[Long-term hemodialysis treatment using femoral vein puncture method (FV-method) as blood access in 12 patients].

It is well known that blood access is essential for long-term hemodialysis treatment. Arteriovenouos fistula (AVF) is the most widely used method. However, this method of access frequently fails (access failure) as a result of stenosis. We attempt simple femoral vein puncture (FV-method) instead of AVF in such patients and have experienced 12 patients who were undergoing hemodialysis treatment using the FV-method, three times a week for more than one year. We devised special needles (18- and 19-gauge) for the FV-method. Generally, we use a 19-gauge needle with 4 side holes. We discuss here the results of 12 patients consisting of 4 males and 8 females with a mean age of 57.9 years, a mean duration of dialysis of 10.0 years, and a mean duration of FV-method of 3.5 years. Their underlying diseases were chronic glomerulonephritis (9 patients), diabetic nephropathy (2 patients) and nephrosclerosis (1 patient). Before the use of the FV-method, AVFs were attempted a man of 3.8 times and an artificial graft, 4 times in 3 patients. Ten patients were outpatients and 2 were inpatients. As for the indications of the FV-method, 11 patients had access failure and another had suffered from heart failure resulting from an over flow of blood through AVF. KT/V, PCR and TACBUN were measured monthly and were within the normal range in almost all of the patients. Concerning complications of the FV-method, hematoma formation after detachment of the needle at the end of dialysis and pain at needle puncture were sometimes noted.(ABSTRACT TRUNCATED AT 250 WORDS)

Mitochondrial encephalomyopathy with A to G transition of mitochondrial transfer RNA(Leu(UUR)) 3,243 presenting hypertrophic cardiomyopathy.

In a 24-year-old woman with mitochondrial encephalomyopathy presenting hypertrophic cardiomyopathy, microscopical examination of myocardial biopsy specimen disclosed severe vacuolar degeneration of myocardium and aggregates of enlarged mitochondria with proliferated cristae. Limb muscle biopsy specimen showed "ragged-red fibers" light microscopically and enlarged abnormal mitochondria with markedly increased cristae ultrastructurally. Mitochondrial DNA analysis by polymerase chain reaction (PCR) revealed an A-to-G transition in the mitochondrial transfer RNA(Leu)(UUR) gene at nucleotide position 3,243 which is reported to be associated with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). However, the clinical features of this case, presenting mainly cardiac abnormalities, were not consistent with the typical MELAS.

[A long-term hemodialysis patient complicated with systemic calciphylaxis].

A 46-year-old male patient underwent long-term hemodialysis treatment had suffered from calciphylaxis (defined by Selye), such symptoms as advanced systemic vascular calcification, rapid progression of gangrene on both fingers and toes, disturbance of consciousness, and sclerosis and obstruction of the superficial vein after venipuncture during 11.5 years of dialysis. Furthermore, he had a long history (30 years) of heavy smoking. He died as a result of sepsis due to pneumonia after 12.5 years of dialysis. He had received dialysis treatment using a small amount of dialysate (50 liters on a recirculating system) for 8.5 years and had been dialysed 2 and 2 or 3 times a week for 10 years. As a result of this insufficient dialysis treatment, his characteristic laboratory data showed hypocalcemia, hyperphosphatemia, elevated calcium-phosphorus product, advanced metabolic acidosis, hyperalkaliphosphatemia and elevated serum parathyroid hormone. Autopsy revealed the following: 1) enlargement parathyroid gland enlarged in two (4.0 g and 2.0 g, respectively) showing adenomatous hyperplasia presenting cord-like arrangement of chief cells and water-clear cells, 2) systemic medial calcification in radial, ulnar, renal, mesenteric and brain arteries, and 3) Berline-blue positive iron deposit in calcified arteries in mesenteric and parathyroid tissue. From these results, we concluded that factors (challengers) related to the appearance of calciphylaxis might be as follows: 1) advanced secondary hyperparathyroidism, 2) long-term uremic state, 3) administration of VD2 and VD3, 4) iron salt injection, and 5) a long history of heavy smoking. We speculated that these challengers might act synergistically to cause calciphylaxis.

Effect of captopril on blood pressure and renin-angiotensin-aldosterone system in hypertensive patients on hemodialysis.

We have performed a long-term (6-16 months) administration of captopril in 6 hypertensive patients with renal failure undergoing hemodialysis. They were divided into two groups according to the basal renin levels (pretreatment plasma renin activity, PRA), that is, high PRA group (3 patients) and normal PRA group (3 patients). 1) In the high PRA group efficient reduction of blood pressure was obtained by small doses of captopril. In the normal PRA group, however, slight or no pressure reduction was observed. Appropriate initial dose was 10-15 mg/day and maintenance one was 75 mg/day in high PRA group. 2) Hemodialysis potentiated the hypotensive action of captopril in the high PRA group through massive removal of sodium and water. 3) In the normal PRA group PRA was regulated by serum sodium concentration and the plasma aldosterone concentration (PAC) was by serum potassium concentration, but in the high PRA group PRA and PAC were mainly regulated by captopril itself. 4) In one patient an adverse reaction consisting of strong bradycardia, dyspnea, chest pain and cold sweat was observed soon after the start of captopril medication. From these results, it was concluded that captopril was as excellent drug for the control of severe hypertension in dialysed patients having a high basal renin level.

Development of malignant hypertension in patients with uremia under hemodialysis: a case report and discussions on its etiology.

A woman, now 28 years old, was diagnosed 6 years ago as chronic glomerulonephritis by renal biopsy. From August 15, 1975 she complained of nausea, loss of appetite and weight (about 7 kg within 2 weeks). Severe hypertension (200/130 mmHg), hyponatremia (123 mEq/liter), anemia, elevated plasma renin activity (PRA), advanced azotemia, and eye ground changes of KW-II were found. Dialysis treatment was started on September 2, 1975. From November 1975 massive amounts of sodium (5,000 mEq or more monthly) and water (26 liters or more monthly) were removed by the dialysis. These intensive dialyses resulted in an elevated PRA with recurrence of severe hypertension. At the end of March 1976 she became almost blind with retinopathy of KW-IV. Potent hypotensive drugs including beta-blockers were administered, but no improvements were obtained. On March 31, 1976 nephrectomy was performed to save her life. Marked hyalinization of glomeruli and heavy thickening of intima in interlobular arteries were found in the removed kidneys. Renal artery stenosis was not recognized either macroscopically or histologically. In this patient, the amount of sodium removed by the dialysis was dependent on her diastolic blood pressure and sodium concentration of the dialysis. It may be concluded that too enthusiastic dialysis may develop malignant hypertension due to excessive renin release.

Analysis of 30 patients with malignant hypertension treated with hemodialysis.

For the past 7 years we have treated 30 patients with malignant hypertension with hemodialysis. The diagnosis of the disease was made according to the criteria recommended by the Ministry of Public Welfare, Japan, as described below. These patients were divided into three groups according to the therapies. Group A (15 patients) were medicated with large doses of beta-blockers for the control of hypertension. Characteristic features of this group were abnormally high reninemia, hyponatremia, and severe hypertension which were not controlled by large doses of beta-blockers in combination with dialysis. Their body weights were quite subnormal. Twelve patients out of 15 had essential hypertension (EH) as an underlying disease, and the remaining 3 had chronic glomerulonephritis (CN). Ten patients out of 15 died of hypertensive heart failure or hypertensive cerebrovascular accidents. Group B (6 patients) were treated by beta-blockers intermittently. They showed good results responding well to the treatment; high reninemia was brought down to normal level by the administration of beta-blockers and dialysis. Their underlying diseases were EH (3 patients) and CN (3 patients). Group C (9 patients) did not receive beta-blockers, because hypertension was easily controlled by dialysis alone. In the Group C patients, normoreninemia, normonatremia, and a favorable clinical course were characteristic. Their underlying disease was CN in all. From these results, it is concluded that the factors influencing the prognosis of te disease may be the existence of EH as an underlying disease, high reninemia, and hyponatremia which are not correctable either by administration of beta-blockers or by hemodialysis.