I'm a dialysis patient in the US. I take fish oils every morning before dialysis instead of using heparin as a blood thinner. The one day I forgot to take my fish oil, the dialysis machine clotted up. Fish oil does work for me.
Certainly! Based on the video transcript, here are the chapters for the video: **Chapter 1: Introduction to IGA Nephropathy and FSGS Webinar** [00:00:05][^1^][1] - Greetings and welcome - Overview of the webinar series - Introduction of speakers **Chapter 2: Diagnosing IGA Nephropathy** [00:01:17][^2^][2] - Pathology basis for diagnosis - Characteristics of IGA Nephropathy - Differential diagnosis and distinguishing factors **Chapter 3: Pathophysiology and Clinical Aspects of IGA Nephropathy** [00:13:22][^3^][3] - Historical perspective of IGA Nephropathy - Clinical trials and targeting pathways - Importance of blood pressure control and lifestyle modifications **Chapter 4: Biopsy Predictors and Stratification** [00:07:24][^4^][4] - The role of renal biopsy in diagnosis and prognosis - International consensus on classification - The Oxford approach to classification **Chapter 5: Clinical Implications of Biopsy Findings** [00:42:42][^5^][5] - The significance of crescents in IGA Nephropathy - The importance of clinical context in treatment decisions **Chapter 6: Lifestyle Modifications and Patient Management** [00:32:23][^6^][6] - Supportive therapy approaches - The impact of diet, obesity, and smoking on IGA Nephropathy - Recommendations for physical activity **Chapter 7: Conclusion and Q&A Session** [00:47:13][^7^][7] - Summary of key points from the webinar - Audience questions and expert responses - Closing remarks and future webinars These chapters provide a structured overview of the video's content, making it easier to navigate through the different topics discussed. If you need more detailed information or specific time stamps for each chapter, feel free to ask!
My protein 24 hour is over 1000. As long as I take cortisol it stays the same but whenever I stop it startd going over 1000. This proves that cortisols are just like painkillers and do not treat IGA and second IGA has no treatment and medical sciences are all defeated by it
Excellent thoughts Several Major issues Lack of concern for humanity and no forethought Total inertia even in application of measures Big pharma driving business for pharmacotherapy using human Guinea pigs paying medical professionals Ruthless greed making cost of newer medicines absolutely unaffordable No one bothered about prevention and no effort made on implementing life style interventions aggressively in real world Great talk appreciate his insight forethought with total compassion and caring He needs to be rewarded
4:12 actually the graph shows less than 30% are anemic (<10 g/dl) even in stage 5, and only 5% are anemic in stage 3a 9:47 The ferritin > 500 had the highest mortality at 1.38. I just looked up the paper. Only 'iron deficiency' at < 100 ferritin had NO increase in mortality. So mortality clearly increased with the level of iron, in the presenter's paper of choice. In her defense, the paper makes the same claims even though the data is right there. I'm not sure why anyone would pick hospitalization data (for which the p value was not even significant) when you have significant mortality data. 11:08 trial results irrelevant for non-dialysis patients 15:36 find-ckd results: "The increase in hepcidin from baseline was significantly smaller with low ferritin FCM or oral iron vs high ferritin FCM at all time points up to week 52." In other words, giving a lot of iron is counterproductive since it increases hepcidin and locks down all that extra iron (aka iron overload). Hepcidin levels more than doubled even in the 'low' iron arm. That being said, 16:05 shows that Hb does respond to adding more iron alone. The question is was it worth it (not according to mortality data, and guidelines not to try to raise Hb all the way to normal), when instead Hb could have been raised with ESA alone. The trial nad no mortality data. I think the trick with excess iron raising Hb is, the targeted, way too high, ferritin levels lead to spilling of Fe iron from the ferritin into the blood, which bypasses iron release by macrophages with ferroportin, ie bypasses hepcidin regulation. That's basically freeing iron by making the liver spill over. Which over time will also end up locked into other body cells by hepcidin. 17:45 the confirm-hf trial did allow anemic patients (no limit on low Hb). So obviously they would wind up with more blood and thus more oxygen to walk a few meters more. There was no benefit to mortality. 19:28 it is not clear if high fgf23 in late ckd worsens or improves the condition 36:04 storage level of vitamin D also strongly raises HIF in hypoxia ie in anemia. So raising D storage levels should work just as well as preventing breakdown of HIF with the drug Roxadustat (note it's the circulating storage form, not the active form of vit D, that potentiates HIF): Regulation of Hypoxia Inducible Factors HIF-1 and HIF-2 by Calcidiol in Hepatocellular Carcinoma Cells Under Normoxia and Hypoxia, 2022 40:20 first time I hear a nephrologist describe lower saturation and ferritin as an improvement. According to the 'guidelines', this improvement just made the patients iron deficient.
I am curious to see if these clinical guidelines align with the VA's 2019 guidelines (approved for VA physicians) in addressing patient-centered care and shared decision-making- an area where the KDIGO 2012 guidelines are lacking. Very interested to see what's ahead.
Curious as well. This was uploaded in June and they say "in the coming weeks"; however, it is now October and the current guidelines are growing more and more outdated as the world has vastly changed (especially for CKD patients) since 2012.
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