Jump to content
IndiaDivine.org

CoQ10 (Coenzyme Q10) and Renal Failure

Rate this topic


Guest guest

Recommended Posts

CoQ10 (Coenzyme Q10) and Renal Failure

 

http://www.coq10supplement.com/herbal-remedies/coenzyme-q10/coq10-renal-failure

 

Chronic renal failure (CRF) is the progressive loss of kidney function.

Chronic Renal Insufficiency (CRI) is the early stage, when the kidneys no longer

function properly but do not yet require dialysis.

 

CoQ10 was studied in a small pilot study involving 21 patients with chronic

renal failure. Researchers administered CoQ10 to 11 of the subjects while 10

received a placebo capsule. To be included in the study patients had to have a

creatinine level of 5 mg/dl or above. After 4 weeks, the subjects receiving

CoQ10 had significant decreases in serum creatinine and urea while creatinine

clearance significantly increased. At the end of the 4 week study the number of

patients on dialysis was significantly less in the CoQ10 group. 36.2% of the

patients in the CoQ10 group were on dialysis at the end of the study while 90.0%

of the placebo group were on dialysis at the end of the study.

 

An increase in blood antioxidant levels and a significant decrease in

indicators of oxidative stress were noted by the study group. (J Nutr Environ

Med,

2000; 10: 281-288)

 

" Randomized, Double-Blind Placebo-Controlled Trial of Coenzyme Q10 in Chronic

Renal Failure: Discovery of a New Role, " Singh RB, Khanna HK, Niaz MA, J Nutr

Environ Med, 2000;10:281-288.36843

 

 

Medical Abstracts of Clinical Studies and Research On Renal Failure and CoQ10

 

 

Malondialdehyde and selected antioxidant plasma levels in conservatively

treated patients with kidney diseases

 

Bratisl Lek Listy 2000;101(9):490-4

 

Gazdikova K, Gvozdjakova A, Kucharska J, Spustova V, Braunova Z, Dzurik R.

 

Institute of Preventive and Clinical Medicine, Limbova 14, SK-833 01

Bratislava 37, Slovakia. gazdikova

 

Oxidation stress and decreased antioxidative capacity participate in the

progression and complications of renal diseases such as hyperlipoproteinemia or

cardiovascular diseases. Many data have been collected on oxidation stress in

dialysed patients, however a shortage of information is evident in

conservatively treated patients.

 

STUDY AIMS: To determine the blood and/or plasma levels of MDA and the

selected antioxidants, i.e. Coenzyme Q10 (CoQ), alpha-tocoferol, beta-carotene

in

conservatively treated patients with kidney diseases.

 

PATIENTS AND METHODS: Fifty five patients (45 with interstitial nephritis and

10 with glomerulonephritis) were included. They were divided into 3 subgroups

on the basis of their clearance of creatinine (Ckr). Only validated methods

have been exploited for the determination of variables.

 

RESULTS: MDA plasma levels were increased (5.37 +/- 0.10, reference range

(rr.) < 4.5 mumol/l) with the highest levels in patients treated by

immunosuppression. CoQ plasma (0.35 +/- 0.04, rr. 0.4-1.0 mumol/l) and blood

(0.30 +/- 0.03

mol/l) were decreased, notably in patients with interstitial nephritis. No

correlation with Ckr was apparent. alpha-tocopherol plasma levels (42.1 +/-

3.04, rr. 15-40 mumol/l) were increased, but the concentrations increased

further

with the decreasing kidney function. beta-carotene plasma (2.14 +/- 0.39, rr. >

0.8 mumol/l) were in reference range but decreased with the decrease of

kidney function.

 

CONCLUSIONS: CoQ plasma levels are decreased and MDA levels increased in

conservatively treated kidney disease patients even in just slightly decreased

renal function. beta-carotene levels decrease only in advanced renal failure.

These changes could participate in kidney disease progression and it is

suggested

that their correction opens the possibility of progression inhibition. (Tab.

3, Ref. 27.)

 

PMID: 11187051 [PubMed - indexed for MEDLINE]

 

 

Quinone-responsive multiple respiratory-chain dysfunction due to widespread

coenzyme Q10 deficiency.

Lancet 2000 Jul 29;356(9227):391-5

Rotig A, Appelkvist EL, Geromel V, Chretien D, Kadhom N, Edery P, Lebideau M,

Dallner G, Munnich A, Ernster L, Rustin P.

 

Unite de Recherches sur les Handicaps Genetiques de l'Enfant, INSERM U393,

Hopital des Enfants-Malades, Paris, France.

 

BACKGROUND: The respiratory-chain deficiencies are a broad group of largely

untreatable diseases. Among them, coenzyme Q10 (ubiquinone) deficiency

constitutes a subclass that deserves early and accurate diagnosis.

 

METHODS: We assessed respiratory-chain function in two siblings with severe

encephalomyopathy and renal failure. We used high-performance liquid

chromatography analyses, combined with radiolabelling experiments, to quantify

cellular

coenzyme Q10 content. Clinical follow-up and detailed biochemical

investigations of respiratory chain activity were carried out over the 3 years

of oral

quinone administration.

 

FINDINGS: Deficiency of coenzyme Q10-dependent respiratory-chain activities

was identified in muscle biopsy, circulating lymphocytes, and cultured skin

fibroblasts. Undetectable coenzyme Q10 and results of radiolabelling experiments

in cultured fibroblasts supported the diagnosis of widespread coenzyme Q10

deficiency. Stimulation of respiration and fibroblast enzyme activities by

exogenous quinones in vitro prompted us to treat the patients with oral

ubidecarenone (5 mg/kg daily), which resulted in a substantial improvement of

their

condition over 3 years of therapy.

 

INTERPRETATION: Particular attention should be paid to multiple

quinone-responsive respiratory-chain enzyme deficiency because this rare

disorder can be

successfully treated by oral ubidecarenone.

 

PMID: 10972372 [PubMed - indexed for MEDLINE]

 

Coenzyme Q10 levels, plasma lipids and peroxidation extent in renal failure

and in hemodialytic patients.

Mol Aspects Med 1994;15 Suppl:s213-9

 

Lippa S, Colacicco L, Calla C, Sagliaschi G, Angelitti AG.

 

Istituto di Chimica e Chimica Clinica, Universita Cattolica del S. Cuore.

 

Coenzyme Q10 (CoQ10), vitamin E, triglycerides and conjugated dienes were

measured in a group of 48 patients on chronic hemodialysis, in 15 uremic

patients

and in a control group of 10 normal subjects. CoQ10 levels were significantly

lower (P < 0.001) in both hemodialytic and uremic patients compared with the

normal group whereas triglycerides were significantly higher (P < 0.001) with

respect to both normal subjects and uremic patients. Conjugated dienes were

significantly higher (P < 0.001) in both hemodialytic and uremic patients with

respect to normal subjects. The predialytic values of vitamin E were higher in

hemodialytic patients with respect to both normal subjects and uremic patients

whereas the postdialytic values were in the normal range. A restoration

mechanism of vitamin E after hemodialytic treatment was hypothesized.

 

PMID: 7752833 [PubMed - indexed for MEDLINE]

 

 

Pathophysiological mechanism of ischemic acute renal failure: protective

effect of coenzyme Q10, Ca channel blocker, superoxide dismutase and protease

inhibitor against ischemic acute renal failure

 

Nippon Jinzo Gakkai Shi 1989 Jan;31(1):15-24

 

Higuchi C.

 

Ischemic insult has been considered a cause of cellular injuries under

certain circumstance, such as the disturbance of energy metabolism, the

alternation

of calcium homeostasis, the production of oxygen radical and the release of

lysosomal protease. The present study was designed to clarify the

pathophysiological effects of coenzyme Q10 (CoQ10), diltiazem, superoxide

dismutase (SOD)

and urinastatin on the development and progression of ischemic acute renal

failure (IARF) of the rat. At 24 hours after reflow following 45 minutes

ischemia,

serum urea nitrogen, creatinine and fractional excretion of sodium were 99.3

mg/dl, 3.14 mg/dl, 5.95% respectively, in non-treated IARF rats. Renal ATP

content was reduced to 0.91 micrograms/mg. prot. from 10.59 micrograms/mg. prot.

at 10 minutes after ischemic insult, and remained at almost the same level

throughout the entire 45 minutes ischemia. Although the subsequent blood reflow

resulted in the recovery of ATP content, it was up to 50% of normal level at 24

hours after reflow following 45 minutes ischemia. During the ischemic period,

the pathological changes were mild, whereas, after reflow, tissue involvement

was mainly localized in the S3 segment of the proximal tubule. Major

alteration were the loss of brush border, high amplitude swelling of

mitochondria with

matrical densities and fragmentation of the epithelial cell. At 24 hours after

reflow, it was observed that renal function was superior in IARF rats treated

with CoQ10, diltiazem, SOD and urinastatin. The treated rats also had higher

ATP contents and showed less pathological changes than non-treated rats. Among

these inhibitory agents, diltiazem exerted the most reliable effect. From

these results, it was concluded that IARF was obviously caused by such

pathophysiological mechanisms as mentioned above. Especially, Ca influx into the

cells

is one of the most important factors on pathogenesis of IARF.

 

PMID: 2746996 [PubMed - indexed for MEDLINE]

 

CoQ10 (Coenzyme Q10) and Parkinsons

http://www.coq10supplement.com/herbal-remedies/coenzyme-q10/coq10-parkinsons

 

 

 

Link to comment
Share on other sites

Renal failure is the most common cause of death in the elderly;

however supplementing with coQ10 doesn't address three underlying

natural biological causes of renal failure.

 

Glutathione, the kidney's natural protection, falls off with age, and

glutathione precursors are very low in the human diet especially in a

cooked food diet. Lipoic acid and to a certain extent CoQ10 recycles

glutathione you do have, but it's the low glutathione precursors that

need to be improved.

 

The body's only fibrinolytic enzyme, plasmin, also falls off with

age, which allows fibrosis, the biggest cause of organ failure, to

accumulate. This can be fixed with nattokinase and serrapeptase.

 

Natural HGH release also falls as one ages, allowing organ and muscle

shrinkage; research also shows that kidney size and function can be

improved with a program of HGH increase.

 

 

Bonnie

 

 

 

, surpriseshan2

wrote:

>

>

> CoQ10 (Coenzyme Q10) and Renal Failure

>

> http://www.coq10supplement.com/herbal-remedies/coenzyme-q10/coq10-

renal-failure

>

> Chronic renal failure (CRF) is the progressive loss of kidney

function.

> Chronic Renal Insufficiency (CRI) is the early stage, when the

kidneys no longer

> function properly but do not yet require dialysis.

>

> CoQ10 was studied in a small pilot study involving 21 patients with

chronic

> renal failure. Researchers administered CoQ10 to 11 of the subjects

while 10

> received a placebo capsule. To be included in the study patients

had to have a

> creatinine level of 5 mg/dl or above. After 4 weeks, the subjects

receiving

> CoQ10 had significant decreases in serum creatinine and urea while

creatinine

> clearance significantly increased. At the end of the 4 week study

the number of

> patients on dialysis was significantly less in the CoQ10 group.

36.2% of the

> patients in the CoQ10 group were on dialysis at the end of the

study while 90.0%

> of the placebo group were on dialysis at the end of the study.

>

> An increase in blood antioxidant levels and a significant decrease

in

> indicators of oxidative stress were noted by the study group. (J

Link to comment
Share on other sites

Join the conversation

You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.

Guest
Reply to this topic...

×   Pasted as rich text.   Paste as plain text instead

  Only 75 emoji are allowed.

×   Your link has been automatically embedded.   Display as a link instead

×   Your previous content has been restored.   Clear editor

×   You cannot paste images directly. Upload or insert images from URL.

Loading...
×
×
  • Create New...