Yasushi Akutsu

Interleukin-6 in cerebrospinal fluid of patients with central nervous system infections

Interleukin(IL)‐6 levels were measured in cerebrospinal fluid (CSF) and serum samples from pediatric patients with central nervous system (CNS) infections by means of an enzyme‐linked immunosorbent assay. Mean IL‐6 concentrations in CSF samples from patients with bacterial meningitis (49017 44 730 pg/ml) were significantly higher than those in patients with aseptic meningitis (10761572 pg/ml) or encephalitis (409835 pg/ml). In aseptic meningitis and encephalitis, IL‐6 levels in serum were within the lower ranges (< 100 pg/ml), in contrast with the highly elevated levels found in bacterial meningitis (14 33218 385 pg/ml). In 5 of the 15 patients with encephalitis, elevated levels of IL‐6 were observed in the initial CSF samples despite normal findings of routine CSF examinations. Also, sequential CSF samples revealed that there was an increase in the CSF cell count in two of the five patients. These results validated the potential of measuring IL‐6 in CSF samples for the purpose of providing additional information on routine laboratory test results. D Central nervous system infection, cerebrospinal fluid, children, enzyme‐linked immunosorbent assay, interleukin‐6.

Urinary Excretion of Terminal Complement Complexes in Glomerular Disease

To evaluate renal terminal complement activation in patients with glomerular diseases, we measured terminal complement complexes (TCCs) in plasma and urine with sandwich enzyme-linked immunosorbent assay (ELISA) using a monoclonal antibody against a C9 neoepitope expressed on TCC and a polyclonal antihuman C7 antibody. TCCs were detectable in plasma but not in urine in most of normal controls. In plasma, TCC levels were elevated in 4 of 22 patients with lupus nephritis and in 6 of 12 with membranoproliferative glomerulonephritis. However all patients with IgA nephritis, focal glomerulosclerosis, idiopathic membranous nephritis and idiopathic minimal change nephrotic syndrome (MC) showed normal values. In urine, TCCs were detectable in almost all patients with heavy proteinuria (greater than or equal to 100 mg/ml) except MC. The TCCs present in urine were partially purified by gel filtration using Sepharose 6B and were found to contain C5, C6, C7, C8, C9 and S protein by ELISA. Although the molecular weight of TCC is similar to that of IgM, the fractional excretion rate of TCC was about 100 times higher than that of IgM. These results suggest that TCCs detectable in urine contain SC5b-9 complexes and are mostly of renal origin.

Spot-Urine Screening for Primary Hyperoxaluria

Noritomo Itami, MD, Hokkaido University, School of Medicine, North 15 West 7, Kitaku, Sapporo 060 (Japan) Dear Sir, In primary hereditary hyperoxaluria (oxalosis), stone formation usually begins in childhood (in 65% of the cases before age 12) and recurs at short intervals. Without treatment, more than 80% of the patients with oxalosis become uremic by 20–30 years of age. Treatment with pyridoxine was reported to reduce endogenous oxalate production as well as stone progression, and to prevent them altogether [1]. Early diagnosis and proper management are therefore essential. The diagnosis of oxalosis rests on the finding of increased urinary oxalate excretion in the 24-hour urine, urinary oxalate excretion > 0.5 mmol/l.73 m2/24 h occurs in primary oxalosis [2]. However, it is sometimes troublesome and inaccurate to collect 24-hour urine volumes in infants and toddlers without bladder catheterization, because they do not void spontaneously. Bladder catheterization should be avoided as much as possible because of the risk of urinary tract infections. We tried to find a more convenient screening method for the diagnosis of primary oxalosis type II. Urinary oxalate excretion might be influenced by diet, and our study was performed in children eating self-selected diets without fluid restriction or special medications. Children with hypospadias (n = 4, aged 1–4 years), a girl with remission of nephrotic syndrome (aged 9 years) and a boy with post-Henoch-Schönlein purpura (aged 7 years), who had normal renal function and neither gastrointestinal disease nor other serious illness and no family history of urolithiasis, were chosen as normal controls with their parents’ consent. In the children < 5 years old, urine collections were performed by means of bladder catheterization. Urinary oxalate excretion in the controls varied among 0.55 mmol ± 0.16/24 h/1.73 m2 when 24hour urinary oxalate excretion per unit of surface area was con-

Hypercalciuria and nephrolithiasis in Wilson disease

nation with a cineloop technique allows the immediate judgement of the coronary vessels over a certain distance, whereas M-mode echocardiography provides a small section only. Irrespective of this, the M-mode-beam should cross the vessel in a perpendicular fashion in order to obtain reliable measurements. In our opinion, this may carry a risk of increased errors in distance measurements, especially for the right coronary artery which is difficult to visualize. Unfortunately, Muscumeci et al. do not report their experience with the right coronary artery. In summary, we would like to recommend the use of twodimensional echocardiography in combination with cineloop techniques for quick and reliable measurements of coronary arterial diameters.

Progressive Renal Failure despite Discontinuation of Mefenamic Acid

NSAID-induced Renal failure was excepted to be reversed with the discontinuation of mefenamic acid. However, the renal failure progressed. This progression may be due to the progression to extensive interstitial fibrosis

Acute Tubular Necrosis in LEC Rats with Hereditary Hepatic Failure — A New Animal Model of Hepatorenal Syndrome

It has been reported that LEC rats are a useful animal model for spontaneous fulminant hepatitis [1] and liver cell carcinoma [2]. At 16–20 weeks of age, 80%–90% of LEC rats spontaneously develop severe hepatic disease, but its etiopathogenesis has not yet been clarified. The clinical features of these LEC rats are marked jaundice, ascitis, subcutaneous bleeding, and oliguria, and their low urinary output suggests the presence of an accompanying renal lesion. In this paper, we present the laboratory data and histopathological findings in the liver and kidney of LEC rats — hepatocellular lipid degeneration and acute renal failure due to acute tubular necrosis — and suggest that LEC rats can serve as an animal model for human hepatorenal syndrome.