Haemolytic uraemic syndrome complicated with norovirus-associated gastroenteritis

Nephrology Dialysis Transplantation, Jul 2007

Toshiro Sugimoto, Nobuyuki Ogawa, Masahiro Aoyama, Masayoshi Sakaguchi, Keiji Isshiki, Masami Kanasaki, Takashi Uzu, Yoshihiko Nishio, Yutaka Eguchi, Atsunori Kashiwagi

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Haemolytic uraemic syndrome complicated with norovirus-associated gastroenteritis

Toshiro Sugimoto 1 2 3 Nobuyuki Ogawa 1 2 3 Masahiro Aoyama 1 2 3 Masayoshi Sakaguchi 1 2 3 Keiji Isshiki 2 3 Masami Kanasaki 2 3 Takashi Uzu 1 2 3 Yoshihiko Nishio 1 2 3 Yutaka Eguchi 0 2 3 Atsunori Kashiwagi 1 2 3 0 Critical and Intensive Care Medicine Shiga University of Medical Science , Otsu Shiga Japan 1 Department of Internal Medicine 2 Acknowledgement. We thank Dr Masanori Matsumoto (Department of Blood Transfusion Medicine, Nara Medical University , Nara , Japan) for the assay of activity of of von Willebrand factor-cleaving protease 3 Rehabilitation Medicine Emory University School of Medicine Atlanta , GA 30322 USA 8. Schalkwijk CG, ter Wee PM, Teerlink T. Reduced 1,2-dicarbonyl compounds in bicarbonate/lactate-buffered peritoneal dialysis (PD) fluids and PD fluids based on glucose polymers or amino acids. Perit Dial Int 2000; 20: 796798 Sir, Norovirus infections run a short self-limiting disease, course characterized by sudden onset of nausea, vomiting and diarrhoea [1,2]. Dehydration is the most common complication, especially among the young and elderly, and may require medical attention; however, there is no evidence of any serious sequelae [1,2]. Here, we describe the occurrence of haemolytic uraemic syndrome in a patient with norovirusassociated gastroenteritis. An 82-year-old Japanese man, with a history of chronic kidney disease (stage 3) due to hypertensive nephrosclerosis [3], was referred and admitted in December 2006, because of rapidly progressive renal dysfunction, consciousness disturbance and convulsion. He had been well until 1 week previously; however, abdominal symptoms (i.e. watery nonbloody diarrhoea, abdominal pain and vomiting) had developed in him and his family members. On admission, he showed no abdominal symptoms, but showed marked renal dysfunction with anuria (blood urea nitrogen, 181 mg/dl; serum creatinine, 9.17 mg/dl); thus, we initiated emergent haemodialysis. Although he had not been noted with marked hypertension during the gastroenteritis, he showed marked hypertension (200/100 mmHg). Furthermore, he also showed thrombocytopenia (11 103/ml), anaemia with red blood cell fragmentation (haemoglobin, 8.0 g/dl) and an undetectable serum haptoglobin level. Coagulation screening and liver biochemistry results were normal. Further laboratory tests (i.e. hypocomplementaemia, direct Coombs test, hepatitis B/C, anti-nuclear antibodies, anti-double-stranded-DNA antibodies, anti-cardiolipin antibodies, blood/urine cultures, parvovirus B 19, cytomegalovirus and EpsteinBarr virus) showed negative results. In his fecal specimens, the cultures of enterohaemorrhagic-Esherichia coli, Clostridium difficile and Campylobacter species and the enzyme-linked immunosorbent assay of verocytotoxins were negative, but norovirus antigen was identified with enzyme immunoassay, indicating norovirus-associated gastroenteritis. After six haemodialysis sessions, his clinical symptoms and laboratory abnormalities were completely improved; renal function, however, did not fully recover, and he was treated with maintenance haemodialysis. We think our patients renal dysfunction might not have been caused by dehydration due to diarrhoea alone, but might have been caused by thrombotic microangiopathy, because he showed the marked hypertension, thrombocytopenia and microangiopathic haemolytic anaemia. Based on these clinical manifestations, laboratory data and the normal plasma activity of von Willebrand factor-cleaving protease (70%), we diagnosed a possible haemolytic uraemic syndrome with diarrhoeal prodrome [4]. Although we did not perform highly sensitive serum-serological assays, haemolytic uraemic syndrome associated with verocytotoxin-producing E. coli might be clinically unlikely because he had not showed bloody diarrhoea or the positive results of fecal assays [5]. Reported other causal/associated factors of this syndrome (e.g. Streptococcus pneumoniae, drugs, malignancy, autoimmuine diseases or viral infections) were not identified in our patient [4]. He had norovirus-associated gastroenteritis before admission; thus, the norovirus infection might have contributed to the development of his haemolytic uraemic syndrome. Norovirus-associated gastroenteritis is typically a non-inflammatory small bowel infection and disease manifestations generally last 4872 h with a full and rapid recovery [1,2]; however, norovirus infections reportedly can lead to an increased duration of diarrhoea in elderly patients, and to severe consequences (e.g. increased levels of C-reactive protein and creatine phosphokinase, hypokalaemia and renal dysfunction) in patients with underlying conditions (e.g. cardiovascular disease and immunosuppression) [6]. To our knowledge, ours is the first case of the occurrence of haemolytic uraemic syndrome in norovirusassociated gastroenteritis. The question remains as to whether our patients norovirus infection was a root cause, a simple coincidence or a precipitating factor of haemolytic uraemic syndrome. Further, there is a possibility that his chronic kidney disease and hypertension might also have contributed to the development of endothelial cell damage, resulting in haemolytic uraemic syndrome, even in the mild norovirus-associated gastroenteritis. Norovirus infections have been emerging this winter and up to 40 deaths of elderly patients associated with these infections have already occurred in Japan. Our observation merits presentation, because further accumulation of clinical studies including case reports is necessary to confirm whether haemolytic uraemic syndrome is a real association in patients with norovirus-associated gastroenteritis. Conflict of interest statement. None declared. UptoDate, CD-ROM: version 14.3, UptoDate, Wellesely, Masschusetts: 2006 6. Mattner F, Sohr D, Heim A, Gastmeier P, Vennema H, Koopmans M. Risk groups for clinical complications of norovirus infections: an outbreak investigation. Clin Microbiol Infect 2006; 12: 6874 Advance Access publication 29 March 2007 Quality of life assessment in a recent haemoglobin trial in CKD (CHOIR) Sir, We read with interest the editorial comment by Levin [1] on methods and lessons learned from recent haemoglobin trials in chronic kidney disease (CKD). Levin identifies a number of issues on the design, reporting and conclusions of one of these trials, the Correction of Haemoglobin and Outcomes in Renal Insufficiency (CHOIR) study, published in the New England Journal of Medicine [2]. Improvement in quality of life (QOL) is an anticipated benefit of correcting anaemia, but in the CHOIR study there were no differences in QOL in the high Hgb group, in contrast to any other study to date [1]. Levin notes that it is not clear when QOL was measured in the CHOIR study [1], and we noted additional issues. One measure used in the CHOIR study to assess QOL was a disease-specific instrument, the Kidney Disease Questionnaire (KDQ). Unfortunately, the correct reference for the KDQ, developed by Laupacis et al. [3], was not provided. The purpose of the KDQ is to assess five distinct QOL domains found to be salient for CKD patients: physical symptoms, fatigue, depression, relationships with others and frustration. Instead of reporting results for each of the five KDQ domains, however, a KDQ total score was reported for CHOIR participants (Table 2) [2]. In the absence of a well-validated composite score, summing across discrete domains of a QOL measure is meaningless. Moreover, important information on QOL differences among patients participating in the CHOIR study may have been obscured. Change may occur in some domains but not in others, as Foley et al. [4] showed when they used the KDQ in their study of the normalization of Hgb in haemodialysis patients. Continued study of Hgb targets, epoetin alfa use and associated clinical outcomes among CKD patients is important [1], and QOL perceptions, appropriately measured and analysed, can furnish valuable information. Conflict of interest statement. None declared. Nancy Kutner Neisseria-cinerea-induced pulmonary cavitation in a renal transplant patient Sir, Neisseria cinerea is a commensal microbe that colonizes the nasal and oropharynx cavities [1], generally considered to be a non-pathogenic organism. Nevertheless, it has been described as an aetiological agent responsible for various diseases. Herein, we report the first case of N. cinerea related pulmonary cavitation to occur in a male renal transplant patient. A routine chest radiography, performed 16 months after transplantation in a 58-year-old renal transplant patient, revealed the presence of de novo cavitation located in the upper lobe of the right lung. A computed tomography (CT) scan showed a single mass in the right upper lobe with a large cavitation and a thick margin (Figure 1A), without lymphadenopathy. At that time, the patient had been complaining of an intermittent non-productive cough and fatigue for a few days, and a low-degree fever (388C). C-reactive protein was 80 mg/l (N < 15 mg/l), and serum creatinine was unchanged (225 mmol/l). His immunosuppressive therapy was based on the combination of sirolimus (trough level 9 ng/ml) and steroids (5 mg/day). Blood and urine cultures, as well as fluid obtained from gastric aspirations, induced-sputum and bronchoalveolar lavage (BAL) were negative for bacteria, mycobacteria including anti-fast bacilli and fungi (culture and polymerase chain reaction). No anaerobic agent grew on specific culture media. Aspergillus antigenaemia was negative. A transthoracic CT-guided biopsy of the peripheral component of the cavity and an aspiration of fluid were performed (Figure 1B). The fluid aspirated from the cavity was inflammatory. Pathological analysis of the biopsy showed a fibrinoinflammatory pulmonary tissue without any granuloma or malignant cells. The culture of the biopsy grew a Gramnegative, oxidase-positive diplococcus, which was further identified as N. cinerea (Apisystem, BioMe rieux, France). The patient was treated with amoxycillin at 2 g three times per day for 3 weeks. The fever disappeared, and C-reactive protein returned to normal range 9 days later. Another CT scan, performed 15 days after starting amoxycillin therapy, showed that the margins were thinner and the cavitation represented the majority of the lesion (Figure 1C, D). Finally, an antero-posterior chest radiography and a CT scan, performed 3 months after completion of amoxycillin therapy, showed a residual cystic lesion with a thin margin (Figure 1E, F). Close monitoring of Aspergillus antigenaemia at 2-monthly intervals was initiated. After 1 year of follow-up, the patient had not presented with a relapse or any symptomatic pulmonary manifestations, though the cavitation was still evident on the CT scan. The main infectious causes of lung cavitation in transplant recipients are aspergillosis, tuberculosis and nocardiosis [2]. In transplant patients in whom a cavitary lung lesion is demonstrated, if a complete investigation procedure including BAL does not yield a pathogen, one should consider


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Toshiro Sugimoto, Nobuyuki Ogawa, Masahiro Aoyama, Masayoshi Sakaguchi, Keiji Isshiki, Masami Kanasaki, Takashi Uzu, Yoshihiko Nishio, Yutaka Eguchi, Atsunori Kashiwagi. Haemolytic uraemic syndrome complicated with norovirus-associated gastroenteritis, Nephrology Dialysis Transplantation, 2007, 2098-2099, DOI: 10.1093/ndt/gfm104