Renin-angiotensin system component gene polymorphisms in Japanese maintenance haemodialysis patients

Summary: The renin-angiotension system (RAS) component gene polymorphisms was examined in 216 patients undergoing maintenance haemodialysis (HD) therapy and in 208 control subjects. the RAS polymorphisms selected for analysis were angiotensin I converting enzyme (ACE) I/D, angiotensinogen (Agt) T235/M235, angiotensin II type 1 receptor (AGT1R) A1166/C1166. the control allelic frequencies was ACE I/D (0.63/0.37), Agt T235/M235 (0.16/0.84), and AGT1R A1166/C1166 (0.94/0.06). Recently, relationships between ACE I/D and the progression of renal disease attract great attention in Japanese and Caucasian populations. ACE D allele was expected to be more frequent in HD population. However, no accumulation of ACE D allele or Agt T235 allele, AFT1R C1166 allele in Japanese end-stage renal disease (ESRD) subjects was detected. to explain the paradoxical result of positive association of ACE D allele with progression of renal disease and no bias of ACE genotype in ESRD subjects, further investigation with systematic prospective study regarding the change of ACE genotype distribution around the period of entering dialysis therapy is required.     

Traumatic renal artery thrombosis with renovascular hypertension

A 15-year-old boy, who tumbled from a fourth-floor window, was transported to our hospital. Enhanced computed tomography (CT) 1.5 h after the injury showed a non-contrasted right kidney, and a repeat CT 6 h after the injury showed a growing retroperitoneal hematoma. The angiography showed complete obstruction of the right renal artery and bleeding from the subcapsular artery, which was successfully embolized. Renovascular hypertension developed on the second day after the injury; therefore, simple nephrectomy was performed.     

Clinico-epidemiological features of infantile hydrocephalus in Japan

In 1988, a nationwide survey was conducted in Japan, in order to examine the prevalence and clinico-epidemiological features of hydrocephalus that developed before 1 year of age. The study was based on questionnaires that were sent to all hospitals in Japan with more than 200 beds. There were 1435 patients who were eligible for the analysis. They were born before 1987 and diagnosed as having infantile hydrocephalus. Approximately two-thirds of the patients had primary hydrocephalus. Neural tube defects were the most frequent cause of the primary hydrocephalus and common among full-term infants. On the other hand, secondary hydrocephalus occurred more often in preterm infants, mainly following intracranial hemorrhage. Intracranial hemorrhage as a cause of hydrocephalus increased over the year, while the incidence of hydrocephalus secondary to intracranial infection decreased during the same period.     

Successful Treatment of Severe Orthostatic Hypotension with Erythropoietin

KAWAKAMI, K., et al .: Successful Treatment of Severe Orthostatic Hypotension with Erythropoietin. A 71-year-old man, who was diagnosed with familial amyloidosis type I, was admitted for treatment of severe orthostatic hypotension associated with recurrent syncopal attacks. Head-up tilt testing demonstrated severe orthostatic hypotension (114/72 mmHg in the supine position and 62/34 mmHg in the upright position) with syncope or presyncope. Oral midodorine and fludrocortisone therapies failed to prevent his symptoms. After administration of subcutaneous erythropoietin, his blood pressure drop in the upright position was decreased and symptoms disappeared unassociated with improvement of anemia. Although previous reports have shown that the mechanism by which erythropoietin improves orthostatic hypotension is related to improvement in anemia, other mechanisms may also play a role. (PACE 2003; 26[Pt. I]:105–107)     

EFFECTS OF IODIDES ON THE HYPOTHALAMIC-PITUITARY-THYROID AXIS IN NEUROLOGICAL ENDEMIC CRETINISM: EVIDENCE FOR COMPENSATED THYROIDAL FAILURE IN ADULT LIFE

Thyroid function studies, performed after iodide administration to five patients with neurological endemic cretinism, were indicative of hypothyroidism. All five subjects had either a low serum thyroxine (T4) or a high basal thyrotrophin (TSH) level and a clearly exaggerated TSH response to thyrotrophin releasing hormone (TRH). These findings are in sharp contrast with those we have previously described in goitrous patients without cretinism from the same geographical area. One interpretation of our observations is that there is an underlying mild defect in thyroid hormone synthesis in endemic cretinism predisposing to iodine induced hypothyroidism.     

Effect of Low Dose Aspirin on Augmented Piasminogen Activator Inhibitor Type 1 Activity in Patients with Permanent Pacemakers

To clarify the activity states of coagulation and fibrinolysis in patients with a permanent pacemaker, we studied 29 patients more than 4 months after operation. They were divided into a single pacemaker lead group (S, n = 14) and a double lead group (D, n = 15). Prothrombin time, activated partial thromboplastin time, fibrinogen, antithrombin III, tissue-type plasminogen activator (tPA) activity, plasminogen activator inhibitor type-1 (PAI-1) activity, and platelet aggregation were measured and compared to those in an age-matched control group (C, n - 7). The effects of low dose aspirin (81 mg/day) in the patients (n = 21) were also studied 2 weeks after administration. PAI-1 activity in groups S and D was significantly higher than that in the group C (53.5 ± 36.5, 86.8 ± 59.2 ng/ mL vs 19.4 ± 7.2 ng/mL; P < 0.01 and P < 0.005). Platelet aggregation induced by collagen was slightly higher in groups S and D than group C. Other parameters were not significantly different. In the patients, low dose aspirin significantly suppressed collagen induced platelet aggregation (71.8 ± 20.3% vs 41.7 ± 28.3%; P < 0.005), but not PAI-1 activity. tPA activity was increased significantly by the low dose aspirin administration (3.94 ± 1.85 ng/mL vs 2.48 ± 1.19 ng/mL; P < 0.005). Thus, PAI-1 activity in patients with a permanent pacemaker is elevated, and the activity is not suppressed by low dose aspirin unlike the platelet aggregation.     

Hepatic and renal expression of senescence marker protein-30 and its biological significance

A novel rat hepatic protein was detected and isolated, the amount of which is down-regulated in an androgen-independent manner with ageing. This protein was designated as senescence marker protein-30 (SMP30). Senescence marker protein-30 turned out to be identical to a hepatic calcium-binding protein called regucalcin (RC). This review gives an overview of SMP30 in its structure, expression and possible physiological function(s). A hypothetical role of SMP30 in ageing and calcium homeostasis is also discussed.