Renal anaemia is a common and important complication in patients with chronic kidney disease (CKD). The current standard‐of‐care treatment for renal anaemia in CKD patients involves ensuring adequate iron stores and administration of erythropoietin stimulating agents (ESA). Hypoxia inducible factor (HIF) is a key transcription factor primarily involved in the cellular regulation and efficiency of oxygen delivery. Manipulation of the HIF pathway by the use of HIF‐prolyl hydroxylase inhibitors (HIF‐PHI) has emerged as a novel approach for renal anaemia management. Despite it being approved for clinical use in various Asia‐Pacific countries, its novelty mandates the need for nephrologists and clinicians generally in the region to well understand potential benefits and harms when prescribing this class of drug. The Asian Pacific society of nephrology HIF‐PHI Recommendation Committee, formed by a panel of 11 nephrologists from the Asia‐Pacific region who have clinical experience or have been investigators in HIF‐PHI studies, reviewed and deliberated on the clinical and preclinical data concerning HIF‐PHI. This recommendation summarizes the consensus views of the committee regarding the use of HIF‐PHI, taking into account both available data and expert opinion in areas where evidence remains scarce.

Nine (10%) out of 90 hepatitis C virus (HCV) isolates from hepatitis patients and commercial blood donors inThailand were not classifiable into any of genotypes I/la, II/lb, III/2a, IV/2b, V/3a or VI/3b by RT-PCR with type-specific primers deduced from the HCV core gene. These isolates were sequenced over a 1-6 kb stretch of the 5'-terminal sequence and 1.1 kb of the 3'-terminal sequence covering 30 % of the entire genome. Based on two-by-two comparison and phylogenetic analyses of the nine Thailand isolates among themselves and with known full or partial sequences of previously reported HCV isolates, the Thailand isolates were classified into five genotypes not reported previously, viz. 6b, 7c, 7d, 9b and 9c. Along with HCV isolates reported already, they make at least nine major genetic groups of HCV which further break down into at least 28 genotypes with sequence similarity in the E1 gene (576 bp) of ~< 80%. As many more HCV isolates of distinct genotypes are expected to be found throughout the world, it will become increasingly difficult to classify them by comparison of any partial sequences of the genome. Complete sequence data will be required for the full characterization and classification of HCV genotypes.Hepatitis C virus (HCV) is a positive-stranded linear RNA virus of approximately 9500 nucleotides (nt), and is the major causative agent of blood-borne non-A, non-B hepatitis worldwide (for a review, see Houghton et al., 1991). It has a genomic structure and organization resembling those of pestiviruses and ftaviviruses (Miller & Purcell, 1990) with 5' and 3' untranslated regions (UTR) flanking the single open reading frame. The coding area of HCV is divided into nine regions-for core protein, envelope 1 (El) glycoprotein, envelope 2/nonstructural 1 (E2/NSl) glycoprotein, and six nonstructural proteins designated NS2, NS3, NS4a, NS4b, NS5a and NS5b (Houghton eta L, 1991 ;Grakoui et al., 1993).Based on sequence similarity across the entire genome, * Author for correspondence. Fax +81 285 44 1557.The sequences reported in this paper have been deposited in the DDBJ, GenBank and EMBL Nucleotide Sequence Databases (accession nos. D3783%D37841, D37843-D37846, D37848-D37850, D37853-D37855, D37857-D37860, D3786~D37864, D37867, D37869, D38078, D38079). five major HCV genotypes designated I, II, III, IV and V were proposed . Another classification scheme depends on the phylogenetic differences of two tiers, with major types designated 1, 2, 3 etc. which divide into subtypes such as a, b, c etc. (Simmonds et al., 1993). Genotype I corresponds to la, II to lb, III to 2a, IV to 2b and V to 3a. Within the past few years, many HCV variants with substantial sequence divergence have been found, resulting in at least nine major genetic groups/types and 28 genotypes/subtypes (Enomoto et al., 1990;Choo et al., 1991;Mori et al., 1992;Bukh et al., 1993Bukh et al., , 1994Simmonds et al., 1993;Stuyver et al., 1993Stuyver et al., , 1994Okamoto et al., 1990Okamoto et al., , 1992aOkamoto et al., , 1994 Tokita et al., 1994a, b)...

BackgroundNon-steroidal anti-inflammatory drugs (NSAIDs) are one of the most commonly prescribed medications, but they are associated with a number of serious adverse effects, including hypertension, cardiovascular disease, kidney injury and GI complications.ObjectiveTo develop a set of multidisciplinary recommendations for the safe prescription of NSAIDs.MethodsRandomised control trials and observational studies published before January 2018 were reviewed, with 329 papers included for the synthesis of evidence-based recommendations.ResultsWhenever possible, a NSAID should be avoided in patients with treatment-resistant hypertension, high risk of cardiovascular disease and severe chronic kidney disease (CKD). Before treatment with a NSAID is started, blood pressure should be measured, unrecognised CKD should be screened in high risk cases, and unexplained iron-deficiency anaemia should be investigated. For patients with high cardiovascular risk, and if NSAID treatment cannot be avoided, naproxen or celecoxib are preferred. For patients with a moderate risk of peptic ulcer disease, monotherapy with a non-selective NSAID plus a proton pump inhibitor (PPI), or a selective cyclo-oxygenase-2 (COX-2) inhibitor should be used; for those with a high risk of peptic ulcer disease, a selective COX-2 inhibitor plus PPI are needed. For patients with pre-existing hypertension receiving renin-angiotensin system blockers, empirical addition (or increase in the dose) of an antihypertensive agent of a different class should be considered. Blood pressure and renal function should be monitored in most cases.ConclusionNSAIDs are a valuable armamentarium in clinical medicine, but appropriate recognition of high-risk cases, selection of a specific agent, choice of ulcer prophylaxis and monitoring after therapy are necessary to minimise the risk of adverse events.