OBJECTIVE: To study the epidemiologic characteristics and underlying conditions that place pregnant women infected with H1N1 virus at increased risk for being admitted to the intensive care unit (ICU). METHODS: In this cross-sectional study conducted in Porto Alegre, Brazil, with 57 pregnant women hospitalized with the H1N1 influenza during the 2009 pandemic, we collected epidemiologic characteristics and assessed the rates of ICU admission according to pregnancy duration and the presence or absence of comorbidities. RESULTS: The median (range) of maternal age was 26years (15-41years), the pregnancy duration at the time of infection was 29weeks (8-41weeks), and the birth weight was 3180g (740-3900g). Five patients (8.8%) were in the first, 22 (38.6%) in the second, and 30 (52.6%) in the third trimester, and (22.8%) had comorbidities. Antiviral drugs were administered to all, and 46 (80.7%) patients received an early treatment. There were no maternal, fetal, or neonatal deaths. Eight patients (14%) required ICU admission and 15 (50%) of the patients who gave birth during their hospitalization underwent a cesarean delivery. The risk of being treated at the ICU did not increase for patients with comorbidities (P=0.22) or an advanced pregnancy (P=0.31). The study revealed a relationship between early initiation of an antiviral treatment and a lower mortality rate. CONCLUSION: Neither an advanced pregnancy nor comorbidities increased the risk of being admitted to the ICU but, compared with the results of other studies, a prompt treatment lowered mortality.
PMID: 20801449 [PubMed - as supplied by publisher]
BACKGROUND: Complement is a key component of the innate immune system, and variation in genes that regulate its activation is associated with renal and other disease. We aimed to establish the genetic basis for a familial disorder of complement regulation associated with persistent microscopic haematuria, recurrent macroscopic haematuria, glomerulonephritis, and progressive renal failure. METHODS: We sought patients from the West London Renal and Transplant Centre (London, UK) with unusual renal disease and affected family members as a method of identification of new genetic causes of kidney disease. Two families of Cypriot origin were identified in which renal disease was consistent with autosomal dominant transmission and renal biopsy of at least one individual showed C3 glomerulonephritis. A mutation was identified via a genome-wide linkage study and candidate gene analysis. A PCR-based diagnostic test was then developed and used to screen for the mutation in population-based samples and in individuals and families with renal disease. FINDINGS: Occurrence of familial renal disease cosegregated with the same mutation in the complement factor H-related protein 5 gene (CFHR5). In a cohort of 84 Cypriots with unexplained renal disease, four had mutation in CFHR5. Overall, we identified 26 individuals with the mutation and evidence of renal disease from 11 ostensibly unrelated kindreds, including the original two families. A mutant CFHR5 protein present in patient serum had reduced affinity for surface-bound complement. We term this renal disease CFHR5 nephropathy. INTERPRETATION: CFHR5 nephropathy accounts for a substantial burden of renal disease in patients of Cypriot origin and can be diagnosed with a specific molecular test. The high risk of progressive renal disease in carriers of the CFHR5 mutation implies that isolated microscopic haematuria or recurrent macroscopic haematuria should not be regarded as a benign finding in individuals of Cypriot descent. FUNDING: UK Medical Research Council and Wellcome Trust.
PMID: 20800271 [PubMed - as supplied by publisher]
BACKGROUND: Complement is a key component of the innate immune system, and variation in genes that regulate its activation is associated with renal and other disease. We aimed to establish the genetic basis for a familial disorder of complement regulation associated with persistent microscopic haematuria, recurrent macroscopic haematuria, glomerulonephritis, and progressive renal failure. METHODS: We sought patients from the West London Renal and Transplant Centre (London, UK) with unusual renal disease and affected family members as a method of identification of new genetic causes of kidney disease. Two families of Cypriot origin were identified in which renal disease was consistent with autosomal dominant transmission and renal biopsy of at least one individual showed C3 glomerulonephritis. A mutation was identified via a genome-wide linkage study and candidate gene analysis. A PCR-based diagnostic test was then developed and used to screen for the mutation in population-based samples and in individuals and families with renal disease. FINDINGS: Occurrence of familial renal disease cosegregated with the same mutation in the complement factor H-related protein 5 gene (CFHR5). In a cohort of 84 Cypriots with unexplained renal disease, four had mutation in CFHR5. Overall, we identified 26 individuals with the mutation and evidence of renal disease from 11 ostensibly unrelated kindreds, including the original two families. A mutant CFHR5 protein present in patient serum had reduced affinity for surface-bound complement. We term this renal disease CFHR5 nephropathy. INTERPRETATION: CFHR5 nephropathy accounts for a substantial burden of renal disease in patients of Cypriot origin and can be diagnosed with a specific molecular test. The high risk of progressive renal disease in carriers of the CFHR5 mutation implies that isolated microscopic haematuria or recurrent macroscopic haematuria should not be regarded as a benign finding in individuals of Cypriot descent. FUNDING: UK Medical Research Council and Wellcome Trust.
PMID: 20800271 [PubMed - as supplied by publisher]
