Renal Failure and CoQ10 - Coenzyme Q10 and Renal Insufficiency
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    Coenzyme Q10

CoQ10 (Coenzyme Q10) and 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@upkm.sk

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]

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