated creatinine concentration to 11.6 mg/dl. Nine treatment sessions of hemodialysis were, therefore, required to recover the loss of renal function. The present case suggests that binge drinking may be a potential risk factor for ARF in the presence of NSAIDs.
Acute Kidney Injury↗
Evidence for amelioration of endothelial cell dysfunction by erythropoietin therapy in predialysis patients.
Evidence for the involvement of endothelial cells in the pathogenesis or erythropoietin-induced hypertension, and for endothelial cell damage in patients with chronic renal failure, has emerged and appears to be of major concern. We, therefore, investigated the effect of recombinant human erythropoietin (rHuEPO) therapy on endothelium-derived hormones in predialysis patients with progressive renal anemia. At the entry to the trial, the serum thrombomodulin concentration (Tm) and plasma endothelin-1 concentration (ET-1) in the predialysis patients were significantly higher than those in age- and sex-matched normal subjects. Following a 16 week period of treatment with 6000IU rHuEPO given intravenously once a week, patients' hematocrit increased from 27.1 +/- 2.6% to 34.6 +/- 3.2% (n = 16, P < .001). A positive correlation was found between Tm and serum creatinine concentration (Cr) (r = 0.61, P < .05 (n = 16), but no correlation was found between ET-1 and Cr. Tm and Tm/Cr significantly decreased from 7.9 +/- 2.8 ng/mL to 6.6 +/- 2.4 ng/mL (P < .01, n = 16), and from 2.1 +/- 0.7 (x10(-10) to 1.6 +/- 0.7 (x10(-10), P < .01, n = 16), respectively. However, there was no change in ET-1 as a result of the rHuEPO therapy. Creatinine clearance (Ccr), Cr, total amount of daily Tm excretion, Tm clearance/Ccr, daily urinary protein and albumin excretion, and blood pressure also remained unchanged throughout the trail. The present study indicates that correcting anemia by rHuEPO therapy reduces an abnormally elevated Tm in predialysis patients while blood pressure and renal function remain unchanged, suggesting that rHuEPO has a beneficial effect on endothelial cell dysfunction in chronic renal failure patients. This effect may be mediated via an improved oxygen supply to the endothelial cells due to the amelioration of anemia by rHuEPO.
Adult↗
Angiotensin I converting enzyme gene polymorphism in non-insulin dependent diabetes mellitus.
A total of 168 patients with non-insulin dependent diabetes (NIDDM) followed over 10 years were recruited in this study. The patients were divided into two groups: Group 1 patients had a stable renal function (N = 96) and Group 2 had a declining renal function (N = 72). Group 1 included those whose serum creatinine was normal five years ago but had increased to > or = 2 mg/dl or those who has reached end-stage renal failure (requiring dialysis) by the time of study. All patients were genotyped for the insertion/deletion (I/D) polymorphism of the ACE gene, the M235T polymorphism of the angiotensinogen (Atg) gene and the A1166C polymorphism of the angiotensin II type 1 receptor (AT1) gene. The genotype frequency distributions of M235T Atg and the A116C AT1 gene polymorphisms were not different between Group 1 versus Group 2. While the frequency of the ACE DD genotype in Group 1 (7.3%) was comparable to that of the general population, the DD frequency was significantly higher in Group 2 (26.4%) than in Group 1 (odds ratio, 4.56; 95% confidence interval, 1.80 approximately 11.56, P < 0.001). Among all 168 patients studied, the renal survival rate was significantly lower among DD than ID (P < 0.005) or II patients (P < 0.001). In patients with a declining renal function (Group 2), those with the DD genotype had a significantly shorter time interval from onset of diabetes to the initiation of dialysis (13.4 +/- 1.4 years) than those with ID (20.7 +/- 1.2 years, P < 0.01) or II genotypes (17.5 +/- 1.1 year, P < 0.01). Analysis of the clinical course of the three ACE genotypes revealed that the majority (95%) of patients with the DD genotype who had albuminuria progressed to end-stage renal disease within 10 years of diagnosis of diabetes. Our analysis also revealed that initiation and continuation of dialysis are associated with a progressive decrease in the frequency of the DD genotype. These results indicate that, in NIDDM, the ACE DD genotype has a high prognostic value for progressive deterioration of renal function. Moreover, the DD genotype appears to increase the mortality once dialysis is initiated.
Albuminuria↗