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BACKGROUND: The prospective Dialysis Outcomes and Practice Patterns Study (DOPPS) has collected data since 2012 in all six Gulf Cooperation Council (GCC) countries (Bahrain, Kuwait, Oman, Qatar, Saudi Arabia, and United Arab Emirates). We report the relationship of PTH with mortality in this largest GCC cohort of patients on hemodialysis studied to date. METHODS: Data were from randomly selected national samples of hemodialysis facilities in GCC-DOPPS phases 5 and 6 (2012–2018). PTH descriptive findings and case mix–adjusted PTH/mortality Cox regression analyses were based on 1825 and 1422 randomly selected patients on hemodialysis, respectively. RESULTS: Mean patient age was 55 years (median dialysis vintage, 2.1 years). Median PTH ranged from 259 pg/ml (UAE) to 437 pg/ml (Kuwait), with 22% having PTH 700 pg/ml. Patients with PTH >700 pg/ml were younger; on dialysis longer; less likely to be diabetic; have urine >200 ml/d; be prescribed 3.5 mEq/L dialysate calcium; had higher mean serum creatinine and phosphate levels; lower white blood cell counts; and more likely to be prescribed cinacalcet, phosphate binders, or IV vitamin D. A U-shaped PTH/mortality relationship was observed with more than two- and 1.5-fold higher adjusted HR of death at PTH >700 pg/ml and 450 pg/ml. Future studies are encouraged for further understanding this PTH/mortality pattern in relationship to unique aspects of the GCC hemodialysis population.

Background Plasma lipid disorders are key risk factors for the development of atherosclerotic cardiovascular disease (ASCVD) and are prevalent in the Middle East, with rates increasing in recent decades. Despite this, no region-specific guidelines for managing plasma lipids exist and there is a lack of use of guidelines developed in other regions. Methods A multidisciplinary panel of regional experts was convened to develop consensus clinical recommendations for the management of plasma lipids in the Middle East. The panel considered existing international guidelines and regional clinical experience to develop recommendations. Results The panel's recommendations include plasma lipid screening, ASCVD risk calculation and treatment considerations. The panel recommend that plasma lipid levels should be measured in all at-risk patients and at regular intervals in all adults from the age of 20years. A scoring system should be used to calculate ASCVD risk that includes known lipid and non-lipid risk factors. Primary treatment targets include low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol. Lifestyle modifications should be first-line treatment for all patients; the first-line pharmacological treatment targeting plasma lipids in patients at moderate-to-high risk of ASCVD is statin therapy, with a number of adjunctive or second-line agents available. Guidance is also provided on the management of underlying conditions and special populations; of particular pertinence in the region are familial hypercholesterolaemia, diabetes and metabolic dyslipidaemia. Conclusions These consensus clinical recommendations provide practicing clinicians with comprehensive, region-specific guidance to improve the detection and management of plasma lipid disorders in patients in the Middle East.

Background: The importance of plasma lipid abnormalities in chronic renal failure (CRF) is well recognized, but surprisingly little attention has been given to the study of some plasma lipid fractions, including cholesteryl esters (CE) and phospholipids, which might be expected to be important factors in the pathogenesis of the disease. Materials and Methods: Fasting blood samples were taken from 25 control subjects and 53 CRF patients (29 predialysis and 24 on hemodialysis). Samples were analyzed for urea nitrogen, creatinine, triacylglycerols, total and individual phospholipids, total and free cholesterol, as well as cholesterol bound to very low-, low- and highdensity lipoproteins (VLDL, LDL and HDL). Plasma CE was calculated and expressed as a percentage of total cholesterol. Results: Over half of the patients had CE levels more than two standard deviations below the control value. In this subgroup of low CE patients, total, LDL- and HDL-cholesterol levels were also significantly lower than for controls, while levels of phosphatidylcholine and lysophosphatidylcholine were decreased and increased, respectively. In patients with high CE, no significant lipid abnormalities were observed. Conclusion: In this study, CE was an excellent marker for lipid disturbances—if CE was high, then the other lipid fractions were normal, but if CE was low, most other lipid fractions were abnormal. The changes noted appear to be consequences of or related to deficiency of the plasma enzyme lecithin-cholesterol acyltransferase. Ann Saudi Med 2001;21(5-6):283-286.

Cardiovascular diseases (CVD) constitute a significant risk and may, in part, explain the high morbidity and mortality rates among haemodialysis (HD) patients. Several studies have implicated reduced insulin like growth factor (IGF-1) levels in the development of CVD. However, it is not clear whether IGF-1, and its relationship with other hormones such as leptin, insulin, and growth hormone (GH), as well as anthropometric variables may explain the high incidence of vascular complications in chronic kidney disease (CKD) patients. This study was designed to measure total serum IGF-1, leptin, insulin and GH levels in CKD patients and in age-matched control subjects and to elucidate the relationship between IGF-1 and GH, leptin, and insulin as well as other known aetiological risk factors for CVD including blood pressure, body mass index (BMI), and age. The study consisted of 50 CKD patients [36 M and 14 F; mean age; 41.8 ± 10.3 years) on maintenance haemodialysis and 50 healthy control subjects (36 M and 14 F; mean age 41.6 ± 10.2 years) matched for age and sex. None of the subject among patients and controls reported either smoking or history of diabetes mellitus. The circulating levels of IGF-1 were significantly lower (P < 0.001) in both male and female patients compared to the control subjects. Moreover, IGF-1 was strongly and inversely correlated with both systolic blood pressure (SBP) (r = −0.360; P < 0.01) and diastolic blood pressure (DBP) (r = −0.512; P < 0.001) in the CKD group, and when the two groups were combined SBP (r = −0.396; P < 0.001) and DBP (r = −0.296; P < 0.01). When adjusted for age, the correlation was more significant, however, when adjusted for BMI no significant correlation was observed between IGF-1 and blood pressure. IGF-1 was inversely correlated with age (r = −0.367; P < 0.01) and BMI (r = −0.310; P < 0.05) in the control group, but not the patient group. In controls and patients, respectively, a positive correlation between leptin and BMI (r = 0.358; P < 0.01; r = 0.640, P < 0.001) was observed. The results show that circulating levels of IGF-1 were significantly lower in CKD patients as compared to healthy normal subjects and were inversely correlated with SBP and DBP independent of age, but not BMI indicative of a strong relationship between cardiovascular risk factors and low IGF-1 levels. Although, the data do not clearly indicate low IGF-1 levels as a cause or an effect of these cardiovascular risk factors, they do point to an interesting relationship between low IGF-1 levels and increased cardiovascular risk factors among CKD patients as compared to age-matched healthy control subjects.

Hepatitis B vaccination is mandatory for all hepatitis B surface antigen (HBsAg)-negative hemodialysis (HD) patients with low hepatitis B surface antibody titers. We report a case of transient hepatitis B surface antigenemia, detected incidentally, in an HD patient after the second dose of Hepatitis B vaccine. The patient had to be isolated on a separate HD machine, in a separate room, until further investigations ruled out a true hepatitis B virus infection. This led to further unnecessary testing and generated great concern and anxiety for the patient. We present this case to emphasize that HD units should be aware of this phenomenon and that HBsAg testing be deferred until 4 weeks after vaccination to avoid HBsAg false positivity.