An awareness of the triggers of relapse is critical for the control of steroid-dependent, frequently relapsing nephrotic syndrome (SDFRNS). We have investigated the triggers, usually described as 'episodes', to such relapses within a temporal context. Thirty-five patients with SDFRNS were analyzed retrospectively. A total of 442 relapses occurred in 2499 patient-months. The relapses were classified into two groups: those with episodes (E+) and those without episodes (E-). There were 135 E+ relapses and 296 E- relapses. The common cold was the most common episode (52%) of E+ relapse, followed by school events (18%). These E+ relapses occurred almost evenly throughout the 4 weeks between each follow-up visit. Conversely, 161 (55%) of the 296 E-z relapses occurred within the 3-day period preceding the patient's appointment (relapse-related hospital visit, RRHV). McNemar's test revealed that the concentration of relapses in this period was statistically significant (P < 0.00011). In addition, 15 out of 26 RRHV without additional therapy showed a spontaneous remission. From a chronological perspective, the common cold and school events as well as up-coming hospital visits may trigger relapses in SDFRNS patients.
Gliadin, one of the major proteins together with glutenin composing gluten, affects the physical properties of wheat flour dough. In this study, nanoscale structures of hydrated gliadins extracted into distilled water were investigated primarily by small-angle X-ray scattering (SAXS) over a wide range of concentrations. Gliadins are soluble in distilled water below 10 wt %. Guinier analyses of SAXS profiles indicate that gliadins are present as monomers together with small amounts of dimers and oligomers in a very dilute solution. The SAXS profiles also indicate that interparticle interference appears above 0.5 wt % because of electrostatic repulsion among gliadin assemblies. Above 15 wt %, gliadins form gel-like hydrated solids. At greater concentrations, a steep upturn appears in the low-q region owing to the formation of large aggregates, and a broad shoulder appears in the middle-q region showing density fluctuation inside. This study demonstrates that SAXS can effectively disclose the nanostructure of hydrated gliadin assemblies.
We treated a 14-year-old boy with Henoch -Schönlein purpura nephritis (HSPN) who died of an intracranial hemorrhage (ICH). Although ICH is a rare complication of HSPN, the consequence of this complication is sometimes very serious. 1 But there are no reports on the pathology and pathogenesis of ICH occurring in the course of HSPN. We examined the autopsied brain tissue and renal biopsy specimen using in situ hybridization (ISH) and polymerase chain reaction (PCR) of human cytomegalovirus (HCMV). The results indicated that he had had latent HCMV infection on admission to hospital. This suggests that reactivation of latent HCMV infection superimposed on HSPN worsened his vasculitis and resulted in fatal ICH. This is the fi rst report investigating the brain pathology of ICH as a result of severe vasculitis of HSPN. Case reportFive years prior to coming to Surugadai Nihon University Hospital , a 9-year-old boy was admitted to a local hospital for abdominal pain and vomiting. He was diagnosed as having HSPN because purpura had appeared on his legs. He was followed as an outpatient by the hospital and was admitted fi ve times after his fi rst admission due to abdominal colic. The patient had proteinuria and hematuria and was given only dipyridamole during these periods. Two months prior to admission to Surugadai Nihon University Hospital he had pretibial edema, hypertension and abdominal distention with heavy proteinuria. He was referred to Surugadai Nihon University Hospital because of his severe nephritis.On admission he was 6 kg heavier than 1 month previously, and he had hypertension (140/92 mmHg) and anasarca. The laboratory fi ndings on admission were as follows: blood urea nitrogen 25.6 mg/dL, creatinine (Cr) 2.29 mg/dL, total protein (TP) 4.1 g/dL, albumin (Alb) 2.3 g/dL, total cholesterol (T-cho) 272 mg/dL, urine red blood cells >100 per high-power fi eld, and urinary protein 819 mg/dL (3.62 g/day), and creatinine clearance (Ccr) 39.6 mL/min, IgG 338 mg/dL, IgA 233 mg/dL, third component of complement (C3) 97.7 mg/dL, fourth component of complement (C4) 19.2 mg/dL, anti-nucleic antibody, anti ds-DNA antibody, proteinase 3 antineutrophil cytoplasmic antibody (PR3-ANCA) and myeloperoxidase antineutrophil cytoplasmic antibody (MPO-ANCA) were negative.Based on these fi ndings a clinical diagnosis of nephronephritic HSPN was made, and treatment with oral prednisolone (2 mg/kg) was started. A renal biopsy showed diffuse mesangial proliferative glomerulonephritis, which was compatible with the International Study of Kidney Disease in Children (ISKDC) grade Vb. Intravenous methylprednisolone pulse therapy in combination with urokinase (3 days/week) was administered for 3 weeks. 2 After this therapy his serum creatinine decreased to 1.5 mg/dL. We then conducted double fi ltration plasmapheresis for 3 days to remove the IgA immune complex (IgA-IC), 3,4 which reduced IgA-IC from 3 mg/dL to 1 mg/dL. But on day 26 he had a fever and complained of a severe headache and delirium. Brain computed tomography (CT) showed a smal...
A 12-year-old girl, who had been diagnosed as having Cockayne syndrome (CS), was admitted for emaciation and dehydration. On admission the patient had mild chronic renal failure (glomerular filtration rate: GFR 50 mL/min) and hyperuricemia. After rehydration, allopurinol was commenced for her hyperuricemia. Then, her renal function rapidly deteriorated (GFR 20 mL/min) with enhancement of proximal tubular dysfunction and hypertension. A renal biopsy showed that the patient had acute tubulointerstitial nephritis (ATIN). Based on this diagnosis, allopurinol was stopped and prednisolone was started (2 mg/kg per day), following which the renal tubular function improved. However, the proteinuria intensified to become nephrotic syndrome. After 1 month the patient developed a gastric ulcer. Famotidine was commenced but GFR deteriorated and renal proximal tubular dysfunction re-occurred. The renal pathology was evaluated by referring to the previous reports of renal pathology in CS. It is suggested that rapid deterioration of the renal function in CS patients might be the result of ATIN. In addition, the present nephrotic syndrome seemed to be accompanied by ATIN, as in other reports.
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