Morphologic Features of the Myopathy Associated With Chronic Renal Failure

Diesel, Wayne; Knight, Bryan K.; Noakes, Timothy D.; Swanepoel, Charles R.; Smit, R van Zyl; Kaschula, R. O. C.; Sinclair-Smith, C

doi:10.1016/s0272-6386(12)80430-6

Cited by 148 publications

(97 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The diagnosis of uremic myopathy is based on clinical features, including weakness (defined as a failure to generate force) and wasting (sarcopenia), which affect predominantly the proximal lower limbs 102. Whereas muscle enzymes levels and electromyographical studies are usually normal, muscle biopsies show atrophy of the fast‐twitch white (type 2) fibres 103, 104. These morphological features are similar from those found in patients with vitamin D deficiency 11, 48…”

Section: Bone and Musculoskeletal Abnormalities In Chronic Kidney Dismentioning

confidence: 55%

Vitamin D, a modulator of musculoskeletal health in chronic kidney disease

Molina

Carrero

Bover

et al. 2017

J cachexia sarcopenia muscle

View full text Add to dashboard Cite

The spectrum of activity of vitamin D goes beyond calcium and bone homeostasis, and growing evidence suggests that vitamin D contributes to maintain musculoskeletal health in healthy subjects as well as in patients with chronic kidney disease (CKD), who display the combination of bone metabolism disorder, muscle wasting, and weakness. Here, we review how vitamin D represents a pathway in which bone and muscle may interact. In vitro studies have confirmed that the vitamin D receptor is present on muscle, describing the mechanisms whereby vitamin D directly affects skeletal muscle. These include genomic and non‐genomic (rapid) effects, regulating cellular differentiation and proliferation. Observational studies have shown that circulating 25‐hydroxyvitamin D levels correlate with the clinical symptoms and muscle morphological changes observed in CKD patients. Vitamin D deficiency has been linked to low bone formation rate and bone mineral density, with an increased risk of skeletal fractures. The impact of low vitamin D status on skeletal muscle may also affect muscle metabolic pathways, including its sensitivity to insulin. Although some interventional studies have shown that vitamin D may improve physical performance and protect against the development of histological and radiological signs of hyperparathyroidism, evidence is still insufficient to draw definitive conclusions.

show abstract

Section: Bone and Musculoskeletal Abnormalities In Chronic Kidney Dismentioning

confidence: 55%

Vitamin D, a modulator of musculoskeletal health in chronic kidney disease

Molina

Carrero

Bover

et al. 2017

J cachexia sarcopenia muscle

View full text Add to dashboard Cite

show abstract

“…Second, O 2 conductance from muscle microcirculation to mitochondria is particularly low in CRF patients (10) and after rHuEPO therapy still remains at ‫ف‬ 70% of that seen in control subjects. The structural basis of this abnormal O 2 transport conductance is likely microvascular rarification and capillarymyofiber dissociation provoked by a uremic myopathy (11)(12)(13). As a result of these changes, the ratio of muscle diffusive to perfusive conductance as defined by Piiper et al (14)(15)(16) may either not vary (10) or even fall after rHuEPO.…”

Section: Introductionmentioning

confidence: 99%

“…Structural and histochemical findings in skeletal muscle biopsies obtained in CRF patents (11)(12)(13) indicate poor capillary network and capillary-myofiber dissociation as the foremost characteristic findings, but also myopathic changes that could decrease oxygen-dependent metabolism. Abnormal oxidative capacity is claimed to exist in CRF patients by some authors (19).…”

mentioning

confidence: 97%

Cellular bioenergetics after erythropoietin therapy in chronic renal failure.

Marrades¹,

Alonso²,

Roca³

et al. 1996

J. Clin. Invest.

View full text Add to dashboard Cite

After erythropoietin (rHuEPO) therapy, patients with chronic renal failure (CRF) do not improve peak O 2 uptake (O 2 peak) as much as expected from the rise in hemoglobin concentration ([Hb]). In a companion study, we explain this phenomenon by the concurrent effects of fall in muscle blood flow after rHuEPO and abnormal capillary O 2 conductance observed in CRF patients. The latter is likely associated with a poor muscle microcirculatory network and capillary-myofiber dissociation due to uremic myopathy. Herein, cellular bioenergetics and its relationships with muscle O 2 transport, before and after rHuEPO therapy, were examined in eight CRF patients (27 Ϯ 7.3 [SD] yr) studied pre-and post-rHuEPO ([Hb] ϭ 7.8 Ϯ 0.7 vs. 11.7 Ϯ 0.7 g ϫ dl Ϫ 1 ) during an incremental cycling exercise protocol. Eight healthy sedentary subjects (26 Ϯ 3.1 yr) served as controls. We hypothesize that uremic myopathy provokes a cytosolic dysfunction but mitochondrial oxidative capacity is not abnormal. 31 P-nuclear magnetic resonance spectra ( 31 P-MRS) from the vastus medialis were obtained throughout the exercise protocol consisting of periods of 2 min exercise (at 1.67 Hz) at increasing workloads interspersed by resting periods of 2.5 min. On a different day, after an identical exercise protocol, arterial and femoral venous blood gas data were obtained together with simultaneous measurements of femoral venous blood flow ( leg) to calculate O 2 delivery ( O 2 leg) and O 2 uptake ( O 2 leg). Baseline resting [phosphocreatine] to [inorganic phosphate] ratio ([PCr]

show abstract

“…Some explanations that have been provided include accumulation of immunoreactive fragments of cardiac troponins due to reduced renal clearance (15,16) or continuous cardiac release from limited areas of clinically silent myocardial necrosis (17). Other possible hypotheses are the reexpression of cTnT isoforms in the skeletal muscle fibers during uremic-induced skeletal myopathy (18), the increase of left ventricular mass index (LVMI) (19), the loss of membrane integrity, constant outflow from the free cytosolic troponin pool (20), and uremic damage on myocardial cells (21). An additional drawback in the diagnostic use of traditional biomarkers of myocardial necrosis is the influence of the dialysis process itself on metabolism of cTnT, CK-MB, and myoglobin (22).…”

Section: Introductionmentioning

confidence: 99%

Effect of hemodialysis on traditional and innovative cardiac markers

Montagnana

Lippi

Tessitore

et al. 2008

Clinical Laboratory Analysis

View full text Add to dashboard Cite

The diagnostic approach to acute coronary syndrome (ACS) is challenging in patients with impaired renal function since most serum biomarkers are commonly increased in this clinical setting. Cardiac troponin T (cTnT), creatine kinase isoenzyme MB (CK MB), myoglobin, and ischemia modified albumin (IMA), were assayed in 45 patients prehemodialysis (pre-HD) and posthemodialysis (post-HD), and results were adjusted for hemoconcentration. The pre-HD values of serum IMA and cTnT were above the respective diagnostic thresholds (IMAo85 K units/L; cTnT o0.03 ng/mL) in six (13%) and 27 (60%) patients undergoing chronic HD, respectively. A significant (105.0 vs. 79.0 K units/L, Po0.0001) and variable (138%; 95% confidence interval [CI], 12-65%) increase of serum IMA was observed post-HD, whereas the other biomarkers significantly decreased (cTnT: 0.029 vs. 0.044 ng/mL, P 5 0.016; CK-MB:2.33 vs.2.50 mg/L, Po 0.0001; myoglobin: 128.1 vs. 148.7 mg/L, Po0.0001). Biomarkers of myocardial injury, especially cTnT and IMA, might be used in HD patients, provided that an appropriate diagnostic interpretation is guarantee, according to individual baseine value, metabolism, and time of sampling. Moreover, IMA might be reliably applied to stratify the long-term risk of these patients, but not for diagnosing an ACS during or immediately post-HD.

show abstract

Morphologic Features of the Myopathy Associated With Chronic Renal Failure

Cited by 148 publications

References 14 publications

Vitamin D, a modulator of musculoskeletal health in chronic kidney disease

Vitamin D, a modulator of musculoskeletal health in chronic kidney disease

Cellular bioenergetics after erythropoietin therapy in chronic renal failure.

Effect of hemodialysis on traditional and innovative cardiac markers

Contact Info

Product

Resources

About