Shigeichi Shoji

Different Impacts of Neck Circumference and Visceral Obesity on the Severity of Obstructive Sleep Apnea Syndrome

Our aim was to investigate the significance of neck circumference (NC) on the presence and severity of obstructive sleep apnea (OSA) syndrome independent of visceral fat (VF) obesity. A total of 219 subjects with suspected OSA underwent a complete polysomnography (PSG) study, along with the measurement of NC, and total body fat (TF) and VF levels (VFLs) measured by bioelectrical impedance analysis. We proposed NC divided by height (NC/H) as the simple index for height‐corrected NC in Japanese subjects. NC/H exhibited a significantly stronger correlation than NC per se with BMI (r = 0.781 vs. 0.675, P = 0.0178), TF (r = 0.531 vs. 0.156, P < 0.0001), and VF (r = 0.819 vs. 0.731, P = 0.0203), indicating that NC/H is a better indicator of visceral obesity than NC per se. Interestingly, despite the strong correlation between NC/H and VFL, VFL was significantly associated with the apnea‐hypopnea index (AHI) ≥5, ≥15, and ≥30, but not with ≥40 or ≥50, whereas NC/H was significantly associated with higher AHI values, i.e., AHI ≥50 but not with lower AHI value. Furthermore, multiple regression analyses revealed that VFL and NC/H were independently associated with the square root of AHI (AHI0.5) levels in obese and nonobese patients, respectively. In conclusion, NC is associated with the severity of OSA independently of visceral obesity, especially in nonobese patients.

Significant correlation of glycated albumin, but not glycated haemoglobin, with arterial stiffening in haemodialysis patients with type 2 diabetes

Objective  We recently reported that glycated albumin (GA) is a better indicator of glycaemic control compared with glycated haemoglobin (HbA1c) in haemodialysis (HD) patients with type 2 diabetes. As poor glycaemic control is considered an independent risk factor for atherosclerosis in diabetes, the relationship between GA, HbA1c and arterial stiffening was examined in HD patients with type 2 diabetes.

Relationship Between Serum Sclerostin, Bone Metabolism Markers, and Bone Mineral Density in Maintenance Hemodialysis Patients

BACKGROUND Sclerostin, which is secreted exclusively by osteocytes, is a negative regulator of bone formation. The role of sclerostin in chronic kidney disease-mineral and bone disorder is not well known. In the present study, we examined the relationship between serum sclerostin levels, bone turnover markers, and bone mineral density (BMD) of the radius in maintenance hemodialysis patients. METHODS This was a cross-sectional study that analyzed sclerostin, bone alkaline phosphatase (a bone formation marker), and tartrate-resistant acid phosphatase 5b (a bone resorption marker) in stored serum samples from 181 hemodialysis patients (age, 68 ± 11 y; 105 males and 76 females; hemodialysis duration, 6.9 ± 5.9 y). The BMD in the distal one-third of the radius and in the ultradistal radius, which are enriched with cortical and cancellous bone, respectively, was examined by dual-energy x-ray absorptiometry. RESULTS Serum sclerostin was 125 ± 53 pmol/L (mean ± SD). Serum sclerostin correlated significantly and negatively with serum bone alkaline phosphatase and tartrate-resistant acid phosphatase 5b (r = -0.265, P < .001; r = -0.218, P < .01, respectively). The BMD in the distal one-third of the radius and in the ultradistal radius both correlated significantly and positively with serum sclerostin levels (r = 0.454, P < .0001; r = 0.329, P < .0001, respectively). In multiple regression analysis, serum sclerostin was associated significantly and independently with BMD of both parts of the radius (β = 0.200, P < .001; β = 0.218, P < .05), after adjustment for age, hemodialysis duration, and bone metabolism markers. CONCLUSION Serum sclerostin was associated significantly, independently, and positively with BMD of both cortical and cancellous bone. Sclerostin is considered to be one of the factors associated with chronic kidney disease-mineral and bone disorder in hemodialysis patients.

Poor muscle quality as a predictor of high mortality independent of diabetes in hemodialysis patients

BACKGROUND Poor muscle quality provides a clinically relevant measure for mortality in general population, particularly in the elderly people. Our previous reports indicating poorer muscle quality in diabetes mellitus (DM) hemodialysis patients than in non-DM counterparts prompted us to examine the association between two parameters in hemodialysis patients, independent of DM prevalence. METHODS The study was performed from 1997 to 2005. Grip dynamometry and dual-energy X-ray absorptiometry (DXA) were used to measure handgrip strength (HGS) and arm lean mass (ALM), respectively, with the muscle quality defined as the ratio of HGS to ALM. RESULTS During the mean follow-up period of 77 months, 90 out of 272 patients died. The patients were divided into higher and lower groups based on the values of muscle quality. In Kaplan-Meier analysis, the higher group revealed lower mortality than the lower group. Cox regression hazards analysis identified higher muscle quality as a significant independent predictor for better survival in hemodialysis patients (HR; 0.889, 95% CI 0.814-0.971; P<0.05), after adjustment for age, sex and the prevalence of DM. Since DM prevalence is a major factor for poorer muscle quality, another analysis was performed after restriction of the subjects to non-DM patients. The result also indicated that muscle quality provides a relevant measure independent of the presence of DM to predict the mortality in hemodialysis patients (HR; 0.849, 95% CI 0.759-0.950; P<0.05). CONCLUSION The study suggested that muscle quality provides a good marker for survival in hemodialysis patients, independently of the presence DM, age and serum albumin.

Greater potency of darbepoetin‐α than erythropoietin in suppression of serum hepcidin‐25 and utilization of iron for erythropoiesis in hemodialysis patients

The potency of darbepoetin‐α (DPO‐α) to improve anemia in hemodialysis (HD) patients is greater than that of recombinant human erythropoietin (rHuEPO).

Significant inverse relationship between serum undercarboxylated osteocalcin and glycemic control in maintenance hemodialysis patients.

SummaryIncreased levels of serum undercarboxylated osteocalcin, which were associated with bone metabolism markers, correlated inversely with indices of glucose metabolism (plasma glucose, hemoglobin A1C, and glycated albumin) in hemodialysis patients with abnormalities of bone metabolism.IntroductionUndercarboxylated osteocalcin (ucOC), a possible marker of bone metabolism and one of the osteoblast-specific secreted proteins, has recently been reported to be associated with glucose metabolism. We tested the hypothesis that ucOC levels are associated with indices of glucose metabolism in chronic hemodialysis patients with abnormalities of bone metabolism.MethodsSerum ucOC, bone alkaline phosphatase (BAP, a bone formation marker), and tartrate-resistant acid phosphatase-5b (TRACP-5b, a bone resorption marker) were measured in 189 maintenance hemodialysis patients (96 diabetics and 93 non-diabetics), and their relationships with glucose metabolism were examined.ResultsucOC correlated positively with BAP (ρ = 0.489, p < 0.0001), TRACP-5b (ρ = 0.585, p < 0.0001) and intact parathyroid hormone (iPTH; ρ = 0.621, p < 0.0001). Serum ucOC levels in the diabetic patients were lower than those of non-diabetic patients (p < 0.001), although there were no significant differences in serum BAP or TRACP-5b between diabetic and non-diabetic patients. Serum ucOC correlated negatively with plasma glucose (ρ = −0.303, p < 0.0001), hemoglobin A1C (ρ = −0.214, p < 0.01), and glycated albumin (ρ = −0.271, p < 0.001), although serum BAP or TRACP-5b did not. In multiple linear regression analysis, log [plasma glucose], log [hemoglobin A1C], and log [glycated albumin] were associated significantly with log [ucOC] after adjustment for age, gender, hemodialysis duration, and body mass index but were not associated with log [BAP], log [TRACP-5b], or log [intact PTH].ConclusionIncreased levels of serum ucOC, which were associated with bone metabolism markers, were inversely associated with indices of glucose metabolism in hemodialysis patients.

Serum type III, IV collagens and TIMP in patients with type II diabetes mellitus.

We investigated serum levels of type III procollagen aminopeptide (CIII), 7S type IV collagen (CIV), and tissue inhibitor of metalloproteinase (TIMP) in 33 patients with type II diabetes mellitus (DM) without uremia (serum creatinine less than 1.5 mg/dl). The patients were divided into three groups based on measurement of the urinary albumin excretion (UAE) index obtained during two morning outpatient clinic visits: non-proteinuric patients (n = 11), UAE index less than 2.26 mg/mmol Cr; patients with microalbuminuria (n = 15), UAE index of 2.26 - 22.6 mg/mmol Cr; and patients with proteinuria (n = 7), UAE index more than 22.6 mg/mmol Cr. Serum levels of CIV and TIMP in patients with microalbuminuria and proteinuria were significantly higher than non-proteinuric patients (ANOVA, p <0.05). Serum levels of CIII in patients with proteinuria were significantly higher than those in non-proteinuric patients (p < 0.05). There was a significant positive correlation between CIV and TIMP (r = 0.502, p < 0.003), but no correlation was observed between CIII and TIMP. These results demonstrated that serum CIII and CIV increases as diabetic nephropathy progresses in terms of increasing proteinuria in type II DM patients, suggesting feasibility and usefulness of measuring serum CIV and CIII in assessing diabetic nephropathy. The increase in TIMP may be, at least in part, a possible cause for the increase in serum CIV in type II DM patients.

A CASE OF CRESCENTIC GLOMERULONEPHRITIS ASSOCIATED WITH POLYMYOSITIS

Masaki Tsunemi, MD, Second Department of Internal Medicine, Osaka City University Medical School, 1-5-7 Asahi-machi, Abenoku, Osaka 545 (Japan) Dear Sir, Polymyositis is an autoimmune collagen disease which preferably involves proximal striated muscles. Though other collagen diseases, such as systemic lupus erythematosus (SLE) and progressive systemic sclerosis (PSS), involve various organs including the kidney, polymyositis is rarely complicated with renal disease. We hereby describe an adult patient with polymyositis which was followed by crescentic glomerulonephritis. Clinical course and laboratory examination suggest an association of two immune-mediated diseases: crescentic glomerulonephritis and polymyositis in this case. The patient, a 56-year-old man, was first seen at another hospital in 1985 because of progressive muscle weakness of the trunk and lower extremities. After several examinations, including muscle biopsy of the deltoid muscle, a diagnosis of primary idiopathic polymyositis was established in 1985, according to the criteria offered by Bohan and Peter [1]. Prednisolone treatment (30 mg/day) was started, with subsequent reversal of muscle weakness and improvement in laboratory data. In July 1990, however, laboratory data showed exacerbation of polymyositis. Serum creatine phosphokinase (CK) gradually increased to 400-529 IU (normal range 30-160) and aldolase was 9.1-10.9 BU (normal range 2-8). Cyclophosphamide (100 mg/day) was subsequently added to steroid therapy. In December 1990, macroscopic hematuria was noted. Serum creatinine was 1.3 mg/l. The patient was admitted to Osaka City University Hospital in May 1991. On physical examination, the patient was 167 cm tall and weighed 58 kg. His temperature was 36.8 °C and blood pressure 166/68 mm Hg. His chest was normal except for occasional irregular heartbeats. There was no edema in the extremities. Neurological examination revealed symmetric weakness and atrophy of the muscles of the trunk and extremities. Laboratory findings on admission were as follows: urine gave a 1 + test for protein (1.52 g/day) and 3 + for occult blood, urinary sediment contained 120-550 red cells, 3-7 white cells, a few granular casts and hyaline casts per high-power field. Erythrocyte sedimentation rate was 50 mm

Heat-insoluble cryoglobulin in a patient with essential type I cryoglobulinemia and massive cryoglobulin-occlusive glomerulonephritis

We report a case of type I essential cryoglobulinemia with massive cryoglobulin-occlusive glomerulonephritis, in which the clinical course and the physical characteristics of the cryoglobulin were unusual. Nine years before appearance of cryoglobulin, this 54-year-old man noted edema and purpura of the lower extremities. Renal biopsy performed 2 years later showed large amounts of amorphous, weakly eosinophilic, weakly periodic acid-Schiff (PAS)-positive materials occluding the glomerular capillaries. Immunostaining showed the material to be weakly immunoglobulin (Ig) G positive, and electron microscopy showed homogeneous, electron-dense deposits. Nephrotic syndrome and azotemia did not respond to steroid treatment, and dialysis was begun 5 years after the biopsy. A small amount of cryoglobulin was first detected 2 years later, 9 years after the onset of disease. The cryoglobulin had a white gelatinous appearance, was resistant to resuspension, and did not redissolve when rewarmed to 37 degrees C. Immunoelectrophoresis of the cryoglobulin, which partially dissolved at 54 degrees C, showed it to be composed of monoclonal IgG-kappa and a small amount of albumin. We consider that the unusual physical characteristics of the cryoglobulin in this case precipitated a massive cryoglobulin-occlusive glomerulonephritis, which progressed to end-stage renal failure in the absence of significant cryoglobulinemia during the initial onset of disease.

An autopsy case of cholesterol embolism following percutaneous transluminal coronary angioplasty and aortography.

A 67‐year old woman with a 6‐year history of angina pectoris underwent percutaneous transluminal coronary angioplasty. Just after manipulation of the guiding catheter during a second attempt at angioplasty and aortography, the patient developed intestinal obstruction with peritonitis. Laparotomy was performed, and surgical specimens taken during surgery revealed necrosis and perforation of the small intestine. Microscopical examination proved that this was the result of multiple fresh cholesterol emboli in the arteries. Postoperatively, renal failure and sepsis developed, and the patient died 13 days after surgery. Autopsy revealed multiple cholesterol emboli in arteries of the intestine, spleen, pancreas, liver and kidneys. This case demonstrates that cholesterol embolism can be a serious complication of percutaneous transluminal coronary angioplasty. Acta Pathol. Jpn. 32: 203∼206, 1989.