We examined the role of oxygen free radicals in cisplatin-induced acute renal failure (ARF). The intravenous injection of cisplatin (5 mg/kg body weight) induced an increase in serum creatinine and tubular damage in the outer stripe of the outer medulla in rats. The renal content of malondialdehyde (MDA) transiently increased. Treatment with the free radical scavengers dimethylthiourea (DMTU) or lecithinized superoxide dismutase (L-SOD) attenuated the increase in serum creatinine. The beneficial effect of DMTU, a hydroxyl radical scavenger, was associated with less accumulation of MDA, less tubular damage, and enhanced expression of proliferating cell nuclear antigen (PCNA) in the damaged tubular cells, but not with improvement of reduced renal blood flow (RBF). On the other hand, the beneficial effect of L-SOD, a superoxide anion scavenger, was associated with preservation of RBF and increased urinary guanosine 3',5'-cyclic monophosphate excretion but not with modification of tubular damage or PCNA expression. These results suggest that (1) cisplatin-induced nephrotoxicity was associated with lipid peroxidation, (2) the hydroxyl radical scavenger prevented ARF through both attenuation of tubular damage and enhanced regenerative response of the damaged tubular cells, and (3) the superoxide anion scavenger did the same through preservation of RBF. It follows that oxygen free radicals may play an important role in cisplatin-induced ARF by reducing RBF and inducing tubular damage.

No abstract

attacks and urolithiasis from the age of 27 years, along pathy; platelet aggregation; polycythaemia vera with mild proteinuria and haematuria and mild polycythaemia 5 years before admission, blood values were haematocrit (Htc) 52%, white blood cell count 13 000/ml, red blood cell (RBC) count 5 600 000/ml, Case report On admission, he presented with a reddish face, injected conjunctivae, and moderate hepatosplenome-Patient 1 a 35-year-old Japanese male, was referred to galy. Neurological signs and the findings on head CT our hospital in June 1994 because of a hypertensive scan were consistent with cranial nerves VIII and IX crisis (224/140 mmHg) with headache, visual disturbdamage due to cerebral infarction. Repeated and freance, and dark urine. He had been normotensive until quent blood pressure measurements were within March 1994 when he developed an upper respiratory normal limits. infection. His past history included recurrent gout Urinalysis in both cases demonstrated intense proteinuria (patient 1, 4.0 g/day; patient 2, 2.8 g/day) and Correspondence and offprint requests to: Eri Muso MD, Third haematuria (20-40 RBCs; 30-40 RBCs per high-power Division, Department of Internal Medicine, Faculty of Medicine, field in the sediments respectively) with numerous RBC

Modern vehicles are equipped with Electronic Control Units (ECUs) and external communication devices. The Controller Area Network (CAN), a widely used communication protocol for ECUs, does not have a security mechanism to detect improper packets; if attackers exploit the vulnerability of an ECU and manage to inject a malicious message, they are able to control other ECUs to cause improper operation of the vehicle. With the increasing popularity of connected cars, it has become an urgent matter to protect in-vehicle networks against security threats. In this paper, we study the applicability of statistical anomaly detection methods for identifying malicious CAN messages in invehicle networks. We focus on intrusion attacks of malicious messages. Because the occurrence of an intrusion attack certainly influences the message traffic, we focus on the number of messages observed in a fixed time window to detect intrusion attacks. We formalize features to represent a message sequence that incorporates the number of messages associated with each receiver ID. We collected CAN message data from an actual vehicle and conducted a quantitative analysis of the methods and the features in practical situations. The results of our experiments demonstrated our proposed methods provide fast and accurate detection in various cases.

Background/Aims: Filtration coefficients (Lp) and plasma volume were estimated in order to investigate whether suppressed Lp associates with intradialytic hypotension and/or diabetic nephropathy. Methods: Twenty-one patients were evaluated. Nine patients were diabetic (DM) and 12 were nondiabetic (non-DM). Three of DM and 4 of non-DM were prone to dialysis-induced hypotension (hypo(+)) and others (hypo(–)) were not. Changes in hematocrit (Ht) were measured for 60 min after the start of ultrafiltration. Lp and plasma volume at the start of ultrafiltration (Vp0) were estimated to fit calculating values of Ht based on Schneditz’s open two compartment model to actual value. Results: There was no significant difference in the mean values of Lp/Vp0 either between hypo(+) and hypo(–) (0.87 ± 0.37 vs. 1.24 ± 0.48 ml/mm Hg·min·liter; n.s.) or between DM and non-DM (1.04 ± 0.32 vs. 1.17 ± 0.56 ml/mm Hg·min· liter; n.s.). However, the comparisons of Lp/Vp0 among the four groups (hypo(+)/DM, hypo(–)/DM, hypo(+)/non-DM and hypo(–)/non-DM) showed significant differences between hypo(+)/non-DM and hypo(–)/non-DM (1.08 ± 0.40, 1.02 ± 0.32, 0.71 ± 0.29*, 1.40 ± 0.53* ml/mm Hg·min·liter; *p < 0.05). Differences in the percentage of Vp0 to body weight (Vp0/BW) among four groups and correlation between Lp/Vp0 and Vp0/BW were not significant. Conclusion: These data indicated that reduction of Lp/Vp0 was not simply caused by decreased circulating plasma volume (Vp0/BW) and that the suppressed filtration coefficients may have substantial association with dialysis-induced hypotension in non-DM. The estimation of Lp using in-line measurement of Ht was a useful method for analyzing intradialytic hypotension.

Acute renal failure (ARF) is a well-documented but infrequent complication in patients treated with low-molecular weight dextran (LMWD). We herein report 3 cases of oliguric ARF following the administration of dextran-40. One case developed ARF totally after 1.200 g of LMWD administration. In contrast, two cases having increased serum creatinine developed oliguria despite the acceptable therapeutic doses (totally 450 and 650 g). Contrast media was also co-administered in these patients. Plasma exchange (PE), double filtration plasmapheresis (DFPP), or continuous hemodiafiltration (CHDF) but not hemodialysis (HD) reduced circulating dextran concentrations by 35-44% during a single session. All patients completely recovered from ARF by 14-32 days after the treatment. Our cases suggested that radiocontrast could predispose to the development of LMWD-induced ARF especially in patients having pre-existing renal dysfunction. In addition, PE, DFPP and CHDF afforded a beneficial effect for removing accumulated LMWD from the circulation.

We report a 70-year-old man with primary (AL) amyloidosis with predominantly vascular deposition of amyloid diagnosed by renal biopsy, who was successfully treated using two chemotherapy regimens. There was rapid elevation of the serum creatinine level without remarkable proteinuria or hematuria. Renal histological examination showed some thickened arterial walls with amyloid fibril accumulation, and only a small amount of amyloid deposition in the glomeruli. Immunohistochemical examination was positive for anti-kappa staining. Serum immunoelectrophoresis and immunofixation testing did not show monoclonal proteins, and urine immunoelectrophoresis did not show Bence-Jones proteins. Serum free light chain (FLC) analysis showed that the serum FLC level and FLC kappa/lambda ratio were abnormally high for his renal function. He received two courses of VAD (vincristine, doxorubicin, and dexamethasone), followed by BD (bortezomib and dexamethasone), resulting in a hematologic partial response. Renal amyloidosis with vascular-limited amyloid deposition has few urinary findings. Early diagnosis of this condition is challenging, because kidney biopsies are not usually performed in patients without significant urinary findings. We suggest several currently available methods of achieving earlier detection of this condition.

We evaluated the causal role of glucocorticoid deficiency in the hyponatremia that developed in a 57-year-old Japanese man with hypothyroidism following the performance of a total thyroidectomy for laryngeal cancer. The plasma concentration of vasopressin (1.78 pg/ml) was not suppressed in the presence of hyponatremia (125 mEq/l). The urinary excretion of sodium was increased, and the plasma renin activity and plasma aldosterone concentration were suppressed. The infusion of hypertonic saline increased the plasma osmolality, but not the plasma concentration of vasopressin. An oral water load (20 ml/kg of body weight) did not suppress the plasma vasopressin level or induce diuresis. Pretreatment with hydrocortisone normalized the response of plasma vasopressin to the water load was well as the diuretic response during the hypothyroid state. The urinary exretion of 17-hydroxycorticosteroids was below normal in the hypothyroid state in the face of normal serum cortisol concentration. The correction of the hypothyroidism returned these abnormalities to normal. A disturbed metabolism of glucocorticoid may have been responsible for the hyponatremia and disturbance in plasma vasopressin regulation observed in this hypothyroid patient.