Urinary α₁-microglobulin levels were studied in 170 patients with various renal diseases and were compared with other parameters of renal function. The urinary α₁-microglobulin level showed good correlation with the values of serum creatinine, BUN, and creatinine clearance.
Urinary α₁-microglobulin was significantly increased in patients with a decreased creatinine clearance whose serum creatinine and BUN values were still normal or only slightly raised, when compared with the α₁-microglobulin level in patients who had normal values of creatinine clearance, serum creatinine, and BUN.
Quantification of urinary α₁-microglobulin is simple, and seems to useful in patients with renal failure to determine the severity of renal dysfunction and/or the need for maintenance hemodialysis, since this test may provide different information from tests of serum creatinine and BUN.

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This study was designed to clarify if high performance membranes are effective in removing Di-(2-ethylhexyl) phthalate (DEHP) by measuring DEHP, which is an endocrine disrupter.
During in vitro experiments, we circulated albumin solution in blood tubes and measured DEHP concentrations. Also, we circulated albumin solution in blood tubes connected to regenerated cellulose membranes (CU) or cellulose triacetate membranes (CTA). DEHP eluted from the tubes was 0.95mg. It consisted of 0.72mg from a CU membrane (AMFP 110), and 0.17mg from a CTA membrane (FB 90 U).
Furthermore, we compared two different models of CTA dialyzers (FB-E (55Å) and FB-F (75Å)) to observe the influence of different pore sizes on DEHP removal. The quantity of DEHP was 0.47mg in FB 50 E, and 0.29mg in FB 50 F, the lower value found in the membrane with a larger pore size.
During in vivo experiments, we measured DEHP in arterial blood before and after hemodialysis sessions. DEHP was not detected in the serum of any patients dialyzed with CU, CTA, or PS membranes over a long period. However, DEHP was detected in the serum of post-hemodialysis patients, and its concentration was 0.69±0.31mg/l in CU, while it was 0.41±0.07mg/l in CTA, and 0.25±0.21mg/l in PS. It was significantly lower in CTA and PS membranes, compared to CU.
In conclusion, we can state that high-performance membranes are useful in the removal of DEHP eluted from blood circulating tubes.

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To examine the possible usefulness of the analysis of femoral artery flow patterns for the assessment of atherosclerosis in patients on regular dialysis treatment, we analyzed femoral artery flow patterns by the pulsed Doppler method.
The subjects consisted of 18 dialysis patients and 18 control subjects. The interval between the top of R wave on ECG and the onset of the femoral artery flow pattern (R-FA), peak systolic forward flow velocity (peak FA), peak reversed flow velocity (rev FA), peak FA/rev FA (R), and the interval between the top of wave on ECG and peak FA (R-PV) were recorded. These parameters were compared between dialysis patients and control subjects, and the correlation of these parameters with aortic pulse wave velocity (C-PWV), an established index of aortic atherosclerosis, was assessed among dialysis patients.
R-FA and R-PV were significantly shorter in dialysis patints than in control subjects. Peak FA and R were also significantly smaller in dialysis patients. C-PWV was significantly larger in dialysis patients. R-FA and R-PV were negatively correlated with C-PWV in dialysis patients, although there were no correlations to C-PWV in other parameters, which are assessed to reflect peripheral atherosclerosis.
We conclude that the analysis of femoral artery flow patterns might be useful to estimate aortic and peripheral atherosclerosis in dialysis patients.

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Left ventricular hypertrophy (LVH) is an extremely common condition in chronic hemodialysis (HD) patients. The clinical importance of LVH resides in the fact that LVH with systolic dysfunction is a predictor of cardiac death in HD patients independent of blood pressure.
We studied whether atrial and brain natriuretic peptides (ANP, BNP) in HD patients represent cardiac dysfunction. For that purpose, we compared the relationship between plasma concentrations of ANP, BNP after the removal of fluid by ultrafiltration and echocardiographic data, H/M estimated by MIBG scintigrahy in 36 HD patients. The following results were obtained.
Both plasma ANP and BNP levels were elevated in these patients. There was a positive correlation between plasma ANP and BNP levels. Plasma ANP concentrations correlated with left ventricular mass index (LVMI), but correlated inversely with H/M. However, plasma BNP levels correlated with A/E and LVMI, but inversely with left ventricular ejection fraction (LVEF) and H/M. Plasma BNP levels showed stronger correlation with these parameters than ANP. BNP/ANP after HD showed correlations with LVEF, A/E, LVMI and A/E. BNP/ANP showed stronger correlation with LVEF and A/E than BNP. HD patients with BNP/ANP above had severe left ventricular hypertrophy and systolic dysfunction.
From these results, we conclude that elevated plasma BNP levels are a more sensitive marker of left ventricular dysfunction in HD patients than plasma ANP. In addition, HD patients with BNP/ANP above showed severe left ventricular hypertrophy with systolic dysfunction and impaired cardiac sympathetic nerve function.

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A 42-year-old female with Klippel-Feil syndrome and chronic renal failure is described. In 1989, she developed nephrotic syndrome. She was diagnosed as having Klippel-Feil syndrome by observation of a short neck, fusion of the cervical vertebrae, and scoliosis. Renal biopsy was not performed because she had alasia of the left kidney. In 1995, her renal function deteriorated, and she needed dialysis therapy. Her arterial malformation caused the failure of the creation of an arterio-venous fistula. Therefore, she started CAPD.

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We herein report a rare case of parathyroid carcinoma in an early hemodialysis patient. In March 1991, a 45-year-old woman with 17-year history of hypertension was admitted to our hospital for further examination of renal failure. On admission, primary hyperparathyroidism was suspected because of the findings of nephrocalcinosis and tendency toward hyrcalcemia, but parathyroid scintigraphy showed negative accumulation of radioactive agents. She finally underwent maintenance hemodialysis (HD) in June 1992. Three months later, she was re-admitted to our hospital because of rapid increase in parathyroid hormone concentration and uncontrollable elevation of serum calcium. Magnetic resonance imaging and CT demonstrated a mass in the anterior meiastinum between the superior vena cava and the trachea, although scintigraphy did not demonstrate any accumulation of radioactive agents at that site. Parathyroid tumor and consequent hyperarathyroidism were highly suspected and the tumor was resected. Histoloicl examination revealed carcinoma of the parathyroid gland. Two other parathyroid glands simultaneously resected did not show any abnormal findings such as hyperlasia.
These findings suggested that the background of our case might differ from that of other previously reported cases of parathyroid carcinoma complicated with chronic renal failure.

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We report a patient with Type Ia glycogen storage disease complicated with rhabdomyolysis. This 47-year-old man developed cardiomegaly, hypertension and hepatorenal dysfunction and was diagnosed with Type Ia glycogen storage disease in 1984. His parents were married consanguineously, and his brother demonstrated the same disease. Complaining of general fatigue for 2 days, he was admitted to our hospital on December 25, 1996, and hemodialysis was performed immediately because of renal failure with hyperkalemia. On December 27, he was diagnosed with rhabdomyolysis based on laboratory findings; i.e., marked elevation of serum CPK, GOT, GPT, LDH, and myoglobin levels. Therefore continuous hemodiafiltration (CHDF) was performed. Anticoagulant therapy for disseminated intravascular coagulation syndrome (DIC) and absorption therapy for hyperbilirubinemia were initiated. The patient responded to these treatments. Sequence analysis of exon 5 of the glucose-6-phosphatase gene revealed a homozygous mutation of G 727 T. Rhabdomyolysis due to Type Ia glycogen storage disease has been reported only rarely. Lactic acidosis exacerbated by the underlying disease may have led to rhabdomyolysis in this patient.

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