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.3)4) 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.5)6)

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.7)8) 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.

Role of Vitamin D Receptor in in chronic kidney disease

Continuously evidence indicates that deficiencies in vitamin D receptorA nuclear receptor located throughout the body that plays a key role in the innate immune response. 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.

M. Cozzolino et al.11)

J Nephrol. 2010 Jun 10. pii: 33B14427-99AC-49E6-89CA-36BC1A6F102F. Vitamin D receptor activators and response to injury in kidney diseases. 12)

Eleftheriadis T, Antoniadi G, Liakopoulos V, Antoniadis N, Stefanidis I, Galaktidou G. Department of Nephrology, General Hospital of Serres, Serres - Greece and Research Institute, Theagenion Anticancer Hospital, Thessaloniki - Greece. Abstract Clinical studies have confirmed that administration of vitamin D receptor (VDR) activators offers a survival benefit in hemodialysis patients and may help in preservation of renal function in predialysis patients. Accumulated clinical and mainly experimental data support that in the context of kidney disease, VDR activators exert their beneficial effect not only due to their action on calcium and phosphorus homeostasis, but also through modulation of the response to injury. They attenuate systemic and renal 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., and they affect the tissue repair process, reducing renal fibrosis. This aspect of the functions of VDR activators in kidney disease is reviewed in the present manuscript.

Selective vitamin D receptor activation: effect on renal physiopathology. 13) Marangella M, Berutti S, Fabbrini L G Ital Nefrol ; 26(S-49) :23-29 Download citation Affiliation S.C. Nefrologia e Dialisi, A.O. Ordine Mauriziano-Torino, Torino - Italy. Abstract The wide distribution of the vitamin D receptor (VDR) suggests that its activators (VDRAs) are involved in diverse organ functions including the cardiovascular, immune, and reproductive systems. These actions are likely to be independent of PTH and calcium/phosphorus levels. Earlier studies had shown that calcitriol was able to favorably influence experimental nephritis, remnant kidney glomerulosclerosis, and interstitial fibrosis, mediated through inhibition of inflammatory cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system.. Recently, VDRAs were shown to inhibit the reninangiotensin system (RAS), acting directly on the renin gene promoter. This action is independent of the systemic RAS blockade. VDRAs also inhibit other important gene promoters including NF-kBA protein that stimulates the release of inflammatory cytokines in response to infection and p65, which are known to foster inflammation and fibrogenesis. These multiple actions result in a decrease in macrophage infiltration, fibroblast activation, and endothelial mesenchymal transition in the kidney. These findings represent the rationale for the use of VDRAs, in association with RAS blocking agents, to counteract the progression of renal injury characterized by inflammation and neofibrogenesis. However, despite promising preliminary results, the human studies available to date do not allow to draw definitive conclusions on this matter.

Kidney Int. 2010 Nov;78(10):975-80. Epub 2010 Sep 15. Direct evidence for a causative role of FGF23 in the abnormal renal phosphate handling and vitamin D metabolism in rats with early-stage chronic kidney disease. 14)

Hasegawa H, Nagano N, Urakawa I, Yamazaki Y, Iijima K, Fujita T, Yamashita T, Fukumoto S, Shimada T. Innovative Drug Research Laboratories, Kyowa Hakko Kirin, Tokyo, Japan. Abstract Circulating levels of fibroblast growth factor 23 (FGF23) are elevated in patients with early chronic kidney disease (CKD) and are postulated to cause low blood levels of 1,25-dihydroxyvitamin DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol., as well as normal phosphate levels. In order to provide more direct evidence for the pathophysiological role of FGF23 in the settings of mineral ion homeostasis typically seen in early CKD, we studied rats with progressive CKD treated with anti-FGF23 neutralizing antibody. Without antibody treatment, rats with CKD exhibited high circulating levels of FGF23 and parathyroid hormone, low 1,25-dihydroxyvitamin D, and normal serum phosphate levels, accompanied by increased fractional excretion of phosphate. Antibody treatment, however, lessened fractional excretion of phosphate, thus increasing serum phosphate levels, and normalized serum 1,25-dihydroxyvitamin D by increased 1α-OHase and decreased 24-OHase expressions in the kidney. These antibody-induced changes were followed by increased serum calcium levels, leading to decreased serum parathyroid hormone. Hence, our study shows that FGF23 normalizes serum phosphate and decreases 1,25-dihydroxyvitamin D levels in early-stage CKD, and suggests a pathological sequence of events for the development of secondary hyperparathyroidism triggered by increased FGF23, followed by a reduction of 1,25-dihydroxyvitamin D and calcium levels, thereby increasing parathyroid hormone secretion.

Subclinical kidney infection

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 inflammation 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 pathogensThe community of bacterial pathogens which cause chronic inflammatory disease - one which almost certainly includes multiple species and bacterial forms., 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 diseaseAny of the chronic inflammatory diseases caused by bacterial pathogens. 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.

Calcium-alkali syndrome

Am J Kidney Dis. 2009 Apr;53(4):711-4. Epub 2009 Jan 29. Calcium-alkali syndrome due to vitamin D administration and magnesium oxide administration. Hanada S, Iwamoto M, Kobayashi N, Ando R, Sasaki S. Department of Nephrology, Musashino Red Cross Hospital, Tokyo Medical and Dental University, Tokyo, Japan. s-hanada@umin.ac.jp 15)

Got Calcium? Welcome to the Calcium-Alkali Syndrome. Patel AM, Goldfarb S J Am Soc Nephrol Apr 2010; Download citation Affiliation Renal-Electrolyte and Hypertension Division, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania. Abstract We recommend changing the name of the milk-alkali syndrome to the calcium-alkali syndrome, because the new terminology better reflects the shifting epidemiology and understanding of this disorder. The calcium-alkali syndrome is now the third most common cause of hospital admission for hypercalcemia, and those at greatest risk are postmenopausal or pregnant women.

The incidence of the calcium-alkali syndrome is growing in large part as a result of the widespread use of over-the-counter calcium and vitamin D supplements.Advertising for treatment or prevention of osteoporosis has long encouraged this use. Intricate mechanisms mediating the calcium-alkali syndrome depend on interplay among intestine, kidney, and bone. New insights regarding its pathogenesis focus on the key role of calcium-sensing receptors and TRPV5 channels in the modulation of renal calcium excretion. Restoring extracellular blood volume, increasing GFR and calcium excretion, and discontinuing calcium supplementation provide best treatment. 16)

Evidence of infectious cause

Patients experiences

The renal bloods are so much better and the doctor 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 creatinine seems to be going down and the eGFR up, towards the end of the zith cycle.

Pundun, MarshallProtocol.com

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 (July '08), MarshallProtocol.com

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, MarshallProtocol.com

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, MarshallProtocol.com

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, MarshallProtocol.com

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, MarshallProtocol.com

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.

Simonc, MarshallProtocol.com

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, MarshallProtocol.com

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, MarshallProtocol.com

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, MarshallProtocol.com

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 “Whoa! Your BP is dropping, you should take less of that Benicar.” The counter-intuitive answer is to TAKE MORE instead.

Claudia, MarshallProtocol.com

Dear MPKB Reader: You have arrived at one of the articles that has not yet completed the development and review process in the knowledge base. Some of the content here may be helpful, but please know that this page is not complete. There are about 400 articles in the KB, and this is one we are still working on. Thanks for your patience.

Notes and comments


  • Avoid foods high in potassium for people with kidney disease?

Atherosclerosis in chronic kidney disease: the role of macrophagesValentina Kon, MacRae F. Linton & Sergio Fazio About the authors

topof page Abstract

Patients with chronic kidney disease (CKD) are at increased risk of atherosclerotic cardiovascular disease and loss of renal parenchyma accelerates atherosclerosis in animal models. Macrophages are central to atherogenesis because they regulate cholesterol traffic and inflammation in the arterial wall. CKD influences macrophage behavior at multiple levels, rendering them proatherogenic. Even at normal creatinine levels, macrophages from uninephrectomized Apoe−/− mice are enriched in cholesterol owing to downregulation of cholesterol transporter ATP-binding cassette subfamily A member 1 levels and activation of nuclear factor κB, which leads to impaired cholesterol efflux. Interestingly, treatment with an angiotensin-II-receptor blocker (ARBA drug which is an angiotensin receptor blocker. One of the ARBs is olmesartan (Benicar). Not all ARBs activate the Vitamin D Receptor.) improves these effects. Moreover, atherosclerotic aortas from Apoe−/− mice transplanted into renal-ablated normocholesterolemic recipients show plaque progression and increased macrophage content instead of the substantial regression seen in recipient mice with intact kidneys. ARBs reduce atherosclerosis development in mice with partial renal ablation. These results, combined with the clinical benefits of angiotensin-converting-enzyme (ACE) inhibitors and ARBs in patients with CKD, suggest an important role for the angiotensin system in the enhanced susceptibility to atherosclerosis seen across the spectrum of CKD. The role of macrophages could explain why these therapies may be effective in end-stage renal disease, one of the few conditions in which statins show no clinical benefit.

From: Jigsaw Date: 2011-03-10 19:19:56 Reply: http://www.marshallprotocol.com/reply.php?topic_id=1448

Hi Trevor. I am pleased to see your positive results from the use of sodium bicarbonate. I started using it (840 mg/ day) in August and have had one favourable result with potassium back into the normal range. Not much effect on creatinine.

A query on your on your test collecting procedure. Was this always done in the morning after an overnight fast? Below is a slightly edited excerpt from a report I made in 3/08.

All values were from blood samples taken in the morning after overnight fasting. Seven days before the the 3/08 readings (urea, 18.3; creatinine, 148; eGFR, 40; potassium 5.5) , I had one set taken in the afternoon after a chicken lunch, where urea was 23.3, creatinine 201 and eGFR 28. Potassium was 5.4.

As I noted in a reply to Inge's thread, my cardiologist/physician and the Path lab said this would have no effect: but http://www.medicine.ox.ac.uk/bandolier/band156/b156-3.html noted that the test was standardised on samples taken in the morning from subjects after an overnight fast and quoting data showing that blood creatinine was raised an average of 25% for samples taken 1-2 hours after a meat meal One might say mine was raised by 53/148 x 100 = 35.5%..

I am not sure that the web link will still come up. I think the tests were done on healthy subjects and imagine that the effect would be greater where GFR is less adequate.

I see the words “kidney failure” loosely bandied around the forums, and I thought the attached article gives a little perspective on what it is like to really have experienced kidney failure, and become reliant on life-long dialysis. Even though their eGFR and blood Creatinine might be the same as people who have experienced “kidney failure,” none of our cohort have become dependent on dialysis (while they remained on Olmesartan).

Here is an article giving a glimpse into what it is like to experience true kidney failure:


and another:


and another from India:



Nuclear receptorsIntracellular receptor proteins that bind to hydrophobic signal molecules (such as steroid and thyroid hormones) or intracellular metabolites and are thus activated to bind to specific DNA sequences which affect transcription. in renal disease. Levi M Biochim Biophys Acta Apr 2011; Full text via publisher | Download citation Affiliation Abstract Diabetes is the leading cause of end-stage renal disease in developed countries. In spite of excellent glucose and blood pressure control, including administration of angiotensin converting enzyme inhibitors and/or angiotensin II receptor blockers, diabetic nephropathy still develops and progresses. The development of additional protective therapeutic interventions is, therefore, a major priority. Nuclear hormone receptors regulate carbohydrate metabolism, lipid metabolism, the immune response, and inflammation. These receptors also modulate the development of fibrosis. As a result of their diverse biological effects, nuclear hormone receptors have become major pharmaceutical targets for the treatment of metabolic diseases. The increasing prevalence of diabetic nephropathy has led intense investigation into the role that nuclear hormone receptors may have in slowing or preventing the progression of renal disease. This role of nuclear hormone receptors would be associated with improvements in metabolism, the immune response, and inflammation. Several nuclear receptorIntracellular receptor proteins that bind to hydrophobic signal molecules (such as steroid and thyroid hormones) or intracellular metabolites and are thus activated to bind to specific DNA sequences which affects transcription. activating ligands (agonists) have been shown to have a renal protective effect in the context of diabetic nephropathy. This review will discuss the evidence regarding the beneficial effects of the activation of several nuclear, especially the vitamin D receptor (VDR), farnesoid X receptor (FXR), and peroxisome-proliferator-associated receptors (PPARs) in preventing the progression of diabetic nephropathy and describe how the discovery and development of compounds that modulate the activity of nuclear hormone receptors may provide potential additional therapeutic approaches in the management of diabetic nephropathy. This article is part of a Special Issue entitled: Translating nuclear receptors from health to disease.

a link to the document http://mpkb.org/home/othertreatments/sodium_bicarbonate would be appropriate somewhere here IMO Sallie Q Jan 2014

made Link — Sallie Q 11.18.2015


1) , 11)
The role of vitamin d receptor activation in chronic kidney disease.
Cozzolino M, Malindretos P
Hippokratia14p7-9(2010 Jan)
The quality of dialysis water.
Pontoriero G, Pozzoni P, Andrulli S, Locatelli F
Nephrol Dial Transplant18 Suppl 7pvii21-5; discussion vii56(2003 Aug)
Defining the microbiological quality of dialysis fluid.
Ledebo I, Nystrand R
Artif Organs23p37-43(1999 Jan)
Identification of culturable bacteria present in haemodialysis water and fluid.
Gomila M, Gascó J, Busquets A, Gil J, Bernabeu R, Buades JM, Lalucat J
FEMS Microbiol Ecol52p101-14(2005 Mar 1)
The hospital water supply as a source of nosocomial infections: a plea for action.
Anaissie EJ, Penzak SR, Dignani MC
Arch Intern Med162p1483-92(2002 Jul 8)
Established and emerging waterborne nosocomial infections.
Merlani GM, Francioli P
Curr Opin Infect Dis16p343-7(2003 Aug)
Efficacy of new point-of-use water filter for preventing exposure to Legionella and waterborne bacteria.
Sheffer PJ, Stout JE, Wagener MM, Muder RR
Am J Infect Control33pS20-5(2005 Jun)
Isolation of infectious cystic fibrosis patients: results of a systematic review.
Vonberg RP, Gastmeier P
Infect Control Hosp Epidemiol26p401-9(2005 Apr)
Viable ultramicrocells in drinking water.
Silbaq FS
J Appl Microbiol106p106-17(2009 Jan)
Vitamin D receptor activators and response to injury in kidney diseases.
Eleftheriadis T, Antoniadi G, Liakopoulos V, Antoniadis N, Stefanidis I, Galaktidou G
J Nephrolp(2010 Jun 10)
[Selective vitamin D receptor activation: effect on renal physiopathology].
Marangella M, Berutti S, Fabbrini L
G Ital Nefrol26 Suppl 49pS23-9(2009 Nov-Dec)
Direct evidence for a causative role of FGF23 in the abnormal renal phosphate handling and vitamin D metabolism in rats with early-stage chronic kidney disease.
Hasegawa H, Nagano N, Urakawa I, Yamazaki Y, Iijima K, Fujita T, Yamashita T, Fukumoto S, Shimada T
Kidney Int78p975-80(2010 Nov)
Calcium-alkali syndrome due to vitamin D administration and magnesium oxide administration.
Hanada S, Iwamoto M, Kobayashi N, Ando R, Sasaki S
Am J Kidney Dis53p711-4(2009 Apr)
Got calcium? Welcome to the calcium-alkali syndrome.
Patel AM, Goldfarb S
J Am Soc Nephrol21p1440-3(2010 Sep)
home/diseases/kidney_disease.txt · Last modified: 03.22.2017 by sallieq
© 2015, Autoimmunity Research Foundation. All Rights Reserved.