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Mai Ots (ESTONIA): Cardiovascular disease in chronic renal disease

Ernesto O. Hoffmann and Syeda Sarwar (USA): Una clasificación práctica para la Nefritis Lúpica.

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Session Start: Thu Feb 22 22:00:00 2000
[22:00] (JBover) welcome Dr Ots!!!!!!!!
[22:00] (JBover) welcome back!!!!!!!!!!
[22:00] (MJesus) Hello Mai Ots, welcome !
[22:00] (maio) Good evening!
[22:01] (JBover) Dr Ots..let me introduce you Dr Hoffman
[22:02] (maio) It is nice to meet you, How dod you do
[22:02] (Ernesto) Nice meeting you maio
[22:02] (JBover) Dr Hoffman is currently working at the Dpt of Pathology in New Orleans in Luoisiana
[22:02] (JBover) Dr Hoffman will talk today about a new classification for Lupus nephritis
[22:03] (JBover) Dr Ots, from the University of Tartu, ESTONIA...will talk about cardiovascular disaease in CRF
[22:04] (MJesus) hello secundino...
[22:04] (MJesus) secundino is from spain, nephrologist
[22:04] (JBover) Dr Cigarran! how are you????
[22:05] (MJesus) I'm pathologist ... from Spain
[22:05] (SCigarran) Hello, How do yo do
[22:05] (JBover) Dr Cigarran...let me introduce you Dr Ots (maio) and Dr Hoffman (ernesto)
[22:05] (MJesus) hello stella, from B. Aires, nephrologist
[22:05] (Ernesto) Hola SCigarran, bienvenido!
[22:05] (JBover) Stella welcome!
[22:05] (SCigarran) I am fun.
[22:05] (Stella) Hola
[22:05] (JBover) Stella is from ARGENTINA!
[22:06] (Stella) Hola Cual es el tema y quien el disertante?
[22:06] (JBover) Stella participated before teaching us her experience in hemolitic uremic syndrome
[22:06] (MJesus) Secundino, estamos de Argentina, Bolivia, España, Estonia, Italia, y Usa
[22:06] (MJesus) hay que hablar ingles
[22:07] (JBover) Stella Dr M. Ots (Maio) will talk about Cardiovascular disease in CRF
[22:07] (SCigarran) OK. Doc
[22:07] (JBover) Stella DR Hoffman from USA will talk about a new classification on Lupus nephritis
[22:07] (SCigarran) Exciting issue
[22:07] (JBover) Dr Ots is located in ESTONIA
[22:07] (JBover) Dr Hoffman n New Orleans
[22:08] (Ernesto) Exciting but obscure!!
[22:08] (JBover) exciting???? heheheehehh I think it is depressing!!!!!!!
[22:08] (JBover) hahaahhahahahaahahahhaahahh
[22:08] (JBover) welcome Dr angoso
[22:08] (Angoso) Buenas Noches a todos
[22:09] (MJesus) gerado, good night
[22:09] (gerardo) buenas noches a todos los puntuales
[22:09] (MJesus) angose, welcome
[22:09] (SCigarran) Wellcome and good night
[22:09] (JBover) good night Gerardo
[22:09] (JBover) Gerardo Torres is the president of This COngress
[22:10] (_gene_) How do you do? Gerado
[22:10] (SCigarran) The big boss
[22:10] (JBover) Gerardo..let me introduce you Dr Ots from ESTONIA (maio)
[22:10] (JBover) welcome _gene_
[22:10] * _gene_ is Medical and Dental Doctor from Spain Europe
[22:11] (_gene_) pleased to meet you
[22:11] (MJesus) hello gurb!
[22:11] (JBover) shall we wait five more minutes???
[22:11] (MJesus) where are you from gurb ?
[22:11] (JBover) is it ok with you Dr Ots???
[22:11] (SCigarran) helo and wellcome Gurb
[22:12] (maio) yes
[22:12] (JBover) Thank you
[22:12] (Gurb) Hello, all
[22:12] * JBover warns everybody that we shall start in five minutes
[22:12] (Gurb) From Spain, MJesus
[22:12] (SCigarran) ok
[22:12] (Ernesto) OK
[22:12] * JBover sets the clock at FOUR minutes
[22:12] (MJesus) hello yooo
[22:13] (JBover) heheehehehehehehe
[22:13] (JBover) do we have simultaneous translation today????
[22:13] (Mapi) hi all
[22:14] (MJesus) yes jordi, and you is the tranlator!
[22:14] (MJesus) gaucho!!
[22:14] (JBover) I cant be translating today!
[22:14] (MJesus) Gaucho is D. Caporale, from Uruguay
[22:14] (JBover) welcome Dr Caporale
[22:14] (gerardo) nelson buenas noches
[22:14] (Gurb) Un saludo cordial desde CÁdiz
[22:14] (MJesus) bermejo. welcome!
[22:15] (SCigarran) Wellcome Tbermejo. Good seeyou again
[22:15] * JBover sets the clock in THREE MINUTES
[22:15] (JBover) we shall start in three minutes
[22:15] * JBover takes off the pastry and champagne
[22:15] (MJesus) hello dr. bermejo..... where are you from Spain?
[22:15] (Tbermejo) Holan jefe, aqui estamos las dos poniendonos al dia
[22:15] (MJesus) las dos ??
[22:15] (JBover) We already have online Dr Ots and dr hoffman
[22:16] * JBover warns that Dr Ots will start in ONE MINUTE
[22:16] (Tbermejo) Yes, i'mSpanish, i'm a nurse
[22:16] (JBover) Welcome Tbermejo
[22:16] (MJesus) tbermejo, we are from Argentina, Bolivia, España, Estonia, Italia, Peru, Usa y Uruguay
[22:17] (Ernesto) Aqui tengo listo el resumen esta en Espanol.
[22:18] (JBover) well.....
[22:18] (MJesus) ok.... ernesto, can writte in Spanish and Englihs ?
[22:18] (JBover) let me introduce MAIO= Dr Ots
[22:18] (Tbermejo) Hello Ernesto
[22:19] (JBover) Dr Mai Ots is in the University of Tartu
[22:19] (JBover) in ESTONIA
[22:19] (JBover) and we are honoured with the presence of such a figure in Nephrology
[22:19] (JBover) we will be delighted to hear the conference on CARDIOVASCULAR DISEASE IN CHRONIC RENAL DISEASE
[22:20] (JBover) CARDIOVASCULAR DISEASE IN CHRONIC RENAL DISEASE
[22:20] (JBover) INTRODUCTION
[22:20] (JBover) Cardiovascular disease (CVD) is the leading cause of mortality among patients with progressive renal failure and renal replacement therapy.
[22:20] (JBover) The risk of atherosclerotic CVD in patients with chronic renal failure,
[22:20] (JBover) especially patients on renal replacement therapy,
[22:20] (JBover) has shown to be 10-20 times greater than in the general population.
[22:20] (JBover) Therefore, patients with chronic renal disease should be considered in the highest risk group
[22:20] (JBover) for subsequent cardiovascular events
[22:20] (JBover) and proper preventive measures should be undertaken.
[22:20] (JBover) The care of chronic renal failure patients cannot start in the period of end-stage renal disease (ESRD)
[22:20] (JBover) or after the initiation of dialysis
[22:20] (JBover) but must set into motion when progressive renal disease is diagnosed and renal failure first begins.
[22:20] (JBover) Optimal treatment prevents detrimental influence of uraemia on the metabolic balance,
[22:21] (JBover) function, and structure of the body.
[22:21] (JBover) The National Kidney Foundation Task Force recommendations
[22:21] (JBover) stress the importance of preventive measures of renal patients early in the course of kidney failure
[22:23] (JBover) when these can be most effective, cost efficient, and of greatest benefit to patients and to society.
[22:23] (JBover) Reduction of both the "traditional" atherosclerosis risk factors
[22:25] (JBover) as well as specific risk factors related to chronic renal failure
[22:25] (JBover) should be one of the main targets of early management of patients with chronic renal disease (1,2,3).
[22:25] (JBover) RISK FACTORS OF ATHEROSCLEROSIS IN CHRONIC RENAL DISEASE
[22:25] (JBover) Several risk factors for CVD manifestations in chronic renal disease patients
[22:25] (JBover) are similar to the progression of atherosclerosis in general population
[22:25] (JBover) because of the higher incidence of ESRD in elderly.
[22:26] (JBover) Atherosclerosis is a multifactorial disease.
[22:26] (JBover) The approach to the "traditional" CVD risks factors like hypertension, diabetes, obesity, hyperlipidemia, oxidative stress, smoking, physical inactivity
[22:26] (JBover) should be guided by the principle that chronic renal disease patients
[22:26] (JBover) belong into the highest risk group for subsequent CVD complications.
[22:26] (JBover) During the course of the renal disease progression excess risk may appear that influence significantly the outcome (4).
[22:26] (JBover) Excellent reviews about the importance of various risk factors
[22:26] (JBover) were recently published in the American Journal of Kidney Diseases (Supplement N 5, 1998).
[22:26] (JBover) Hypertension and diabetes are serious risk factors
[22:26] (JBover) for the development of atherosclerosis, and for all-cause mortality (5,6).
[22:27] (JBover) Hypertension is also a significant risk factor for the development of glomerulosclerosis in various etiologies (7,8).
[22:27] (JBover) Thus, kidney disease may be either a cause or consequence of hypertension and atherosclerotic cardiovascular disease.
[22:27] (JBover) In the general population and among patients with chronic renal disease,
[22:27] (JBover) CVD is more prevalent among individuals with diabetes than those without diabetes.
[22:27] (JBover) According to the data of three large registries covering the United States, Europe, and Australia and New Zealand
[22:27] (JBover) it appears that diabetic nephropathy is the main cause of end-stage renal disease in many countries.
[22:27] (JBover) And, hypertension and diseases of the larger arteries constitute the second major cause of renal failure (9).
[22:27] (JBover) Hypertension complicates the clinical course of patients
[22:27] (JBover) with chronic renal failure and,
[22:27] (JBover) if inadequately controlled,
[22:27] (JBover) may hasten the deterioration of renal function (10,11).
[22:27] (JBover) On the other hand, the presence of hypertension in chronic renal disease
[22:27] (JBover) is associated with adverse outcomes of cardiovascular disease.
[22:27] (JBover) The development of hypertension among chronic renal disease patients involves various pathogenic factors:
[22:28] (JBover) 1) sodium and volume balance,
[22:28] (JBover) 2) renin-angiotensin aldosterone stimulation,
[22:28] (JBover) 3) increased sympathetic activity,
[22:28] (JBover) 4) endogenous digitalis-like factors,
[22:28] (JBover) 5) endothelium-derived factors,
[22:28] (JBover) 6) erythropoetin administration,
[22:28] (JBover) 7) nephron number,
[22:28] (JBover) 8) hyperparathyroidism and calcified arterial tree,
[22:28] (JBover) 9) renal vascular disease,
[22:28] (JBover) 10) worsening of pre-existing essential hypertension (12).
[22:29] (JBover) Patients with chronic renal disease should be screened
[22:29] (JBover) also for hyperlipidemia
[22:29] (JBover) because the prevalence of hyperlipidemia is increased in patients with
[22:29] (JBover) chronic renal insufficiency compared with general population.
[22:29] (JBover) Atherogenic lipoproteins are major risk factors
[22:29] (JBover) implicated in the pathogenesis of atherosclerotic cardiovascular disease.
[22:29] (JBover) It has been suggested that determination of at least triglycerides,
[22:29] (JBover) total, HDL and LDL cholesterol levels
[22:29] (JBover) should be regularly monitored in predialysis patients and renal replacement therapy patients (13).
[22:29] (JBover) Other cardiovascular risk factors also play an important role in the progression of atherosclerotic CVD.
[22:29] (JBover) However, smoking, obesity or physical inactivity has not been intensively investigated in the early stages of renal disease (4,14-17).
[22:29] (JBover) Several specific risk factors due to chronic renal failure
[22:30] (JBover) significantly influence the progression of atherosclerosis.
[22:30] (JBover) The excess risk, which contribute to the progression of atherosclerosis may be caused
[22:30] (JBover) by the hemodynamic and metabolic factors like progressive proteinuria, hypoalbuminemia, malnutrition,
[22:30] (JBover) electrolyte imbalance, increased extracellular volume, anaemia, uremic toxins, hyperphosphatemia,
[22:30] (JBover) hyperuricemia, high levels of fibrinogen and homocysteine (18-23).
[22:30] (JBover) Anaemia is associated with the progression of left ventricular hypertrophy
[22:30] (JBover) in chronic renal failure patients and should be treated
[22:30] (JBover) with iron and erythropoetin in order to achieve the target hematocrit. A tendency toward phosphate retention begins early in renal disease
[22:30] (JBover) and diet modification as well as drug treatment of secondary hyperparathyroidism
[22:30] (JBover) is often necessary before the initiation of dialysis (24,25).
[22:30] (JBover) Recently, it has been shown that hyperhomocyst(e)inemia
[22:31] (JBover) is an independent risk factor for CVD in the general population and in patients with chronic renal disease.
[22:31] (JBover) A combination of high-dose folic acid, vitamin B12 and vitamin B6 reduces homocysteine levels by 25%,
[22:31] (JBover) which may restore normal levels in patients with chronic renal insufficiency.
[22:31] (JBover) However, the effects of decreasing homocysteine levels on the risk for CVD are not exactly known (1,20).
[22:31] (JBover) PROGRESSION OF ATHEROSCLEROSIS AND GLOMERULOSCLEROSIS
[22:31] (JBover) As described,
[22:31] (JBover) various risk factors and mechanisms are involved in the progression of premature atherosclerosis in renal failure patients.
[22:31] (JBover) Risk factors such as hypertension, humoral factors, hyperlipidemia, lipid deposition in vessels
[22:31] (JBover) and later development of atherosclerotic lesions play a central role in the progression.
[22:31] (JBover) Cardiovascular risk factors play important role also in the progressive renal disease (26).
[22:32] (JBover) Moreover, in-vitro and in-vivo studies have shown that atherosclerosis and glomerulosclerosis are pathobiologically
[22:32] (JBover) analogous processes where several common biochemical and histological abnormalities are noticed (27,28).
[22:32] (JBover) There is strong evidence that atherosclerosisshould be fundamentally viewed as chronic inflammatory disease as for instance glomerulosclerosis,
[22:32] (JBover) cirrhosis, rheumatoidarthritis and pulmonary fibrosis (26).
[22:32] (JBover) Hormonal, cellular and molecular responses of each particular tissue or organ depends on its characteristic architecture.
[22:32] (JBover) Similar characteristic lesions for atherosclerosis and glomerulosclerosis are endothelial-cell injury and dysfunction. Hyperlipidemia and atherogenic
[22:32] (JBover) lipoproteins can be the initiating factors for both conditions because abnormalities in lipids and lipoproteins are often present.
[22:32] (JBover) Usually hyperlipidemia is more associated with ongoing atherosclerotic process (29).
[22:32] (JBover) Nevertheless, experimental studies have shown that lipid abnormalities themselves can influence
[22:32] (JBover) the progression of renal disease and lipid oxidation has been increased in animal and human glomerular diseases (30,31).
[22:32] (JBover) Increased nephron oxygen radical generation leads to renal tissue lipid peroxidation.
[22:32] (JBover) Antilipemic therapy (32) may be beneficial in ameliorating renal disease progression.
[22:33] (JBover) Central to the pathogenesis of atherosclerosisis the interaction
[22:33] (JBover) of blood cells and endothelial cells with subsequent macrophage accumulation,
[22:33] (JBover) proliferation of smooth muscle cells and enhanced production of collagen (26).
[22:33] (JBover) The mechanisms that appear to be responsible for this increased proliferative response are growth factors,
[22:33] (JBover) cytokines, and local alterations in the extracellular matrix proteins (ECM).
[22:33] (JBover) Participation of cellular and molecular factors and subsequent accumulation of ECM proteins
[22:33] (JBover) are closely related also with the kidney disease progression (33).
[22:33] (JBover) Similar to atherosclerosis, the kidney fibrosis in human or experimental glomerulonephritides
[22:33] (JBover) and even in classical glomerulosclerotic model e.g. remnant kidney involves inflammatory component.
[22:33] (JBover) Infiltration of mononuclear leukocytes in glomerular and tubulointerstitial areas,
[22:33] (JBover) upregulation of proinflammatory cytokines and growth factors after the initiation of the disease play important role in the progression (34-37).
[22:34] (JBover) The glomerulosclerosis process includes mesangial expansion with mesangial cell proliferation,
[22:34] (JBover) mesangial foam cell accumulation, tissue necrosis, and eventual sclerosis.
[22:34] (JBover) Substances that interfere with the interaction between the different cell types, such as endothelial cells,
[22:34] (JBover) macrophages, and platelets, and with the proliferative responses of both vascular
[22:34] (JBover) and mesangial cells may be of therapeutic value in both diseases (26,38).
[22:34] (JBover) Much attention has recently been paid to chemokines and also,
[22:34] (JBover) for growth factors, e.g. transforming growth factor-ß (TGF-ß)
[22:34] (JBover) because the key actions of this growth factor is the induction of the ECM production.
[22:34] (JBover) Specific matrix proteins are known to be induced by TGF-ß, which were increased in experimental kidney diseases rat glomeruli.
[22:34] (JBover) TGF-ß, monocyte chemoattractant protein -1 (MCP-1) mRNA and protein expression
[22:34] (JBover) as well as macrophage infiltration dynamics have been investigated in experimental diabetic nephropathy (39).
[22:35] (JBover) In these studies sustained TGF-ß and MCP-1 overexpression was also observed.
[22:35] (JBover) This particular gene expression was closely associated with the extent of macrophage infiltration and proteinuria (39).
[22:35] (JBover) The principal factors associated with macrophage accumulation in the lesions of atherosclerosis include also
[22:35] (JBover) macrophage colony stimulating factor and MCP-1 (26).
[22:35] (JBover) RECOMMENDATIONS
[22:35] (JBover) Strategies for risk factor identification and reduction should target
[22:35] (JBover) both the traditional coronary risk factors and specific risk factors related to chronic renal disease.
[22:35] (JBover) Hypertension is a major risk factor for all types of atherosclerotic CVD.
[22:35] (JBover) The prevalence of hypertension in chronic renal disease patients ranges 60-100% and most patients require antihypertensive treatment.
[22:36] (JBover) Renin-angiotensin system inhibitors proved its effectiveness in the treatment of essential hypertension
[22:36] (JBover) and congestive heart failure (40,41).
[22:36] (JBover) Studies on experimental and human diabetic and nondiabetic renal diseases
[22:36] (JBover) revealed that the progression of the renal disease can be slowed by renin-angiotensin system blockade that modulate hemodynamic and non-hemodynamic factors
[22:36] (JBover) contributing to the progression of glomerulosclerosis (42-44).
[22:36] (JBover) Thus, renin-angiotensin system blocking agents have been proved to be vaso- and renoprotective and,
[22:36] (JBover) therefore, prescribed not only for antihypertensive but also for vaso- and renoprotective purposes
[22:36] (JBover) in diabetic nephropathy
[22:36] (JBover) and in other chronic glomerular diseases with and/or without systemic hypertension.
[22:36] (JBover) Monitoring and accurate treatment of patients with chronic renal disease needs specialised training.
[22:36] (JBover) It is reasonable to follow current clinical guidelines, which are based on the highest level of current evidence (24,45).
[22:36] (JBover) Various national organisations have developed clinical guidelines regarding prevention of CVD in the general population.
[22:37] (JBover) These are the interventions the Task Force considered in chronic renal disease (1).
[22:37] (JBover) In addition, several specific risk reduction strategies were included.
[22:37] (JBover) The report of the National Kidney Foundation Task Force on CVD
[22:37] (JBover) in chronic renal failure is a first attempt to provide evidence-based recommendations
[22:37] (JBover) for this holistic approach to the care of patients with renal disease (2).
[22:37] (JBover)
[22:37] (Tbermejo) Plas plas plas
[22:37] (JBover) THANK YOU VERY MUCH DR OTS!!!!!!!!
[22:38] (JBover) It was great!!!!!!!
[22:38] (Angoso) Excellent lecture
[22:38] (maio) You are welcome
[22:38] (MJesus) Congratulations Dr. Ots!
[22:38] (maio) Thank you for your attention
[22:38] (SCigarran) Thanks a lot. Great
[22:38] (JBover) Just FOCUSED ON TARGET!!!!
[22:38] (Tbermejo) I'm sorry but i don't know very much internet
[22:38] (Stella) Thank you Dr Ots
[22:38] (JBover) as we said before...this is an EXCITING issue ...but DEPRESSING at the same time
[22:39] (JBover) to start with the discussion.....
[22:39] (maio) If there are any questions - then i will be happy to try to answer
[22:39] (gerardo) dr Ots shall hypercoleterolemia and hyperlipidemia be aggressively treated in patient with hemodialysis?
[22:40] (JBover) should ALL patients with renal failure be treated with ACEI or AII blockers???
[22:40] (gaucho) congratulations Dr. Ots,and what about factors linked with myocardial fibrosis un uremic patients?
[22:40] (maio) Maybe there is no long lasting works about treatment of hyperlipidemia inHD pt-s
[22:40] (JBover) even regardless of blood pressure..?********** *******+
[22:40] (Angoso) The use of angiotensin II receptors antag in normotensive CRF PATIENTS
[22:41] (Angoso) jbover read my mind:)
[22:41] (maio) But it would protect from atherosclerosis
[22:41] (maio) About RAS blocking treatment
[22:42] (maio) I would suggest to treat not only diabetics but also pt-s with chronic glomerulopathieas with RAS blocking agents
[22:43] (Stella) the patients with renal failure be treated with ACRI or AT1 Bloquers Who is better to reduced the Hyperlipidemia?
[22:43] (SCigarran) Thanks Dr Ots for your excellent lecture. I would like made two questions: first, correction of the anemia is a target complicated by LVH. How high is the Hto Target?, and secondly, How often do you recomend a screening for LVH by acho?
[22:43] (maio) because thera are experimental evidence that these drugs have renoprotective
[22:43] (maio) aslo clinical evidence
[22:43] * JBover would suggest to write ******** at the end of an answer or question to avoid problems with lag
[22:44] (Charlie) patients on dialysis often must lower their insulin dosage: does this mean diabetes is less harmfull in dialysis?**
[22:44] (gaucho) I asked about prevention of myocardial fibrosis*******
[22:45] (maio) As we know there are a target Hct - that we need to achieve 33-36%
[22:45] (maio) Abot echo - depends of pt- once a year
[22:46] (maio) RAS have also cardioprotective
[22:46] (Stella) Do you experience with the use of statins XXXXX
[22:47] (maio) We have actually few patients still
[22:47] (JBover) should high dose-statins be used in all nephrotic patients ?
[22:47] (Angoso) why about achieving higher Hct close to 40% ??
[22:48] (maio) Higher Hct leads to BP rise and also trombosis of AVF
[22:49] (maio) Nephrotic patients need to treat at first the main disease
[22:50] (JBover) obviously we have to treat first the main disease but...many times we cant control proteinuria not even with ACEI ..should we then treat secndary hyupercholesterolemia aggressively?
[22:50] (JBover) **********
[22:50] (Angoso) That true for grafts but not for native fistula plus pstinets feel much better with higher Hct ( as a secundary gain )
[22:50] (maio) It depen's
[22:51] (MJesus) Vaheta keelt .... Dr. Maio..... is there any evidence to rather use ACEI or AII blockers regarding renoprotection? ****
[22:51] (Stella) In the patients corticorresistent the mos importan treatment is AntiHyperlipidemia and ENALAPRIL.What Abot the treatment in this patientsde
[22:52] (maio) ACEI and ATRA have very similar effects
[22:53] (maio) concerning BP lowering and renoprotection
[22:53] (JBover) welcome back Ernesto
[22:53] (maio) There are several experiments where tose drugs are compared
[22:54] (maio) but clinical studies are still not completed yet
[22:54] (Angoso) Hyperchol is a marker for poor prognosis and may contribute to glomerular sclerosis and renal injury
[22:55] (maio) There are probably several biomarkers which are necessary to monitor
[22:56] (maio) Not only TChol but also LDL, HDL, Lp(a)
[22:57] (maio) There are for instance also autoantibodies which people have been found and correlated with severity of atherosclerosis - anti-ox-LDL
[22:57] (SCigarran) What about lifestyle modifications simultaneous drug therapy?
[22:58] (Angoso) What about USE of Vit E ??? aS AN ANTI OXIDANT agent
[22:58] (Charlie) in wich percentage your dialysis patients need antihypertensive drugs?
[22:58] (Angoso) It has shown to decrese LDL oxidation
[22:58] (maio) ~ 90%
[22:59] (Charlie) it seems a little bit high to me!
[22:59] (maio) Yes vit E now have been also suggested even prophylactically
[22:59] (Angoso) and a second question related to Vit
[22:59] (maio) 90% HD patients, but PD less
[23:00] (Charlie) are they very uncompliant whit weight control?
[23:00] (Angoso) Hyper Hcya is significant higher as renal function declines
[23:00] * JBover warns that Angoso's is the last question
[23:01] * JBover tells Dr Hoffman to be ready
[23:01] (Angoso) Should me treat our CRF once there GFR goes down to 50 ml/min
[23:01] (maio) Thank you very much for the attention
[23:01] (Angoso) Thank you for your time
[23:01] (Charlie) thank you dr Ots
[23:01] (gerardo) Thak dr ots
[23:01] (JBover) Dr Ots
[23:02] (JBover) It was great!!!!! you know we would be here speaking for hours about this important issue
[23:02] (maio) Thank you
[23:02] (JBover) Dr Hoofman....
[23:02] (gaucho) of course, you forgot my myocardial fibrosis
[23:03] (JBover) we count on you for next YEAR dr OTs!!!!!!!!
[23:03] (MJesus) Dr. Caporale, luego podremos preguntar mas, y ademas en la web hay un panel dediscusion
[23:03] (maio) Thank you again
[23:03] (SCigarran) AND MY LIFESTYLE MODIFICATIONS ANDRUG THERAPY
[23:03] (JBover) mind answering Dr Caporale's question on myocardial fibrosis???
[23:04] * JBover thinks that there were so many simultaneous questions that we overwhelmed Dr Ots' ability to read!
[23:04] (maio) There is no consensus recommendations about lifstyle
[23:04] (maio) you should use in mild and moderate CRF pt-s general suggestiopns
[23:04] (JBover) Thank you ver much Dr Ots..it was a GREAT PLEASURE!!!!!!!!!
[23:05] (JBover) Dr Hoffman is gonna now teach us .....
[23:05] (maio) but about ESRD pt-s individual programs
[23:06] (JBover) his experience in a new practical classification for Lupus nephritis beyond classical WHO's
[23:06] (Ernesto) clasificacion de la nefritis lupica de la OMS necesita una revision.
[23:06] (JBover) He works in the Dpt of Pathology of the VAMC in New Orleans
[23:07] (Ernesto) Esto con el objeto de mejorar las intercomunicaciones entre patologos y nefrologos.
[23:07] (JBover) welcome Dr Hoffman
[23:07] (JBover) thanks for coming
[23:07] (Ernesto) y para facilitar la evaluacion de la actividad y cronicidad del proceso.
[23:08] (Ernesto) Patogenéticamente hay dos formas de nefritis lupica, una frecuente, la glomerulonefritis y una menos frecuente la forma extra glomerular.
[23:08] (Ernesto) Aqui discutiremos solamente las glomerulonefriitis.
[23:08] (Ernesto) Patogeniticamente hay dos tipos de glomerulonefritis lupica (NN)
[23:09] (Ernesto) GN = glomerulonefritis.
[23:09] (Ernesto) La glomerulonefritis mal llamada proliferativa,
[23:09] (Ernesto) nosotros la llamamos pleomorfica pan glomerular
[23:10] (Ernesto) por aue tiene depositos pleomorficos que se depositan en cuanquier elemento anatomico del glomerulo.
[23:10] (Ernesto) Y la GN membranosa.
[23:10] (Ernesto) Cuando se estudian las GNPP sin complicaciones esta tiene tres grados de agresividad
[23:11] (Ernesto) leve, moderado y severo. La forma membranosa tiene dos grados de ag45resividad, la GNMB pura y la con depositos en el mesangio.
[23:12] (Ernesto) Hay una forma mixta GNPP asociada a GNMB la llamaremos glomerulonefritis mixta
[23:12] (Ernesto) GNMX. Cualquiere de estas formas de GN puede presentar complicaciones. Estas
[23:12] (Ernesto) puedemn ser activas y cronicas o esclesosantes
[23:13] (Ernesto) Las complicaciones activas deben ser avaluadas por separado en complicaciones leves, moderadasa y severeas
[23:14] (Ernesto) Las complicacionews cronicas determinan el estadio del proceso
[23:14] (Ernesto) temprano intermedio y avanzado.
[23:15] (Ernesto) Antes de que se vayan todos creo debemos abrir la discusion
[23:16] (MJesus) atencion, preguntas para el Dr. Hoffmann ?
[23:16] (Angoso) Creo que deberiamos agradecer al Dr Hoffmann por su excellente conferencia
[23:16] (Angoso) Tengo 2 preguntas
[23:16] (MJesus) adelante angoso, la primera ??
[23:16] (Angoso) 1-Numero de glomnerulos minimos para realizar la clasificacion
[23:17] (Angoso) 2-EXISTE DEBATE del uso de
[23:17] (Angoso) criterios de cronicidad /actividad en la WHO TIPO IV
[23:17] (Ernesto) No se debe aceptar una biopsia para cuantificacion sin menos de 20 glomérulos, el diagnostico es posible con 10
[23:17] (MJesus) ernesto.... "en mis tiempos" decian 5 !
[23:18] (SCigarran) Ernesto, felicitaciones . Tengo una pregunta¿ cuales son los criterios de evaluación leve,moderado y severo?
[23:18] (Ernesto) La actividad se mide con dos parametros, la actividad del proceso basico (complejos inmunes) y la actividad de las complicaciones
[23:18] (Ernesto) La cronicidad se mide por el avance de las lesiones cronicas, fibrosis y esclerosis
[23:19] (gerardo) Ernesto que piensas del tratamiento con genoxal via oral o bolus?***
[23:19] (Ernesto) Depende si se trata de avaluar la forma basica (complejos inmiunes o las complicaciones.
[23:19] (Ernesto) No hablamos de tratamiento hasta que resol\vamos el problema de actividad y cronicidad, y grados del LES
[23:19] (gerardo) gracias
[23:20] (MJesus) mas preguntas ??
[23:20] (Ernesto) Las complicaciones se avaluan como leves si son reversible y no dejan cicatriz, son moderadas las que producen trastornos fiuncionales o pueden dejar cicatriz
[23:20] (Angoso) Dr Hofmann la pregunta es pertinente dado que clinicamente una SLE TIPO IV la diferenciacion de su grado de actividad no tiene reoercusion clinica
[23:20] (Ernesto) son severas cunado producen ytrastorno funcinal y dejan cicatriz
[23:22] (Ernesto) SLE IV es un grado , es el grado mas aqvanzado del LES
[23:22] (MJesus) esta documentada la reversibilidad de las lesiones ?
[23:22] (Angoso) Muchas Gracias
[23:23] (Ernesto) La confusion radica en que las clases de la OMS I a IV no son realmente clases sino hgrados de un mismo proceso.
[23:23] (Ernesto) La reversibilidad de lesiones esta documentada en nefropatologia
[23:24] (SCigarran) Me gustaría saber cómo clasifica el daño vascular, bien depósitos hialinos bien arteritis necrotizante?
[23:25] (Ernesto) Toda lesion activa puede graduarse, si se tiene primero en cuanta el tipo de lesion, 2, la extension y 3 el organo encvuelto
[23:25] (Ernesto) En las vasculitis el grado de agresividad es dificil de hacerlo pro que las lesiones no representan la realidad del proceso anatomico
[23:26] (Ernesto) Pero basicamente, una vasculitis necrotizante, primero no tiene cambios hialinos, 2. los cambios llamados hialinos son areas de necrosis,
[23:26] (Ernesto) Toda necrosis es una lesion grave porque altera la funcion y deja cicatriz. El problema es determinar su extension
[23:27] (Ernesto) Nunca he escrito tan rapido y tan mal
[23:28] (SCigarran) No se preocupe, nosotros tampoco
[23:28] (gerardo) te entendemos perfectamente
[23:28] (MJesus) pero tenemos mas tiempo para leer....
[23:28] (MJesus) es que esto del directo, es asi
[23:28] (MJesus) pero tiene su encanto.... no ?
[23:28] (MJesus) de todas formas, para todos hubo una primera vez.....
[23:29] (Ernesto) El encanto es en la relacion con los amigos
[23:29] (SCigarran) Me gustaria tocar ligeramente el tema del uso del MMF en el SLE. Alguna experiencia?
[23:29] (Angoso) Dr Hoffmamm leyendo su conferencia me da la impresion que lo mismo se podria decir de la clasificacion actual de las membranosas
[23:29] (gerardo) nosotros no
[23:29] (MJesus) ernesto.. y en la oportunidad de hacer mas amigos!!
[23:30] (Ernesto) Las membranosas tiene un problema no simepre detectado por los patologos y que creo es serio, es su combinacion con la otra forma
[23:30] (SCigarran) Si, tambien qué hacer con las membranosas puras?
[23:30] (Ernesto) Las membranosas puras pueden tener complicaciones al igual que la otra GN
[23:30] (Angoso) Si te sirve la opinion de Jim Winchester dice que es lo mismo que la azatriopina = pobre
[23:31] (SCigarran) Lo digo porque está apareciendo reports con esperanzadores resultados
[23:32] (Ernesto) Tengo la intencion de traer este problema del LES a la lista NEPHRONOL para que entre todos, patologos y clinicos hagamos una clasificacion practica clinicamente practica
[23:33] (Ernesto) Uno de los problemas que tiene el clinico es con la confusion de "la proliferacion celular"
[23:33] (MJesus) aja... y al nephrol ?
[23:34] (Ernesto) En nephrol no nos permiten mensajes bilingues
[23:34] (Angoso) En que sentido ?
[23:34] (MJesus) ah!! no sabia
[23:34] (Ernesto) La membranosa y la llamada proliferativa pueden tener proliferacion celular
[23:35] (Ernesto) Si el patologo informa una proliferative cuando tiene una membranosa con proliferacion celular, el tratamiento y los resultados seran diferentes
[23:36] (Angoso) pero la proliferacion es habitualmente en el mesangio
[23:36] (Angoso) en la membranosa
[23:36] (Ernesto) Y la confusion persiste por que las llamadas formas proliferativas pueden no tener proliferacion celular pero ser potencialmente muy graves
[23:37] (Ernesto) La proliferacion puede ser mesangial endotelial o de la Capsulade Bowman
[23:37] (Ernesto) No siempre, he visto membanosas con semilunas
[23:38] (gerardo) Queridos todos llevamos mas de 90 minutos nos quedan muchos dias
[23:38] (Ernesto) tanto en les
[23:38] (SCigarran) Ernesto, en esas formas en las que el glomerulo esta respetado y se afecta el tubulo (tubulitis) qué pronostico tienen
[23:38] (Angoso) pero serian mas bien una membrano- proliferativa
[23:38] (Ernesto) Bueno muchas gracias y hasta pronto
[23:38] (gerardo) se puede continuar la discusion en el panel os parece?
[23:39] (gerardo) Ernesto muchas gracias
[23:39] (gerardo) ha sido muy clarificadora
[23:39] (Angoso) MUCHAS GRACIAS
[23:39] (Ernesto) Gracias a Uds por su tolerancia y su rapidez para leer
[23:39] (SCigarran) Gracias por tu presencia y hasta pronto Ernesto
[23:39] (MJesus) BRAVO ERNESTO!!!!!!!!!!!!!!!!!!
[23:39] (MJesus) FELICIDADESSSSSSSSSSSSSSSSSSSSS
[23:39] (Ernesto) Creo que lo haremos mejor por NEPHRONOL
[23:40] (Ernesto) Chau
[23:40] (MJesus) vale... continuaremos ahi!
[23:40] (gaucho) el tiempo se nos hace corto, lo que es una muy buena señal
[23:41] (MJesus) casi dos horas!
[23:41] (MJesus) a ver.... lo de ernesto esta tanto en conferencias como en comunicaiones
[23:41] (Angoso) Creo que ha sido una muy buena experiencia
[23:41] (MJesus) en ambos hay panel
[23:41] (gaucho) felicitaciones y saludos para ernesto, y también tenemos nephronol
[23:41] (MJesus) el de la comunicaiones ya esta puesto....
[23:41] (MJesus) el de la conferencia esta en http://lore.uninet.edu/cgi-bin/cin2000/paneles?base=conf
[23:45] (Angoso) Buenas Noches y hasta mañana
[23:45] (gerardo) gracias por vuestra presencia
[23:46] (gaucho) hasta mañana para todos