Palmer: Case 1: Hyponatremia after traumatic subarachnoid hemorrhage. What is the cause? Case 2: Hyponatremia after trans-urethral resection of the prostate gland. What is the etiology? Why did symptoms worsen with treatment? Case 3. Anion gap metabolic acidosis in a patient with apparently (but not really) compromised bowel. Case 4. Anion gap acidosis in a ventilated patient on lorazepam infusion. Case 5. Extreme hyperkalemia post-operatively in a patient receiving coronary artery bypass surgery. Case 6. Acute renal failure in a post-operative patient after volume expanders. Case 7. Malignant hyperthermia intra-operatively. Case 8. Acute renal failure, anion-gap acidosis, and hyperkalemia post-operatively. Case 9. Hyperkalemia and profound weakness in a post-operative patient. Already know the answers? The CME post-test for this activity will be posted in the coming week.
Got D? Vitamin D in CKD: Is it Helpful? How Much? How Measured?
Clues in Pregnant Hypertensives: Suspects? Venue? Weapons?
Nocturnal and Frequent Dialysis: Are These the Preferred Therapies for Patients with Cardiovascular Disease?
Chan: Cardiovascular risk is greatly increased in stage 5 CKD patients treated with conventional 3x/week schedules. What are the mechanisms whereby more frequent dialysis, either as short daily or long nocturnal, might alter this outcome? What is the impact of these newer dialysis schedules on intradialytic complications? On systolic and diastolic blood pressure? On left ventricular mass index? What are the differences in effect on LVMI between short daily and long nocturnal schedules? What is the relation to control of serum phosphorus? What are the effects of the more frequent schedules on vascular reactivity? Exercise capacity? Inflammatory markers? Endothelial progenitor cell number?
Endothelial Function/Dysfunction: What Does It Mean and Why Does It Matter?
Michael S. Goligorsky, MD, PhD.
Moshe Levi, MD, FAHA, FASN.
Why Does the Glomerulus Leak?
Chavers: What are the factors impacting on sudden death in ESRD patients? What are the demographics? Trends? Is there a race or gender gap? What are the potential causes? What cardiovascular factors are most importantly associated with sudden death? What treatment fators? Which are potentially correctible? What about geographic variation? Do some dialysis chains do better in this area than others?
Tuttle: What are the new KDOQI guidelines regarding treatment of diabetes in CKD patients? How aggressively should we manage hyperglycemia? When should we use insulin? Which oral medications are of use in CKD and ESRD? Which are contraindicated, and why? Which may have special advantages? Which ones require dosage adjustment? What types of combination therapy are useful?
Easom: What are we doing and what could we be doing better? How do we organize a team approach to optimize patient hemogloblins? What is annual blood loss on average, and how does this argue for maintenance iron therapy? How do we use a collaborative approach in implementing change? Juergensen: How can we develop and establish a maintenance IV iron protocol to enhance patient outcomes? How do we pilot new protocols and evaluate their effectiveness? What is an example of a simplified protocol? Amerling: How does emerging outcomes information encourage us to rethink the way we treat patients with anemia? What is a more appropriate anemia treatment paradigm based on new data? What are some illustrative case studies?
Kamyar Kalantar-Zadeh, MD, PhD, MPH.
Kalantar-Zadeh: Is a heavier BMI better in dialysis patients? How can we reconcile this with data in nonuremic patients? Are there other populations where a higher BMI is protective? If so, what are they? What are the possible reasons for so-called reverse epidemiology in terms of BMI? How robust is this data? What are other areas of apparent reverse epidemiology in CKD patients? What are potential physiologic explanations for the high BMI survivor paradox?
Carl M. Kjellstrand, MD, PhD., Rodney S. Kenley, MS, MM.
Fredric O. Finkelstein, MD., John M. Burkart, MD., Salim Mujais, MD., Alexandra Voineseu, MD., Dana Negoi, MD., Martin Schreiber, MD.
Beddhu: Elevated BMI is supposedly a survival factor in ESRD. Is this true in CKD, or is obesity associated with more rapid progression of renal insufficiency? What did the HDFP (Hyperternsion Detection and Follow Up Study) show? The Physician Health Study? Other large databases? What are the potential mechanisms of kidney damage in obesity? What are the roles of hyperfiltration vs. other aspects of the metabolic syndrome as well as inflammatory mediators? What if we control for the degree of insulin resistance using HOMA? Can weight loss affect progression in CKD patients? Is this clinically desirable? CME will be combined with the next week's talk.
Norris: What are the complications associated with cocaine use? What are its pharmacokinetics? What are the renal complications and what is their pathogenetic mechanism? How does cocaine modify the course of CKD in the African Ammerican community? What are cocaine's affects in causing rhabdomyolysis, acute and chronic hypertension? What are its effects on the RAAS, catecholamines, thromboxane, and inflammatory mediators?
Mathers (Dr. Richard Sherman's slides: What is the pathogenesis of hyperphosphatemia in CKD? How well is phosphate controlled? How does mortality relate to serum levels? What are the 3 factors affecting phosphorus control? What does KDOQI say? Which beverages contain lots of phosphate? What is the role of food additives? How much is removed during dialysis? How is compliance affected by pill burden?
Mathers: What are the various phosphate binder options? What are the advantages and disadvantages of each? How do the non-calcium binders compare? How is binding affected by pH? To what extent is it specific? How is choice of binder related to pill burden? How can nurses become patient advocates against hyperphosphatemia?
Sally Burrows-Hudson, MS, RN, CNN; Carol Headley, DNSc, RN, CNN; Sally Campoy, DNP(c), MS, APRN, BC.
Burrows-Hudson: What is the importance of Standards of Practice and Guidelines for Care in the nursing care of patients withe CKD? What are the traditional and non-traditional risk factors for cardiovascular disease? Headley: What is the role of controlling blood pressure and minimizing proteinuria in CKD? What is the nurse's role? What are the recommended lifestyle modifications and pharmaceutical drugs? How is bone metabolism altered? How does this affect calcification and vascular risk? What are the specific dangers of calcification in terms of the cardiovascular system? Campoy: How does anemia impact on cardiovascular disease in CKD? What are potential benefits of anemia treatment? What are the potential risks, and what are the newer target Hb values given the results of the CHOIR and CREATE studies? What is the new 2007 KDOQI recommendation? What are the disorders of cholesterol and triglycerides in CKD patients? When should they be treated, and to what serum levels?
Perazella: What are the renal issues pertaining to proton-pump inhibitors. Do they affect potassium or proton secretion in the kidney? How are they metabolized? What implications are there for interactions with calcineurin inhibitors? How does their metabolism differ in terms of P450 enzymes? How frequently do they cause acute interstitial nephritis? What are the clinical features? Is steroid treatment beneficial? To what extent is this a clinically significant problem? CME: Will become active next week, as this talk is grouped with the one that follows it.
ASDIN 3rd Annual Meeting. American Society of Diagnostic and Interventional Nephrology. April, 2007. Part 6 of 7. Note: Access is FREE for ASDIN members.
Vascular Access Education: Do we need this tool?
Sodium Profiling: The Key to Reducing Symptoms of Dialysis?
Burkart: Why do so few patients remain on PD after 5 or 10 years? What are the main reasons leading to technique failure? What characterizes patients who do remain on PD for the long-term? How does peritoneal transport change over time, and how is this affected by glucose load, glucose degradation products, and use of icodextrin? What are the current theories relating to AGE and inflammatory mediators in causing peritoneal membrane changes over time, including those of peritoneal sclerosis?
Central Venous Stenosis: To Stent or Not to Stent?
Basilic Fistulae: Is Superficialization Needed?
Does Hemodynamic Assessment During Angioplasty Help?
Peri-anastomotic Stenosis: Surgery or PTA?
Cephalic Arch Stenosis: PTA, Stent or Surgical Revision?
Secondary Arteriovenous Fistulae: How to Find Candidates and When to Convert Them?
Vascular Access Research: What Do We Need?
Hise: What are the requirements for a successful vaccine? How does a vaccine interact with T and B cells? What is the history behind Staphylococcal vaccine trials in dialysis patients? What did the NEJM study show? How can we explain the results? Were there promising indications of future success? What happened with the confirmatory study of StaphVax™? What are the current staphylococcal vaccines under development? What is the role of intravenous Staph. aureus immune globulin?
ASDIN 3rd Annual Meeting. American Society of Diagnostic and Interventional Nephrology. April, 2007. Part 5 of 7. Note: Access is FREE for ASDIN members.
Toto RD, De Zeeuw D, Singh AK, Weir MR, Falkner BE, Townsend RR, Norris KC, August P, Sarnak MJ, London GM, Shlipak MG, Kramer HJ, Tuttle KR, Calhoun DA, Dworkin LD.
Lentino: At least 7 new antibiotics (not all approved by the FDA) are available for certain indications in patients infected with VRE or MRSA who either fail vancomycin treatment or need alternative treatment: Quinupristin/dalfopristin, linezolid, daptomycin, tigeycline, dalbavancin, oritavancin, and teicoplanin. What are potential indications for each of these? What particular resistant organisms is each one good against? Bad against? Which are not indicated for treatment of pneumonia? What are their peculiar side effects?
ASDIN 3rd Annual Meeting. American Society of Diagnostic and Interventional Nephrology. April, 2007. Part 4 of 7.. Note: Access is FREE for ASDIN members.
Pflederer TA, Miller PL, Lewis JL, Beathard GA, Abreo KD, Miller KA, Work J, Saad TF, Neill WC, Mishler RE, Hoggard JG, Samaha AL, Urbanes AQ, Brouwer DJ, Francisco LL, Krivitski NM, Besarab A, Asif A.
Cantley LG, Krause D, Kaushansky K, Fuller MT, Li L, Blanpain C, Rao M, Rosenberg ME, Yoder MC, Prockop DJ, Singla DK, Horwitz E, Grompe M, Crooks GM, Bonventre JV, Stappenback T, Lavik, E.
Allon: How has fistula first affected the rate of catheter insertions? How do we handle an infected catheter - what are the options? What are the causative organisms? What should coverage be? How can catheter lock solutions be used to help manage an infected catheter? What was the success rate at University of Alabama Birmingham? At other institutions? How easy is it to use catheter lock solutions? What is the protocol? When should the catheter absolutely be removed?
ASDIN 3rd Annual Meeting. American Society of Diagnostic and Interventional Nephrology. April, 2007. Part Three. Note: Access is FREE for ASDIN members.
Murray PT, Matthay M, Chawla LS, Tolwani AJ, Corwin HL, Davenport A, Mehta RL, Star RA, Palevsky PM, Paganini EP, Marshall MR, Goldstein S, Dowling TC, Goldfarb DS.
Hans Henrik Parving, MD, and Geroge Bakris, MD.
Parving: Four studies have questioned the renoprotective effects of ACE inhibitors. What are their potential weaknesses? What are the different stages of renoprotection, and which trials studied which stage? Should all type 1 diabetic patients receive ACE inhibitors? What did BENEDICT, IRMA2, RENAAL, and IDNT show? What do observational data of Danish patients show in terms of median survival time of type 1 diabetics treated with ACE inhibitors? Bakris: To what extent is microalbuminuria a cardiovascular marker in addition to being a renal progression marker? How important is the level of blood pressure control? Do ACE-I or ARBs affect eGFR, or only proteinuria? What did we learn from the ABCD trial, form ALLHAT, and from other similar studies?
ASDIN 3rd Annual Meeting. American Society of Diagnostic and Interventional Nephrology. April, 2007. Part Two. Note: Access is FREE for ASDIN members.
Thrombectomy of an AVG: What Technique to Use?
Are Calcineurin Inhibitors Still Useful in Transplantation?
Does Fetal Programming Influence Adult Hypertension?
Jay B. Wish, MD; William M. McClellan, Jr, MD; Richard A Lafayette, MD.
Wish: Framing the issues. Consequences of anemia. Anemia as a mortality multiplier. Importance of RCTs. Current state of K/DOQI guidelines and their anticipated revision. McClellan: Impact on Patient Outcomes and Health Care Costs. What is the prevalence of anemia in CKD patients? What is the economic burden of untreated anemia in elderly patients with CKD? What do the quality of life studies show? What do observational studies show in terms of anemia, CVD risk, and risk of progression? Wish (again): What is the rationale for early anemia treatment? How have the results from CHOIR and CREATE affected our target Hb levels? How do we define anemia? What are the K/DOQI 2006 opinions? What did a meta-analysis of RCTs prior to CHOIR and CREATE show? What did CHOIR show? What did CREATE show? What do the now RCTs mean? Lafayette: How often should we dose ESAs to treat anemia? How do the different available ESAs differ in this regard? What are the results with less frequent dosing of epoetin alfa? Darbepoetin alfa? What did the POWER, RAPID, and PROMPT studies show? How much do ESAs cost in an ambulatory setting? In a hospital setting? What are cost comparisons between darbepoetin and epoetin alfa? How do we minimize cycling when using the new, lower Hb targets?
Improving Efficiency in the Nephrologist's Office. Part Two of Two.
ASDIN 3rd Annual Meeting. American Society of Diagnostic and Interventional Nephrology. April, 2007. Part One. Note: Access is FREE for ASDIN members.
Estimating GFR - Quo Vadis?
Molecular Traffic Jams: Cargo No-Go?
Improving Efficiency in the Nephrologist's Office. Part One of Two.
RRI RRI Ninth International Conference on Dialysis, January, 2007. Part Four.
Motto DG, Asahara T, Ponticelli C.
Wetmore JB, Stenvinkel P, Hung AM, Schindler R.
Epithelial-Mesenchymal Transition in Fibrosis: Whither the Controversy?
Morrissey JJ, Liu Y, Lovett DH, Barnes JL, Kriz W.
Heeger PS, Quigg RJ, Morgan BP.
Quaggin SE, Igarashi P, Lieberman J.
Towler DA, Shanahan CM, Hruska KA.
Redd M, Serhan CN, Hirschberg RR.
Levin A, Van Wyck DB, Nelson RG, Depner TA, Besarab A.
Ghabrial A, Kreidberj JA, Tufro A.
Kaufman T, Pontoglio M, Yoder BK, Bell PD.
RRI RRI Ninth International Conference on Dialysis, January, 2007. Part Three.
Biofilms are everywhere: What is its relevance for CKD, PD and HD?
Hartmut H. Malluche, MD, Stuart M. Sprague, DO, and Dennis L. Andress, MD (Moderator: Peter Salgo, MD).
Malluche: Case of a patient with calciphylaxis. How do we approach this case? What is the changing picture of metabolic bone disease in CKD during the past 5-10 years? How is bone turnover linked to vascular calcification? How good is PTH as a method of diagnosing bone turnover? What effects do lanthanum-containing Pi binders have on serum Pi, Ca, and PTH? On bone turnover markers? Sprague: Case of a young male with periarticular shoulder calcification. How does PTH associate with death risk in CKD patients? How do calcification types differ, and what is the relationship to mortality with each type in CKD? What are factors affecting vascular calcification? How do calcium-containing binders vs. non-calcium containing binders affect vascular calcification? What did the DCOR study show? DOPPS? Is there an effect on mortality? Andress: Vitamin D has a primary role in control of PTH. What other organs have the Vitamin D receptor (VDR)? How do different activators of VDR differ? What do studies show regarding mortality vs. use of VDR activators? What effect do VDR activators have on bone mineral density?
Then we have discussion, peer exchange, and more discussion, all archived from the original Medical Crossfire video. All discussions have been transcribed and separated out for ease of use.
RRI RRI Ninth International Conference on Dialysis, January, 2007. Part Two.
Robert W. Schrier, MD, and Arthur Greenberg, MD.
(ASN Renal Week, Official Symposium. November, 2006.) Schrier: Who were the key players in discovering the osmotic and non-osmotic pathways of vasopressin release, the structure of AVP, the V2 receptor, the aquaporin channel, and the first orally- acting nonpeptide V2-receptor antagonist? How does vasopressin regulate aquaporin expression and trafficking in the nephron? Which mutations cause diabetes insipidus? What is the mechanism of the urinary concentrating and free water excretion defects in primary polydypsia? In hypothyroidism? In glucocorticoid deficiency? In mineralocorticoid deficiency? Pregnancy? How is AQP2 involved in all of these conditions? How is AQP2 involved in acquired, nephrogenic diabetes insipidus? How are vasopressin and AQP2 involved in the hyponatremia and water excretion deficits associated with heart failure and liver cirrhosis? What effect do V2-receptor antagonists have in these conditions, and what are their effects on AQP2? Greenberg: What are the vasopressin receptor subtypes, where does each act? Which V-receptor antagonists are specific for V2? What effects do vasopressin (VR) antagonists have treating the hyponatremia and free water excretion deficits associated with SIADH, congestive heart failure, and cirrhosis? What did the SALT-1 and SALT-2 trials show? What are the risks associated with rapid correction of hyponatremia? What are safe correction rates? How do VR-antagonists fit into this? What is an overall diagnostic approach to hyponatremia?
George Kaysen, MD, PhD; Mark Sarnak, MD; Peter Stenvinkel, MD, PhD.
(ASN Renal Week, Official Symposium. November, 2006.) Kaysen: Biomarkers - To what extent does CRP give additional prognostic info apart from traditional risk factors like LDL cholesterol and in ESRD patients, low serum albumin? Are there other, better markers? Especially, IL-6? How does EPO/Hct ratio correlate with inflammatory markers and survival? Sarnak: Is CRP higher in CKD patients or isn't it? Do elevated levels in pre-ESRD patients predict progression or incident hypertension? To what extent to inflammatory markers perdict cardiovascular disease outcomes in CKD patients? Stenvinkel: Eating nuts, soy, or fish: do such dietary changes impact on inflammatory markers or outcomes? What is the effect of statins on CRP and other inflammatory markers in CKD? ACE inhibitors? What is the alpha vs. gamma tocopherol story? How do heparin, N-acetylcysteine, sevelamer and PPAR-gamma activators impact on inflammatory markers? Are there outcomes studies showing that lowering CRP in CKD is of clinical benefit?
(ASN Renal Week, Official Symposium. November, 2006.) Gaston: How has our view of CMV evolved from 1964 to the present? What are the direct vs. indirect effects of CMV infection in transplant recipients? What is the impact of CMV infection or CMV prophylaxis on acute rejection? On long-term allograft function? On metabolic syndrome and post-transplant diabetes? On secondary viral and bacterial infection? On post-transplant lymphoproliferative disorder? Brennan: To what extent does CMV prophylaxis prevent vs. delay post-transplant CMV disease? What is a pre-emptive vs. a prophylactic strategy? Is a pre-emptive strategy better? Is it cheaper?
Should We Change Our Organ Allocation Policies for Kidney Transplantation?
Berns JS, Bruggeman LA, Gharavi AB, Alpers CE.
(ASN Board Review Course, 2006).
Drs. Berls and Stokes present their interesting patients: (1) A woman with flank pain on heparin with hypotension and hyponatremia; (2) a middle-aged male with nephrotic syndrome and severe edema (how would you manage his refractory edema?); (3) Hyponatremia and elevated urinary sodium excretion after subarachnoid hemorrhage. What equation does one use to correct sodium in patients with hyponatremia? (4) Woman with progressive edema and dyspnea. Why does she have edema? (5) Woman with chronic diuretic use and now diuretic-dependent edema without obvious cause.
The CKD that Follows Renal Transplantation: How to Best Manage these Patients?
Anil Chandraker, MD; Warren Kupin, MD; Moderator: Gabe Danovitch, MD.
(ASN Renal Week Official Symposium, 2006).
Chandraker: The long-term survival of allografts has not improved. What is the pathogenesis of chronic allograft nephropathy (CAN) and dysfunction (CAD)? How is the changing (decreasing) quality of organ donors (brain-dead donors, expanded criteria donors) affecting this? What alloantigen-dependent factors affect CAD? How are HLA antibodies involved? What are the main alloantigen- independent factors? How can we mitigate these? How does hyperlipidemia impact on CAD? What are the mechanisms? How is CKD after transplant different from CKD in predialysis patients? Kupin: What is the prevalence of stage 3 and 4 CKD after kidney transplant? After transplantation of other organs? What are the new KDIGO staging recommendations? How should we treat hypertension after transplant? Which CCBs? Are ACE-Is and ARBs particularly beneficial? How prevalent is anemia post-transplant? Are there any particular immunologic concerns related to EPO use? How aggressively should we manage lipids? How do immunosuppressive drugs impact on this? What is the latest info on how best to manage post-transplant bone disease (osteoporosis, hyperparathyroidism)?
Olson: Biopsy interpretation depends on circumstances and time frame. First two weeks, first 6 months, and months to years after transplant, one tends to think of different causalities. What does acute humoral rejection look like? What about acute rejection? How do we use the Banff and CCTT classifications? What about ATN post-transplant? How do we identify calcineurin inhibitor nephrotoxicity? Renal toxicity due to OKT3? Rapamycin? IVIG? Acute interstitial nephritis due to antibiotics? How do we approach polyomavirus nephropathy? What are the findings we can expect in biopsies taken months to years after transplant? What characterizes CAN? Recurrent disease, esp. FSGS? Diabets? Anti-GBM in Alport syndrome? Post-transplant lymphoproliferative disorder?
The New KDOQI Guidelines for Anemia, a Debate: Should the Upper Hgb Limit be 12 or 13 g/dL?
Allen Nissenson, MD; Daniel Coyne, MD; Moderator: Brian Pereira, MD.
Nissenson: What should the lower Hgb limit be? What do the May 2006 KDOQI guidelines recommend? What do the CPRs recommend regarding an upper limit? What do CARI, the Canadians, and the Europeans recommend? Which clinical outcome may continue to improve at higher Hgb levels? What might be the benefits of raising the upper limit to 13? What would be the potential risks? What did the Besarab and Parfrey RCTs show? What parts of CREATE and CHOIR are relevant to the debate? Coyne: Is a target between 11 and 12 too narrow? What is the evidence that an upper level of > 13 may be associated with harm? Is there evidence that QOL is benefited at a target of 12-13 vs. a target of 11-12?
Hudson: What are signs and symptoms of anemia? What is the economic impact of anemia? What are the basics of erythropoiesis in CKD patients? How does functional iron deficiency arise? How do we measure iron deficiency? What are limitations of the TSAT and serum ferritin? What is the pharmacokinetics of IV iron compounds? What are the label-approved indications? What are their safety profiles? What effect does iron therapy have on ESA requirements? What are the relevant pharmacoeconomic considerations?
Debates in Renal Failure: Calcimimetics: Are They Effective Treatment for Secondary Hyperparathyroidism in Patients with Chronic Kidney Disease (CKD)?
Calcimimetics: Monotherapy for Secondary Hyperparathyroidism?
Goodman: What is the conventional approach for managing secondary hyperparathyroidism, involving control of phosphate and use of vitamin D? To what extent does the conventional approach fail to achieve KDOQI Ca, Pi, and PTH targets? What is the calcium-sensing receptor, how to its allosteric activators work, and how does this interact with the physiology of the parathyroid cell? What effects does cinacalcet have on serum Ca, Pi, and PTH, and how is this modulated by usage of vitamin D and degree of hyperparathyroidism? When might we use cinacalcet in patients already on vitamin D? When might we use it as monotherapy? What are potential pitfalls in use of cinacalcet? What is a rational algorithm for its use?
Ronald J. Falk, MD; Gerald B. Appel, MD.
Falk: What are the current views regarding pathogenesis of SLE? What genetic predispositions have been identified? What potentially could cause a relapse? How do we define remission in lupus, and how do we define a relapse? What have been definitions given in the literature? What are serologic and urinary clues to relapse? How do we distinguish between relapse and smouldering disease? Appel: What did the early NIH trials tell us about the best lupus regimens in terms of relapse? What regimen did the Euro-lupus trial use, and what did they find regarding relapses? What did we learn from studies recently published in the New England Journal of Medicine by Contreras et al, and by Ginzler et al? What is my personal approach to treating lupus flares?
(ASN Board Review Course, 2006). Townsend: Renin system activation, mineralocorticoid excess states, pheo, aortic coarctation, and primary renal disease are the main types. What is the best means to diagnose renovascular HTN? What are less common types of RV HTN? How do we approach low renin, high aldo HTN? What are diagnostic criteria (aldo/renin ratios, urinary aldos, etc.), and what are the treatment options besides surgery? How do we approach Cushing's, pheo, and hyper- and hypothyroidism and HTN? What are the main genetic disorders? Liddle, GRH, activating MR receptor mutations, and 11-beta-hydroxysteroid dehydrogenase? What is Gordon's syndrome? What are the main drug-induced causes, including anti-angiogenesis agents? What's new in treating HTN associated with CKD?
John W. Adamson, MD; Stephen Fishbane, MD; Ajay K. Singh, MB, MRCP; (Moderator: Jay Wish, MD).
(ASN Renal Week Official Symposium, 2006). Adamson: What controls iron accumulation in the liver? What is hepcidin, and how do hepcidin knockouts or gain of function mutations affect gut absorption of iron and release of iron from the RE system? Fishbane: What happens to ferritin and TSAT as GFR falls? What was the thinking behind the upper ferritin limit of 500 ng/mL in the KDOQI Workgroup? How is reduced serum iron during inflammation an adaptive response? How is hepcidin involved in all of this? What did the DRIVE study results show in terms of giving IV iron to patients with moderately elevated serum ferritin levels? Singh: Glycosylate, pegylate ... what are the strategies to increase ESA half-life? Why does CERA have such a long half-life? How is EPO receptor affinity involved? What is HIF? How does it affect EPO synthesis, and how do prolyl hydroxylase inhibitors affect HIF and EPO? How might hepcidin fit into this?
Coyne: Where is magnesium stored in the body? What governs absorption by the GI tract? How is magnesium handled in the kidney? In what tubular segments is excretion regulated? What is the role of paracellin? Of the calcium-sensing receptor? Which diuretic class reduces magnesium excretion? What are the effects of Gitelman and Bartter syndromes? What are the important genetic abnormatlities? What are the consequences of hypopmagnesemia? How do we diagnose and treat? What are effects of hypermagnesemia, and how do we treat that? (ASN Board Review Course, 2006).
Foley: How are classic and novel risk factors related to outcome in CKD patients as well as in dialysis patients? What can we learn from Framingham data? From NHANES? Which of the classical risk factors works in the opposite direction when GFR is low? To what extent have patients with mild-moderate CKD been excluded from the major cardiovascular trials? What can we learn from analysis of these subsets? How do the observational data differ from randomized, controlled trials?
Sica: How are the pathogenses of CKD and CVD (cardiovascular disease) related? Where do both impact the RAS (renin-angiotensin system)? How does ACE inhibition affect different parts of the cardiovascular system? What conclusions can we draw from AASK? How can we rationally choose drugs from different classes to treat hypertension? How should different calcium-blockers and ACE inhibitors be used in CKD? How do ACE inhibitors and ARBs compare? (ASN Renal Week Official Symposium, 2006).
Iron Management: We Can Do More!
Bennett: What is the basis for the standard immunosuppression protocols in use currently? When do we use lymphocyte depleting agents or anti-IL2 monoclonal antibodies? How do we assess immunologic and non-immunologic risk and tailor immunosuppression accordingly? Which is better, cyclosporin or tacrolimus, and how is each drug best monitored? What is the basis for chronic allograft nephropathy, and how can we prevent and treat this? What is the state of knowledge regarding steroid avoidance or reduction regiments? When is it appropriate to reduce or eliminate calcineurin inhibitors from the mix? What are indications for expanded criteria donor kidneys? What are the transplant complications relating to osteoporosis, uric acid, and electrolyte disorders? How do we prevent or lower the risk for anemia and cancer? How do we approach fever in the transplant recipient? How do we treat polyomavirus nephropathy? What are the drug interactions among immunosuppressive medications? (ASN Board Review Course, 2006).
Sweeny: For those who did not know this, the National Association of Nephrology Technicians / Technologists has an excellent annual meeting. We are happy to archive one of the talks from the 2006 meeting focusing on technology by a person who has a long experience in the field. How has dialysis therapy evolved and how have membranes changed? What are the potential benefits of on-line hemodiafiltration and hemofiltration? What are the trends and challenges relating to use of ultrapure water for dialysis solution production? How can one practically implement a double-dialyzer solution to treat larger patients, both in-series and in-parallel? How does blood volume monitoring work and when is it useful? When is bioimpedance useful to determine patient fluid status? How can one measure clearance on-line using conductivity? What is being overlooked today and what are the keys to the future? Access to this talk is free for all members of NANT. Please contact the NANT office for the access code. (NANT Annual Meeting, 2006).
Frequent Dialysis: Does It Have to Be Daily?


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Home » Business » Sharjah International Air Port
Sharjah International Airport
Sharjah International Airport's design reflects traditional Islamic architecture and is one of the most modern in the region, offering state-of-the art facilities. Situated approximately 10 km from Sharjah town, it is linked by a four lane highway with Port Khalid and Port Khorfakkan, as well as the other Emirates.
The airport boasts modern passenger handling facilities and has an annual capacity of over 2.5 million passengers. The terminal is designed for ultimate comfort and convenience and is comparable to the best in the world.
The Airport's main features include jet ways to the aircraft, full passenger services, including air-conditioned waiting lounges, well-equipped duty-free areas, banks, rent-a-car companies, hotel reservations, restaurants, a well-appointed Airport Hotel and excellent transit facilities with a minimum turnaround time. Apart from these, the Airport boasts modernized first class and business class lounges have been modernized, well coordinated ground services and a high standard of aircraft line maintenance.
Cargo handling facilities include four warehouses, each with a 7,400 sq. meters storage space, separate cargo apron for up to 6 aircraft, 24-hour customs clearance, free zone facilities and speedy and efficient document procedures.The airport handles the largest amount of air cargo in the Middle East and is the main air cargo handling center for Lufthansa Cargo in the region.
Warehouses offer the customer security for his shipment and protect it against cargo handling irregularity, including theft. The warehousing facilities may be utilized as a distribution center for the Gulf. For those operating from Sharjah, goods can be stored at the airport without incurring any liability for duties, unless the goods are for internal distribution, Foreign goods may be stored safely for re-export. Furthermore a repair and spare parts service is offered on a worldwide scale.
The airports facilities have recently been upgraded. The runway has been extended of by 300 meters, making the complete distance available for take off of an aircraft 4060 meters and a 3 site runaway visual range system has been installed. There are individual packages available, tailored to meet the needs of different companies by offering flexible facilities, the airport promises the best possible assistance to companies.
Click here to go to the official Sharjah Airport website
PO Box 8, Sharjah, United Arab Emirates
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A Twitter friend, @ArcturusOrdo sent me the following image and poem from his 4th book, "Yuletide Sequence".
Calamity Politics is a Progressive on-line news magazine focusing on the Washington DC nightmare with caustic comment and mildly jaundiced opinion. Join the Resistance.
Our image of Santa is pretty much the result of an effective advertising campaign. Santa Claus wasn't always a rotund omniscient gift-giver who circumvents the world on December 25th propelled by flying reindeer, assisted by an army of adorable elves. The Santa we know today, a jolly man in a red suit and full white beard was the vision of Haddon Sundblom. Sundblom was commissioned in 1930 to develop advertising images for Coca-Cola to use during the next Christmas season. Sundblom used the 1822 classic poem "A Visit From St. Nick" by Clement Clark Moore as his inspiration for his new image of Santa Claus. Previous images of St. Nicholas had ranged from a tall gaunt religious man to a tiny elf creature. Moore and Sundblom together created the image of our Santa as a warm, friendly, pleasantly plump humanoid.
The historical basis of Santa Claus is St. Nicholas. St. Nicholas was the renowned Bishop of Myra-a Roman town near Demire, Turkey, around 300 A.D. St. Nicholas even before he was appointed Bishop was known for his generosity. A well told story was one in which he came to the assistance of a poor man who could not afford a proper dowry to marry off his three daughters. In those times, it would mean that the daughters would remain unmarried, making it likely they'd be forced into prostitution. St. Nicholas wanted to spare the family any embarrassment yet wanting to help, he traveled to the man's house in the dark of night, and threw three purses filled with gold coins through the peasant's window.
After St. Nicholas died he became a beloved patron saint, but during the Protestant Reformation of the 16th century, the importance of Catholic saints was rejected and St. Nicholas' popularity dwindled across Europe. However, in the Netherlands he remained popular, living on as a mythical figure, known as Sinterklass, who went from house to house on the eve of St. Nicholas's name day, December 5th, leaving treats and gifts for children. Sinterklaas traditionally wore red bishop's clothes and employed elves, and he traveled with horses that could walk across rooftops.
When the Dutch emigrated in droves to America during the 17th and 18th centuries, they brought the kindly St. Nick to the new colonies, but it wasn't until the 1930's that Coke and Sundblom introduced today's version of the beloved winter visitor.
Calamity Politics is a Progressive on-line news magazine featuring news of the day accompanied by comment and opinion.
The story featured 4 amazing women from 81-87 years of age. Each of the women offered 3 stay young secrets. I thought they were good enough to share with my friends.
1.) Spend time with people of various ages. Having a broad social network helps you to feel and act younger, it helps you keep in mind that age is just a number.
2.) Recognize that some aches and pains are normal and natural. It is your body giving you feedback. Listen to it and change , but don't stop moving.
3) Exercise your brain. Stay engaged intellectually. Volunteer. Do crossword puzzles.
2.) Go meatless. Ruth states it is the most important health change she has ever made.
3.) Focus on the rewards. Exercise improves sleep, lowers blood pressure, reverses Type 2 diabetes, prevents heart disease and osteoporosis.
3.) Believe in yourself. "We are all capable of far more than we think we are, instead of saying 'I can't' say 'I'll try.' Those words can make all the difference.
Wow. Some pretty insightful suggestions. I think the information is as good for a 25-year-old as an 80-year-old.
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Habits affect us in every aspect of our lives, home, school, work, church. It could be nail-biting, thumb-sucking, over eating, procrastination, avoidance. Each one of us has habits we wish we could break. How do we escape these unwanted behaviors, when often we do not understand the basis of the behavior?
The first part of Duhigg's book investigates the "habit loop." The habit loop comprises the "cue" (the situation that stimulates the habitual behavior), the "routine" (the behavior or activity) and the "reward" (the emotional satisfaction resulting from engaging in the behavior).
Duhigg also takes a look at the habits of successful organizations. As a business owner, the habits you instill in your staff go a long way in determining the success of the venture. He looks at organizations as big as Target and as intimate as the structure of NFL teams. It is the owner's job to create positive habits in the staff. If as an owner, you notice a way to replace a bad operational habit with a good one, you have the ability to improve productivity and employee happiness.
Duhigg details four steps to changing any habit. 1.) Pinpoint the "routine" (the habit) 2.) Examine the "reward" that the behavior provides 3.) Isolate the situations that "cue" the unwanted behavior 4.) Develop a "plan" to change the behavior.
Lastly, Duhigg says, "You have to actually believe in your capacity to change for habits to permanently change." With the tools and examples provided in "The Power Of Habit" you should be able to take control of habits you thought were unbreakable. In business and life the ability to change unwanted behaviors is a valuable asset.
Many years ago when I was taking a graduate psychology class I participated in a stop smoking study. The study was very simple. Each participant kept a "smoking journal." We were required to make a note of the emotion experienced when we felt the desire to have a cigarette (the cue/trigger), the action itself (the behavior), and how we felt after the cigarette (the reward).
We were required to journal for six weeks. At the end of the six-week period we met with the study designer and talked about our experience, and designed a plan to stop smoking based solely on the journaling information. This all took place forty years ago, but even now I can remember how amazed I was with my reactions to the journaling experience. First, the journaling made me intently aware of the behavior. Second, I became aware for the first time the situations that triggered the habit. Third, I became aware of the reward. And, lastly, with the information I had learned about the behavior I was able to create a plan to change the undesirable activity.
If I had not participated in that study I may never have been able to quit smoking, but with the isolation of the "behavior loop" it was easy. In fact, by the end of the six weeks I had stopped smoking and have never smoked again. So, like Duhigg says, break the loop.
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I love week ends. On Fall and Winter days I hang out with the dog, drink Irish coffees and watch old movies. On Sundays I try to think of things that make me smile. Here are my 27 things to make you smile.
That's it. Thanks for joining me for a few smiles.
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The time commitment required for a new puppy is often ignored. Before you start looking for that new pup, make sure that you have the time and the energy required to daily commit to your new best buddy. Puppies will need to go out every hour until they are house trained. You or your children will need to be ready to commit no less than two hours daily for play, exercise, socialization and stimulation. Additionally, puppies because they are rapidly growing, need to be fed and watered three times a day.
I was getting packed for my third move in two years. I know, too many, too often, but it was a strange set of circumstances and not worth talking about here. Usually I just go into the bathroom and dump the drawers into a box and then sweep the contents of the cabinet shelves into another box, and voila, the bathroom is packed. But, I picked up the first bottle, a bottle of Aspirin and glanced at the expiration date. Holy Moly, it had expired three years ago. That knowledge shook me up a bit. The next bottle, a prescription for Flexeril, was outdated by 10 months. I was two for two. Not good. Next, was a bottle of cough syrup, expired the previous year. I was batting 100%.
If your medicine chest is full of outdated medications or medications you no longer need and you are wondering how to dispose of them I have some information for you. The best option is to use community-based drug disposal programs. Go to the DEA (Drug Enforcement Agency) website, dea.gov and use their search tool to find an authorized drug disposal collector in your area.
If you don't find a program in your area call your local police department or country sheriff. Often these law enforcement centers have disposal programs. As a last resort you may be forced to dispose of them yourself. Please do not flush down the toilet, or sink. These toxins are dangerous to animals, fish and water systems.
Many medications include specific disposal instructions, please follow any specific disposal instructions. The FDA advises that if there are no disposal instructions, do as follows: If the medication is tablets, crush thoroughly. If medication is capsules, open capsules and release contents. 1). Mix medication with used coffee grounds, kitty litter or dirt/sand to disguise the medication making it less desirable to children, pets and drug seekers. 2). Place the mixture in a sealable bag, empty can or other container to prevent the medication from leaking out of the garbage bag. 3) Be sure to obliterate any personal information on the prescription bottle to protect your identity and health information.
Hope this little piece of life experience helps you think before you just toss medication into the trash, or flush it down the toilet. Be a good citizen, dispose of drugs responsibly.
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If you have ever watched "Tiny House Nation" or "Tiny House" you have seen a growing trend in the United States toward minimalist living. Many people are attracted to the prospect of financial freedom, a simpler lifestyle, and a smaller human environmental footprint. The downsize revolution promotes living structures with sizes between 300 and 700 square feet. In general, the tiny home is 400 sq. ft or less. In some cases, the homes are even on wheels. Despite the stated positives, they are not for everyone.
Small does not necessarily equate with cheap. A tiny house can cost anywhere from $10,000 to $150,000. Holy Moly. The cost is dependent on a series of factors: location, building complexity, materials, and finally are you doing it yourself, or are you having it built. A contractor construction package will generally cost twice as much as a "do it yourself" house.
Not always identified, but a serious matter, are the extra building costs for appliances, fixtures, water heaters and heating & cooling systems because of their reduced size. The rule it seems is that the smaller, the more expensive. It is important that you do some very careful figuring before you commit yourself to building a tiny home. One recommendation would be to get a minimum of three bids. Many builders do sizeable markups on small projects.
Before you decide to DIY you need to understand that construction of a tiny home can take from three to six months if you are working at it full-time. When taking on such a project you should take into consideration that while you are trying to save money on contractors you need to account for the money you won't be earning while you are acting as your own contractor. And, unless you are an experienced carpenter the frustration and potential areas of significant error should be added into your equation. Weigh those pros and cons carefully.
There are pre-fab tiny homes being made, but this is a case where buyer beware. Avoid potential pitfalls by making sure the NOAH (National Organization of Alternative Housing) certifies the plan and the builder. Things like windows, framing, roofing, insulation, become very expensive if you need to go back and fix things done incorrectly the first time.
I know it looks like fun, and even exciting when seen on TV, but before you commit the time, energy, and money required to build a tiny house, please do some big time research. Self education is essential before you go tiny. This should not be a decision made one Sunday night after watching a television show. There are books, magazines, videos, workshops and even Facebook groups which provide excellent information.
I saw one article where the writer recommended that anyone considering building a tiny home to try it out first. I thought that was a great idea. You can rent tiny cabins all over the country. Give it a try. For at least a week, I would suggest. And bring a lot of stuff with you, and remember, this tiny space could potentially be your full time home, with all of your junk, and the necessities, that go with actually living in a home.
I can imagine a lot of people loving their tiny home and never wanting to go back. However, I can also visualize a significant number of people not adapting well to the smaller lifestyle, and regretting their purchase. Please, don't be a regretter, be a planner, be a student, before you build.
Have fun. Even if you don't decide to go "tiny" you will have learned a lot about the industry, yourself, and your needs.
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TheQuintillionTimes
Conjuring images of masses, of velocities, of ubiquity. Ours is a Quintillion Times.
Deconstructing Commercials
Future Comms
← From Benny Hill to Internet memes: Media continues to inspire the decline of deference
Empire of Illusion: The End of Literacy and the Triumph of Spectacle – A book Review
Posted on August 5, 2013 by erictronix
Empire of Illusion is a narrative describing America's descent into a fatuous experience of voyeurism and self-satisfaction.
The Quintillion Times is a chronicle of how media and emerging media technologies affect our culture and those who live under their influence. The content of this book seems particularly apt to comment on in this blog.
Click to hear Chris Hedges on CBC Radio.
View Chris Hedges interview on TVO.
Chris Hedges obtained a master's degree at Harvard Divinity School and has travelled the world reporting on a variety of human experiences for The Christian Science Monitor, National Public Radio and The New York Times. He was awarded the Pulitzer Prize for his coverage of global terrorism. He's also been a professor at Columbia, Princeton and New York Universities as well as the University of Toronto.
Empire of Illusion offers a fascinating opinion on the role of media in casting a kind of somniferous spell on the American public.
He echoes the voice of Noam Chomsky in describing how the American public has become distracted by the vast media circus. To add depth to his story, Hedges cites many authoritative voices including authors like Naomi Klein and political philosophers such as John Ralston Saul and Sheldon S. Wolin.
We live under an anonymous corporate state which inundates the media-scape with mesmerizing diversions
Quoting Wolin, Hedges describes the American state as approaching an inverted totalitarianism. Rather than charismatic leaders, it is an anonymous corporate state which inundates the media-scape with mesmerizing diversions: Lascivious details about the lives of media stars through whom we live vicariously, and political pseudo-events that distract people away from meaningful civic participation or any real understanding of fundamental issues.
How did the U.S. government fabricate "facts" in support of the Iraqi invasion?
Hedges illustrates how consent for the Iraqi war after 911 was manufactured by actions such as Dick Cheney supplying media outlets with top secret information about Saddam Hussein's preparations for an atomic bomb. The secret "facts" were presented as coming from anonymous government sources. Once published for the world to see, it allowed Cheney to appear on Meet the Press and (while attributing the story to the New York Times) validate the story that Saddam had attempted to obtain parts needed for a uranium enrichment project.
Similarly, the CBC documentary series Love, Hate and Propaganda revealed in its episode The War on Terror, the story of a 15 year old Kuwaiti girl who testified before the American congressional caucus on human rights. She tearfully conveyed witnessing first hand how Iraqi soldiers removed babies from incubators and let them die on the floor. The story was all over the news. Its shocking content helped drive support for the first war between America and Iraq. The problem is, the whole story was fabricated. That 15 year-old girl was the daughter of the Kuwaiti ambassador to the United States, and further, she was not even present during the Iraqi invasion to witness any such event.
Thus unfolds the theme of "news as spectacle" in Empire of Illusion.
Hedges describes how the news has become dominated by content like celebrity gossip and quasi-advertising (such as new product announcements) written by corporate public relations officers. Corporate dominated news outlets become complicit in validating lies, even acting like a government mouthpiece.
Hedges' book identifies how independent thought has withered during a period where "spoiled, intellectually limited and wealthy elitists [get] churned out by" ivy-league schools. For-profit universities train this elite not in the art of independent thought, but as extensions of self-interested corporations. Education becomes instruction of how to accumulate wealth. Rather than nurturing knowledge for its own sake, "some forty-five colleges and universities" have become listed on the NYSE or the NASDAQ. The economic imperative has taken over.
Hedges identifies the emergence of an economic "oligarchy" which has seized important influence over elected officials.
Ralph Nader called it "the corporate state" when he appeared on the CBC's Lang and O'Leary Exchange. All the while, American freedoms are being curtailed – with the public cowed into submission by tales of terrorist cataclysms.
We have just learned of the effect of this mode of thought on government. Edward Snowden's revelations show just how far the NSA has taken its mandate to subpoena "any tangible thing" including meta-data from telecom giants. This broad and vague definition (as described in the congressionally approved rules governing the federal domestic telephone records program) was approved by congress. Whether or not the congressmen and women truly understood what they were authorizing was debated on the June 17, 2013 episode of TVO's the Agenda: Secrecy and the Limits of Transparency.
Hedges also claims that the "capitalist ideology of unlimited growth has failed", a sentiment echoed by – ironically – Jeff Rubin, the former Chief Economist and Chief Strategist at CIBC World Markets.
But this book does not dwell only on politico-economic issues. The second chapter entitled The Illusion of Love describes the hollow experiences surrounding both the consumers and producers of pornography. The chapter is a metaphor for the objectification of human beings as commodities, as objects to be used and discarded in a culture defined by corporate greed; alas – devoid of any capacity for empathy.
Look around you and ask yourself: Do we live in an environment dominated and increasingly defined by an ever-present dissemination of commercial messages? As we are bombarded by subliminal and overt messages from birth, do they inform our values? Does news as spectacle contribute to a voyeuristic fascination with celebrities? And does all this stimulation distract from real learning, greater understanding of the objective world and truer empathy towards others?
These are questions particularly suited to the age of Quintillion.
This entry was posted in Culture and Media and tagged 911, Allan Gregg, Amanda Lang, CBC Radio Ideas, Chris Hedges, culture, Edward Snowden, Empire of Illusion, inverted totalitarianism, Iraq, Jeff Rubin, John Ralston Saul, Kuwait, Lang O'Leary Exchange, Love Hate and Propaganda, media, media and culture, Naomi Klein, news as spectacle, Noam Chomsky, NSA, oligarchy, pornography, pseudo event, Ralph Nader, Saddam Hussein, Seeing through Transparency, Sheldon S. Wolin, TVO, USA, war on terror. Bookmark the permalink.
From Benny Hill to Internet memes: Media continues to inspire the decline of deference
How ads "hack" our mind


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Chennai vs Mumbai Match Prediction
After a brief hiatus, the Indian T20 League is all set to make its comeback. The first game of the UAE leg is the el Classico of the Indian T20 League, a Chennai vs Mumbai battle. They will be playing the 30th match of the 2021 season.
The match will be starting at 7:30 PM (IST), and the live streaming will be available on Disney+ Hotstar. Chennai and Mumbai will be playing this game at the Dubai International Cricket Stadium, Dubai.
They also played the 27th match of the season on 1st May at the Arun Jaitley Stadium, Delhi. Mumbai won the toss and was elected to field. Chennai made 218 runs for the loss of four wickets in 20 overs. Ambati Rayudu was the highest scorer for the team as he made 72 runs off just 27 deliveries. Kieron Pollard picked two wickets in the match in two overs and gave away 12 runs.
Quinton de Kock and Rohit Sharma opened the innings for Mumbai. They added 71 runs for the first wicket in 7.4 overs. Kieron Pollard finished the game for the blue team with an innings of 87 runs off just 34 balls. Mumbai won the match by four wickets, and Kieron Pollard has adjudged the player of the match.
In this article, we have mentioned the Chennai vs Mumbai today match prediction, probable playing 11 today, live pitch report today match, weather report today, and fantasy cricket tips.
Chennai vs Mumbai Head to Head
Chennai and Mumbai have played a total of 33 games against each other. Chennai has won 13 games, while Mumbai has won 20 games. Chennai and Mumbai are two of the most successful teams in the Indian T20 League. Chennai has won the title thrice, and Mumbai has won five times. Chennai has won six games while playing first and seven games while batting second.
Mumbai has won 10 matches each while batting first and second. Mumbai has won eight games in the last ten matches, while Chennai has won just two games. Chennai's previous win against Mumbai came in the 2020 edition of the league. Mumbai has dominated Chennai in the Mumbai vs Chennai head-to-head records. Would Mumbai be able to repeat history, or Chennai be able to overcome the power of Mumbai? Please read this article until the end to know our prediction.
Chennai vs Mumbai Playing 11 Today Indian T20 League Match
This section contains today match playing 11 predictions for both teams:
Chennai Playing 11
Ruturaj Gaikwad, Robin Uthappa, Moeen Ali, Suresh Raina, Ambati Rayudu, MS Dhoni (c & wk), Ravindra Jadeja, J Hazlewood, Shardul Thakur, Lungi Ngidi, Deepak Chahar
Mumbai Playing 11
Rohit Sharma (c), Ishan Kishan (wk), Suryakumar Yadav, Hardik Pandya, Krunal Pandya, Kieron Pollard, Rahul Chahar, Piyush Chawla, Dhawal Kulkarni, Jasprit Bumrah, Trent Boult
Chennai vs Mumbai Key Players in Today's Match
Key Players for Chennai in today T20 match:
1. Shardul Thakur
Shardul Thakur has become a meme lord in the past couple of days. Fans made several memes related to him during the fourth test against England. Thakur made half-centuries in both the innings of the game and picked three wickets.
In the last season, Thakur picked ten wickets in nine games at a strike rate of 19.4. The form is currently on Thakur's side, and he would be hoping to continue from where he left in England.
2. Deepak Chahar
Deepak Chahar will be traveling with the Indian team in the T20 World Cup as a reserve. He is one of the few bowlers who have been in red hot form for India in white-ball cricket. His omission from the squad had raised a lot of eyebrows.
In the recently completed limited-overs series against Sri Lanka, Chahar helped India won the second ODI with his all-around skills. He picked two crucial wickets while bowling and made 69 runs off 82 balls to seal the game for India. The UAE leg of the Indian T20 League is an essential tournament for Chahar to prove his worth and cement a position in the Indian team.
Key Players for Mumbai in today's Indian T20 League Match
1. Rohit Sharma
Rohit Sharma was one of the few Indian players who dominated the England bowling attack in the test series last month. He was India's leading run-scorer in the tournament, with 368 runs across his name. He made runs at an average of 52.57.
Mumbai had a dream run in the Indian T20 League last year as the team lifted the trophy for the fifth time, and Rohit Sharma was one of the key players for the team. He is likely to play the same role in this as well as the remaining games.
2. Suryakumar Yadav
Suryakumar Yadav finally arrived on the scene as he made it to the final squad for the T20 World Cup. The remaining seven games for Mumbai will be necessary for Surya as he would be using them for game practice. Also, Surya has been a critical member of the Mumbai team. He is the backbone of the middle-order and is likely to play the same role in this game.
Chennai vs Mumbai Fantasy Team
This section contains today's match fantasy team suggestions.
Batsman: Suryakumar Yadav, Rohit Sharma, Suresh Raina, Ambati Rayudu
Wicketkeeper: Ishan Kishan
All-rounders: Kieron Pollard, Ravindra Jadeja
Bowlers: Jasprit Bumrah, Trent Boult, Shardul Thakur, Deepak Chahar
You can pick Suryakumar Yadav or Ambati Rayudu as the captain of the today's Indian T20 League match. You can pick Shardul Thakur or Kieron Pollard as the vice-captain of the Indian T20 League match today.
Today Indian T20 League Match Pitch Report and Weather Report
Today Match Pitch Report
Chennai and Mumbai will be playing this match at the Dubai International Cricket Stadium, Dubai. The ground has hosted a total of 93 domestic t20 games. The team batting first has won 38 games, while the team batting second has won 54 games. The average score on this ground is 155 runs. The cricket pitch is expected to support both batters and bowlers.
Today's Weather Report
The match will be starting at 6:00 PM local time. The temperature during the game is expected to be around 34°C and 31°C. The probability of precipitation and the cloud cover throughout the match is zero.
Chennai vs Mumbai Today's Match Prediction
Chennai might be missing the services of both Faf du Plessis and Sam Curran in this game. Sam Curran arrived in UAE on Wednesday and now be serving the mandatory six-days quarantine. Faf du Plessis has suffered a groin injury.
Sam Curran is the leading wicket-taker, and Faf du Plessis is the leading run-scorer for the team. Mumbai will have the entire squad at its disposal, which would be an advantage for the team. Our prediction is Mumbai might win this game. It was our Chennai vs Mumbai match prediction today article. Fantasy Power 11 is one of the best fantasy cricket apps. Do use the suggestions provided by us to make your team.
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