According to recent reports, deformity and size of mesothelial cells reflect mesothelial condition. We applied flow cytometry (FCM) to the analyzation of mesothelial cells in peritoneal dialysis effluent (PDE) and the relationship between the period of peritoneal dialysis (PD) and peritoneal function. Eighteen patients treated for two to 89 months by PD were selected. Their dialysate: plasma creatinine ratio (D/P creatinine) was 0.67±0.086(0.53 to 0.87). Overnight PDE was drained and centrifuged. The cell population of peritoneal cells identified by anti-cytokeratin, CD14 and 45 antibodies was studied by FCM. Cytokeratin-positive cells were identified as mesothelial cells, distinct from macrophages, granulocytes or lymphocytes. The forward scatter (FSC) of cytokeratin positive cells, fluorescence intensity of cytokeratin and percentage of cytokeratin-positive cells in PDE were 395.6±55.5 (298.31 to 527.72), 333.9±272.9(67.55 to 1, 071.95), and 6.75±6.1% (0.44 to 21.14), respectively. There was a positive correlation between D/P creatinine and FSC, and a negative correlation between D/P creatinine and cytokeratin fluorescence intensity or the percentage of cytokeratin-positive cells. However, there was no correlation between the period of PD and FSC, cytokeratin fluorescence intensity or the percentage of cytokeratin-positive cells. It was suggested that the alteration of mesothelial cells is not necessarily influenced by the period of PD, but influences peritoneal function. It was found that the analysis of cell population by FCM reflects the morphological and functional changes in the peritoneum of patients on PD.
This retrospective study was conducted to evaluate changes in the clinical features of MPGN type-I in childhood during a 30-year period from 1970 through 1999. Renal biopsies were performed on 2, 260 children with glomerulonephritides, among whom were 71 patients with MPGN type-I. Changes in the mode of onset were investigated in patients separated according to the period of onset into two groups by 1974 in which school urinary screening had been widespread. The difference in symptoms after onset was examined between patients with the onset in the 1980s and 1990s under the same circumstances of school urinary screening and of our steroid regimen. Finally, the incidences of this disease in each of the three decades were analyzed. Chance proteinuria and/or hematuria increased (p=0.0107) and acute nephritic syndrome decreased (p=0.0237) in the ratio of the initial symptom on and after 1974. Regarding the clinical presentation after onset, non-nephrotic range proteinuria increased (p=0.0415) and nephrotic syndrome decreased (p=0.0415) in the 1990s, in comparison with the respective rates in the 1980s. The incidence of this disease decreased (p<0.01) in chronological order. Conclusion: The clinical features of this disease definitely changed over three decades suggesting that the clinical presentation has ameliorated in recent years, regardless of effective palliation of severe symptoms afforded by our steroid regimen.
Advanced Medical Research Center, Nihon University School of Medicine, Tokyo, Japan A 44-year-old woman was diagnosed as having chronic renal failure due to rapidly progressive glomerulonephritis (RPGN) from one year earlier. She has been managed with steroid therapy and hemodialysis. The patient was admitted to our hospital because of fever and sudden disturbance of consciousness with generalized convulsion on October 30, 2003. She showed mild meningeal irritation. Cerebrospinal fluid (CSF) examination demonstrated a cell count of 60/μl, protein level of 70mg/dl, glucose level of 52mg/dl, and chloride (Cl) level of 116 mEq/l. Both the CSF culture for Mycobacterium (M.) tuberculosis and the conventional single polymerase chain reaction (PCR) for M. tuberculosis DNA in CSF were negative results on admission. In contrast, nested PCR of preserved CSF samples obtained at admission demonstrated positive results. We diagnosed her conditions as tuberculous meningitis (TBM) and administered a total of 3 anti-tuberculosis agents over a period of about 2 months. Her clinical condition and CSF examinations improved immediately in response to anti-tuberculosis treatment. Serial CSF cultures for M. tuberculosis and the serial single PCRs for M. tuberculosis DNA in CSF were all negative during the course of anti-tuberculosis treatment. However, serial nested PCR results gradually converted from positive to negative, correlating with the improvement in clinical conditions during the course of anti-tuberculosis treatment. Therefore, nested PCRs were much more useful for the rapid and accurate diagnosis of TBM and for assessment of the clinical course and anti-tuberculosis treatment response of TBM than conventional CSF cultures and single PCRs. To the best of our knowledge, there have been few previous reports of diachronic study in which the serial nested PCR was used to test CSF samples obtained earlier in the clinical course of TBM. In conclusion, our findings suggest that nested PCR for M. tuberculosis DNA in CSF was highly useful not only for rapid and accurate diagnosis of TBM, but also for assessment of the antituberculous treatment response in cases highly suspected of TBM despite negative results on conventional cultures and single PCRs.
Fabry disease is an X-linked recessive disease resulting from a deficiency of the lysosomal hydrolase α-galactosidase A. In male patients with the classic hemizygous form, acroparesthesias, hypohidrosis, corneal opacities, and dysfunction of the heart, brain, and kidney are observed. Recently, it was reported that 0.5-1.2% of male chronic hemodialysis (HD) patients were diagnosed as having Fabry disease based on the measurement of α-galactosidase A activity. Fabry disease is thought to be an important cause of end-stage renal disease. There are a few reports of patients with Fabry disease on long-term HD. Here we report two male siblings with classical type Fabry disease on HD. They had acroparesthesias, and hypohidrosis. Their mother had severe heart failure due to a heterozygous form of Fabry disease. Case 1 is a 44-year-old male. He had mid-cerebral apoplexy at 30 years of age. He started maintenance HD in 2000. Remarkable left ventricular hypertophy and conduction disorders of the heart were found. In 2004, he collapsed and ventricular-tachycardia and severe hypoxic brain damage were found. Now his consciousness level has been in the range of 100 to 300 on the Japan Coma Scale. Case 2 is a 40-year-old male. He started maintenance HD in 1993. Malnutrition due to chronic diarrhea and severe ischemic change in the brain were found. In 1998, he had severe joint pain of shoulders and fingers with ectopic calcifications detected by X ray. The ectopic calcifications were extended to the whole body. In 2004, his dementia by ischemic change in the brain has rapidly progressed. In conclusion, cardiovascular complications, cerebrovascular manifestations, painful ectopic carcifications, and chronic diarrheas in our patients were considered to be specific symptoms of Fabry disease. Young HD patients with these symptoms will need to be examined for Fabry disease.