Kidney disease

Dialysis is primarily used to provide an artificial replacement for lost kidney function in people with renal failure. The death rate from cardiovascular disease for dialysis patients is much higher than the general population, regardless of age.¹ Patients with renal failure are not only exposed to higher volumes of water in their lifetime than the general population, but the barrier between blood and dialysis fluid is generally in the form of a nonselective semipermeable membrane, providing a direct route for any contaminants into the bloodstream. Consequently many of the permitted levels of contaminants in drinking water have the potential to cause problems in dialysis patients.²

It is known that tap water harbors potentially pathogenic micro-organisms that can pose a significant health threat to patients, especially those people with compromised immune systems and haemodialysis.³⁴ For decades, hospital water sources have been known to be reservoirs of nosocomial pathogens, especially organisms of the Pseudomonas sp. yet guidelines for preventing such infections do not exist.⁵⁶

Today, specialists in infectious diseases are considering point-of-use filters. They presume that the filters achieve a greater than 99% reduction in total heterotrophic plate count of bacteria in the immediate and postflush samples.⁷⁸ They conclude that such filtration units would prevent exposure of high-risk patients to waterborne pathogens. However, the results of Silbaq's 2009 study show that viable ultra-microcells pass through 0.2 micron filtration, and can be cultured on agar, as early as 72 hours after collection. The bacteria were identified using 16S ribosomal DNA sequences. The presence of those ultra-small bacteria in water filtrates would remain undetected by the standard and total heterotrophic plate count.

From the results in this study, one might conclude that the filtration strategies may remove most microbes from water, but cannot prevent it. The ability of UMC to pass through the 0.2 m filters and even 0.1 m filters might select for new emerging pathogens from diverse phyla such as S. maltophilia and Pandoraea sp. which are well recognized as pathogens among cystic fibrosis patients.⁹

F.S. Silbaq¹⁰

This work shows that chlorinated tap water harbors opportunistic microbes that can pose some health threat to dialysis patients.

Continuously evidence indicates that deficiencies in vitamin D receptor activation represents one of key players in adversely affecting cardiovascular health, as well as inducing to secondary hyperparathyroidism in chromic kidney disease patients…. Potentially, selective VDRThe Vitamin D Receptor. A nuclear receptor located throughout the body that plays a key role in the innate immune response. activators not only reduce serum parathyroid hormone levels minimizing the risk of hypercalcemia and hyperphosphatemia, but also may improve patient health, reducing the risk of cardiovascular disease.¹¹

M. Cozzolino et al.

Patients who start the MP are often unaware of the fact that their kidneys or liver are infected until blood work comes back out of range. This is due to the fact that inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. in these organs tends to be “silent.” Before the MP, the kidneys are inflamed because they are infected with the Th1 pathogens. But the patient is largely unaware of the problem because their immune system, which has been weakened by the pathogens, doesn’t kill enough of the pathogens to cause a rise in bacterial byproducts that would be picked up on a blood test.

Once patients activate the innate immune system with olmesartanMedication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. Also known by the trade name Benicar. and begin rapidly killing the Th1 pathogens, the resulting immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed. causes a rise in bacterial death, the effects of which are finally high enough to show up on lab tests.

Kidney immunopathology is unavoidable and is necessary for recovery using the Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis.. Thus, people on the MP should not be surprised to learn their kidneys are infected. Patients with Th1 disease have a high risk of kidney inflammation, and many doctors are unaware of the problem because they have no idea how sick their Th1 patients really are. Kidneys are also one of the organs that suffer significant fibrosis (collagen deposition and scarring) from the inflammatory disease process.

-Have been to have my kidney function and BP checked and everything is much improved! Having increased my Benicar frequency to 6-hourly (and I've reduced my abx except mino to give my body a rest) my blood pressure has risen to a respectable 94/57. This is remarkable, as it had stabilized at 80/40 since I was in Phase 1. Creatinine, Urea, Urate and eGFR all returning to bearable levels. Only my anaemia remains but I will hope for that to improve slowly.

So this is a lesson to others whose doctors panic and say “woah! your BP is dropping, you should take less of that Benicar”. The counter-intuitive answer is to TAKE MORE instead. ~Claudia

-My doc also worries about creatinine, but I never pushed for the 24hour test. What I did instead was to try to reduce herx, under the theory that creatinine was related to herx and both related to dying bacteria. What worked was to reduce the herx. It worked like a champ, my creatinine was normal.

What works to stop the herx seems to depend on the person and on the stage of MP. What works to convince a Doc that the Benicar isn't the problem is even more variable, but somehow you have to do it. ~Chris

-Finally my creatinine values are down in the normal range (101) (first time since I measured them in April). Hemoglobin is also up (11,5). Will slowly increase mino after having been to a nephrologist next week (only reason for seeing the specialist is to maintain a good relation to my doc). Think it is wise to keep creatinine low when I go see the specialist, so that no stopping of meds or anything will be enforced. Just finished a year on the MP, it has been a lot tougher than expected. And the time it takes seems so long. But hanging in there. ~inge 01/04/08

-I will have been off abx for 25 days. My serum creatinine is now back down to 71 umol/L (0.81 mg/dL), with an eGFR of 80 mL/min. These are the same as before starting the MP, so my GP was “relieved” when I spoke to her this morning. I haven't been able to stop smiling all day! ~Asilan

-I've had some blood tests back today and creatinine has gone down to 200. Potassium has gone down to 5.2. Urea has slightly gone down to 22.5. Haemaglobin and lymphocyte count are slightly low. So obviously slowing down the herx has helped with bloods. Bloods for me are a definite way of registering the herx because I'm always herxing and I'm not knowing the difference between tolerable and intolerable. Every since I took Benicar I found I was always herxing without the antibiotics and now I've been off Prednisilone for a year I feel like my immune reactions are very turned on and working stronger than when I started so I have found myself also dropping the antibiotic dose to cope with the herx. ~Simon Elrahi

-I received some good news during my doctor appointment. My kidney functioning tests were normal. My doctor had taken me off the MP meds back in May due to the increase in my creatinine and BUN. I wasn't sure how my tests results would be right now since I was now at the maximum doses of the MP meds. I was keeping my fingers crossed that the results would be good so my doctor wouldn't take me off the MP meds again. My doctor and I were both surprised to see that both my creatinine and BUN were normal. ~Mike9a

-Mino 25mg every two days Benicar 40mg every 3 to 5 hours. One week past kidney” crisis”: New test results are almost normal. Whew. ~Somadoc

-Just to let you know, that since stopping all abx and reducing the Beni to three times a day, things are much improved- as expected they would be. Kidney function: creatinine -89 ( was 103), eGFR =62 ( was 52). ~Kas

-only benicar every 4 hours during day time and a few times once at 3 am. creatinine down from 138 to 116 (two days ago) (range 60-105). it was comforting to see that an increase in benicar did not lead to an increase in creatinine, as my nephrologist speculated it would. ~inge

-the renal bloods are so much better & the Dr will no longer blame the Benicar for the abnormal readings. During all of that time I was on the 40mg q6h Benicar, plus the occasional 20mg. The creatinin seems to be going down & the eGFR up, towards the end of the zith cycle. ~Pundun

-My eGFR was retested at 53 up from 45 which my doc informally calls a percentage. Proof that decreased light and more Benicar increase it and therefore that it is IP :). ~PatrickBurke Jul08