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PubMed2005

Hypertension and the kidney.

Hypertension is an important and widely prevalent risk factor for the development of chronic kidney disease (CKD), which unfortunately may progress to end-stage renal disease. CKD is a progressive condition that causes significant morbidity and mortality. Diabetes is the leading cause of end-stage renal disease in the Western world. Both hypertension and diabetes are the causative factors for the occurrence of CKD and its consequences. Aggressive control of hypertension and diabetes is indicated to reduce the risk for kidney disease in the community. Certainly, effective control of hypertension is a proven modality to prevent renal disease. The concept of decreasing the systemic blood pressure as well as the intraglomerular pressure has led to the application of rational therapeutic options in patients with renal insufficiency. Although treatment of hypertension alone is critical, drugs that block the renin-angiotensin system have been shown to have special renal (and cardiovascular) benefits. Early detection and treatment of microalbuminuria is an integral part of disease management. This article reviews the pathophysiologic and therapeutic implications of the link between hypertension and the kidney.

Cardiovascular Diseases↗
PubMed2005

Heart disease in diabetic patients.

Cardiac artery disease and heart failure are major causes for morbidity and mortality in diabetes in general and in those with chronic kidney disease (CKD) in particular. Hypertension and dyslipidemia are more common in diabetes and the prevalence of coronary artery disease in diabetics is two-fold to four-fold higher than in nondiabetics. In those with CKD the incidence of cardiovascular complications is nearly two-fold higher than those without CKD. Recent studies suggest that the pathophysiology of cardiac disease is complex process involving both microvascular and macrovascular disease. In addition, myocardial lipotoxicity may be a novel contributing factor particularly in type 2 diabetics. Compelling evidence from cardiovascular outcomes trials indicates that treatment with drugs that block the renin-angiotensin system are cardioprotective in diabetics with microalbuminuria and early stages of kidney disease. Multiple risk factor intervention aimed at optimal blood pressure control (BP <130/<80 mmHG), lowering LDL cholesterol below 100 mg/dl, lowering triglyceride level to 150 mg/dl, A1C <6.5%, treatment with an ACE inhibitor or an angiotensin II receptor blocker, administration of once daily low-dose aspirin and smoking cessation together reduce cardiovascular morbidity and mortality in type 2 diabetics. Novel studies including diabetics with nephropathy aimed at improving outcomes in diabetics by treatment of anemia and optimal control of dyslipidemia are now underway. These and other clinical trials should provide important new insights into improving the quality of life in diabetics and ultimately preventing cardiac disease.

Blood Glucose↗
PubMed2006

Therapy of hyperhomocysteinemia in chronic kidney disease.

Recent published evidence suggests that the correction of the multiple remethylation pathway abnormalities in chronic kidney disease (CKD), beyond folate-related disturbances, enhanced removal of uremic toxins and/or homocysteine (Hcy), and maneuvers aimed to displace Hcy from protein-binding sites, may represent valuable strategies to normalize total Hcy concentrations in CKD patients. The relevance of decreasing Hcy levels for cardiovascular disease in CKD patients should be shown definitively by the results of ongoing randomized trials.

Cardiovascular Diseases↗
PubMed2006

Nutrition and metabolism in kidney disease.

Nutritional and metabolic derangements are highly prevalent in patients with chronic kidney disease (CKD) and patients on renal replacement therapy. These derangements, which can be termed uremic malnutrition, significantly affect the high morbidity and mortality rates observed in this patient population. Uremic malnutrition clearly is related to multiple factors encountered during the predialysis stage and during chronic dialysis therapy. Several preliminary studies suggested that interventions to improve the nutritional status and metabolic status of uremic patients actually may improve the expected outcome in these patients, although their long-term efficacy is not well established. It therefore is important to emphasize that uremic malnutrition is a major comorbid condition in CKD and renal replacement therapy patients, and that all efforts should be made to try to understand better and treat these conditions effectively to improve not only mortality but also the quality of life of chronically uremic patients. In this article we review the current state of knowledge in the field of nutrition and metabolism in all stages of CKD and renal replacement therapy, including kidney transplant. We also address questions that face investigators in this field and suggest where future research might be headed.

Disease Progression↗
PubMed2005

Chronic kidney disease in renal transplant recipients.

UNLABELLED: The aim of the present study was to investigate the utility in renal transplant patients of the guidelines for the diagnosis and classification of chronic kidney disease (CKD) based on the estimated glomerular filtration rate (GFR) elaborated by the Kidney Disease Outcomes Quality Initiative (K/DOQI) of the National Kidney Foundation. PATIENTS AND METHODS: Four hundred forty-seven cadaveric kidney transplants performed between 1980 and 1994 with graft function at 12 months were included in the study. The GFR was calculated according to the MDRD equation. RESULTS: The mean GFR at 12 months was 54.5 +/- 20.3 mL/min/1.73 m(2): 23 patients (5.1%) had a GFR > or =90 mL/min/1.73 m(2); 136 patients (30.6%), 60-89; 246 (54.7%), 30-59; 35 patients (7.8%), 15-29; and 7 patients (1.6%), GFR <15. Similar distribution of CKD stages was observed at 5 and 10 years. Unadjusted graft survival at 10 years was better among patients with a higher GFR at 12 months: 87% in patients with GFR >90 mL/min/1.73 m(2); 83% of GFR 60-89 mL/min/1.73 m(2); 63%, GFR 30-59 mL/min/1.73 m(2); and 23%, GFR <30 mL/min/1.73 m(2) (P < .001). The association between GFR and graft survival persisted when adjusted by the age and gender of the recipients and donors, time on dialysis, body mass index, immunosuppression, delayed graft function, rejection, and HLA mismatches. The prevalence of complications, such as anemia, hypertension, dyslipidemias, and number of drugs increased as GFR declined. CONCLUSIONS: More than 60% of recipients presented chronic kidney disease. GFR was a predictive factor for graft survival at 10 years. The classification of renal transplant patients by CKD stages may help to identify patients with increased risk of graft loss and also to design strategies to improve outcomes.

Body Mass Index↗
PubMed2001

Considerations for optimal iron use for anemia due to chronic kidney disease.

BACKGROUND: Availability of recombinant human erythropoietin (rHuEPO) has improved the treatment of anemia due to chronic kidney disease (CKD). Iron deficiency is the most common cause of resistance to rHuEPO therapy, contributing to ineffective erythropoiesis and hematocrit/hemoglobin values below the recommended target range (33%-36%/11-12 g/dL). I.v. iron supplementation is necessary to meet increased iron demands from stimulation of erythropoiesis and chronic blood loss; however, questions remain as to the optimal supplementation strategy to maintain appropriate yet safe iron status. Treatment guidelines for anemia management have been developed through the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF-K/DOQI). OBJECTIVE: This review presents the basis of need for the NKF-K/DOQI guidelines and includes detailed information concerning iron physiology, metabolism, iron preparations, and evaluation of iron status. METHODS: This review was based on a MEDLINE search and complemented by references from the NKF-K/DOQI guidelines (whose review extended beyond MEDLINE). References focusing on normal iron physiology and metabolism, alterations in iron physiology in patients with CKD, laboratory evaluation methods, and strategies for iron supplementation were obtained from MEDLINE and reviewed for content. RESULTS: Controversy over appropriate use of iron supplementation has led to disparity in accepted practice procedures. Oral iron (ferrous salts and polysaccharide iron complex) and i.v. iron preparations (iron dextran, sodium ferric gluconate, and iron sucrose) are available. Problems with oral iron supplementation include limited absorption and patient noncompliance. Although most available data on i.v. iron use in the United States are specific to iron dextran preparations, published information based on clinical use of sodium ferric gluconate and iron sucrose products has been promising. The use of chronic i.v. iron administration to sustain iron stores has been more widely accepted to prevent development of absolute and functional iron deficiency. CONCLUSIONS: Although iron therapy is commonly warranted in patients with CKD, questions remain as to the most favorable supplementation strategy to optimize therapy through improvements in hematocrits, efficient use of rHuEPO, and maintenance of appropriate and safe iron levels. Clinicians will need to devise strategies based on the compilation of information from clinical experience and the available literature. Clinical practice guidelines devised by the NKF-K/DOQI have provided a useful tool for the medical community using both these resources.

Anemia↗
PubMed2003

Ambulatory GFR measurement with cold iothalamate in adults with chronic kidney disease.

BACKGROUND: The purpose of this study is to develop a method that eliminates the use of radioactive agents, reduces the length of inpatient visits, and does not require urine collection for the measurement of glomerular filtration rate (GFR) in adults with chronic kidney diseases (CKD). METHODS: We measured simultaneous urinary and plasma clearance of iothalamate using high-performance liquid chromatography in 30 patients with CKD after a continuous subcutaneous infusion of iothalamate at a rate of 125 microL/h for a 24-hour period. To ascertain whether a steady state was achieved with a 24-hour infusion, in 20 additional patients, we infused iothalamate continuously for 48 hours and measured GFR after 24 and 48 hours. RESULTS: Plasma iothalamate levels and urinary excretion rates obtained after 24- and 48-hour infusions were similar. GFR estimated by plasma clearance (44.4 mL/min; 95% confidence interval [CI], 37.0 to 53.3) was similar to urinary clearance (41.6 mL/min; 95% CI, 34.7 to 50.0) and without bias (average difference, 7%; 95% CI, +18% to -38%; P = 0.866). There also was acceptable agreement between plasma and urinary clearance of iothalamate (coefficient of variation [CV], 19.6% between techniques). Reproducibility of day-to-day plasma continuous infusion clearance technique was less than 12%. There was good agreement (CV, 19.9%) between inulin and renal iothalamate clearances. CONCLUSION: These data show that ambulatory infusion of iothalamate can be used to measure GFR in adults with CKD without the need for urine collections with acceptable precision and without exposure to radioactivity.

Adolescent↗
PubMed2006

[Continued late referral of patients with chronic kidney disease. Causes, consequences, and approaches to improvement].

OBJECTIVES: Efforts in recent years have aimed at increasing physicians' awareness of the frequent and harmful consequences of late referral to nephrologists of patients with chronic kidney disease (CKD), shown in repeated concordant studies. We sought to determine whether these efforts have led to improved predialysis care of these patients. METHODS: This study included all 1391 consecutive patients who began maintenance dialysis at Necker Hospital between January 1989 and December 2000. We examined baseline data and outcomes and determined for four three-year periods the percentage of patients who received early specialized care (at least 6 months before onset of dialysis). RESULTS: Late referral (<6 months before dialysis) did not change significantly over the four periods, remaining around 30%, even during the most recent period (1998-2000). Clinical condition and laboratory indicators of patients referred early but not those referred late improved in the latest period, compared with the initial period (1989-1991). Overall, prevalence of major cardiovascular events (myocardial or cerebral infarction, peripheral arteriopathy, or heart failure) was more than twice as high in patients who received nephrologic care for less than 6 months and nearly twice as high even in those followed 6-35 months than in patients followed for at least 36 months before beginning dialysis. Subsequent mortality after maintenance dialysis was also significantly higher in patients with late referral than in those followed at least 3 years before dialysis. Multivariate Cox proportional model analysis identified graded duration of predialysis nephrologic care as a significant independent factor predictive of risk of mortality while on dialysis. CONCLUSION: Late referral of CKD patients for specialist care remains frequent, around 30%, although it is most often unjustified. Late referral deprives the patient of early implementation of a reno- and cardioprotective therapeutic strategy that reduces cardiovascular comorbidity and mortality. Better coordinated cooperation between family doctors and nephrologists, through the implementation of regional healthcare networks, now appears as the most effective way to improve the care of CKD patients.

Acute Kidney Injury↗
PubMed2005

Short-term effects of a very-low-protein diet supplemented with ketoacids in nondialyzed chronic kidney disease patients.

OBJECTIVE: To evaluate the effects on the nutritional and metabolic parameters of a very-low-protein diet supplemented with ketoacids (VLPD+KA) in comparison with a conventional low-protein diet (LPD) in chronic kidney disease (CKD) patients. DESIGN: Prospective, randomized, controlled clinical study. SETTING: Outpatient Clinic of the Nephrology Division of Federal University of Sao Paulo, Brazil. SUBJECTS: The study involved 24 patients with advanced CKD (creatinine clearance <25 ml/min) that were randomly assigned to either a VLPD+KA (VLPD+KA group, 12 patients) or to a conventional LPD with 0.6 g/kg/day (LPD group, 12 patients). The patients were followed for 4 months. RESULTS: Nutritional status was adequately maintained with both diets for the studied period. Protein intake and serum urea nitrogen decreased significantly only in the VLPD+KA group (from 0.68+/-0.17 to 0.43+/-0.12 g/kg/day, P<0.05; from 61.4+/-12.8 to 43.6+/-14.9 mg/dl, P<0.001; respectively). Ionized calcium did not change in the VLPD+KA group but tended to decrease in the LPD group. Serum phosphorus tended to decrease in the VLPD+KA group probably as a result of a significant reduction in dietary phosphorus (529+/-109 to 373+/-125 mg/day, P<0.05) associated to the phosphorus-binding effect of the ketoacids. No change in these parameters was found in the LPD group. Serum parathormone increased significantly only in the LPD group (from 241+/-138 to 494+/-390 pg/ml, P<0.01). The change in PTH concentration was negatively correlated with changes in ionized calcium concentration (r=-0.75, P=0.02) and positively correlated with changes in serum phosphorus (r=0.71, P=0.03) only in the LPD group. CONCLUSION: This study indicates that a VLPD+KA can maintain the nutritional status of the patients similarly to a conventional LPD. Besides, an improvement in calcium and phosphorus metabolism and a reduction in serum urea nitrogen were attained only with the VLPD+KA. Thus, VLPD+KA can constitute another efficient therapeutic alternative in the treatment of CKD patients.

Adult↗
PubMed2006

Hemodialysis reduces inhibitory effect of plasma ultrafiltrate on LDL oxidation and subsequent endothelial reactions.

Oxidative modification of low-density lipoprotein (LDL) and its deleterious effect on endothelium is implicated in the pathogenesis of atherosclerosis. Endothelium responds to such an insult by upregulating the synthesis of heme oxygenase-1 (HO-1) and ferritin. Endothelial cell damage and dysfunction have been observed in patients with chronic kidney disease (CKD) on maintenance hemodialysis (HD). We studied the effect of low-molecular-weight components of uremic plasma on LDL oxidation and LDL-oxidation-provoked endothelial cell reactions, such as the induction of cytotoxicity and the upregulation of cell-protective HO-1 and ferritin. Plasma ultrafiltrate (molecular weight<5000 Da) from CKD patients on HD or when treated conservatively exhibited a pronounced inhibition on heme-mediated oxidative modification of LDL. Endothelial cell cytotoxicity provoked by LDL oxidation was also attenuated by plasma ultrafiltrate from CKD patients. During HD treatment, a dramatic drop occurred in the retardation of oxidative reactions, and a loss of endothelial cytoprotection exerted by plasma ultrafiltrate was noted. The upregulation of HO-1 and ferritin in response to oxidative stress of LDL was blunted by uremic plasma ultrafiltrate that was released by the end of HD. The decreased antioxidant capacity of ultrafiltrate after HD occurred as a consequence of the intradialytic removal of L-ascorbic acid, uric acid, bilirubin, 3-indoxyl sulfate, indoxyl-beta-D-glucuronide, p-cresol, and phenol. Intradialytic removal of L-ascorbic acid, uric acid, bilirubin, 3-indoxyl sulfate, indoxyl-beta-D-glucuronide, p-cresol, and phenol increases the risk of LDL oxidation and subsequent endothelial cell damage, which underlines the importance of activation of cytoprotective HO-1 and ferritin in endothelium.

Adult↗
PubMed2006

Progression of kidney disease: blocking leukocyte recruitment with chemokine receptor CCR1 antagonists.

Chronic kidney disease (CKD) is usually associated with interstitial leukocytic cell infiltrates, which may contribute to disease progression by production of proinflammatory, proapoptotic, and profibrotic mediators. Recruiting leukocytes into the kidney involves local expression of chemotactic cytokines, that is, chemokines, that interact with respective chemokine receptors on the leukocyte's outer surface. Thus, specific chemokine receptor antagonists may represent an attractive therapeutic concept to interfere with renal leukocyte recruitment. Among the proinflammatory chemokine receptors, chemokine receptor (CCR)-1 has nonredundant roles for leukocyte adhesion to activated vascular endothelium and for transendothelial migration. In fact, blocking CCR-1 with specific small-molecule antagonists was shown to retard progression in various types of rodent CKD models. Here we discuss the perspective of CCR-1 as a new potential target for the treatment of CKD.

Animals↗
PubMed2006

Chronic kidney disease in the elderly: is it really a premise for overwhelming renal failure?

Increasingly, the majority of patients being diagnosed as affected by chronic kidney disease (CKD) are elderly. Nonetheless, only a rather small proportion of elderly CKD patients actually progress to end-stage renal disease, whereas many more die before this stage is reached, largely because of cardiovascular disease. This underscores the urgent need for cardiovascular prevention, even more importantly than for renoprotection, among elderly patients with CKD.

Age Factors↗
PubMed2006

Peripheral tissue release of interleukin-6 in patients with chronic kidney diseases: effects of end-stage renal disease and microinflammatory state.

To examine if uremia influences muscle interleukin-6 (IL-6) metabolism we studied the exchange of IL-6 across the forearm in 16 patients with chronic kidney disease (CKD) (stages 3 and 4), in 15 hemodialysis (HD)-treated end-stage renal disease (ESRD) patients (n=15), and in six healthy controls. In addition, we performed an analysis of both IL-6 protein and IL-6 mRNA expression in muscle of CKD (stage 4) patients showing evidence of inflammation and in controls. A release of IL-6 from the forearm was observed in patients with elevated IL-6 plasma levels. Arterial IL-6 was directly related to released IL-6 (r=0.69; P<0.004) in HD patients. Both IL-6 protein and IL-6 mRNA expression were increased in muscle of inflamed CKD patients vs controls (P<0.05). Although muscle net protein balance was similar in all patients, it was significantly more negative in HD patients with high than in those with low IL-6 plasma levels (P<0.05). In addition, net protein balance was related to the forearm release of IL-6 in HD patients only (r=0.47; P<0.038). These data demonstrate that IL-6 expression is upregulated in muscle, and that muscle tissue, by releasing this cytokine, may contribute to the inflammatory response in HD patients. The release of IL-6 from peripheral tissues is associated with an increase in muscle protein loss in HD patients, suggesting that muscle release of IL-6 is linked to protein catabolism in these patients. The release of IL-6 from peripheral tissues may act as a signal for the inflammatory response and contribute to functional dysregulation in uremia.

Aged↗
PubMed2006

Risk factors for de novo acute cardiac events in patients initiating hemodialysis with no previous cardiac symptom.

An initial major adverse cardiac event (MACE) is an important predictor of future cardiovascular events in patients with chronic kidney disease (CKD). We sought to identify factors influencing occurrence of initial MACE in new maintenance hemodialysis patients without previous cardiac symptoms during the predialysis phase of CKD. Among 112 participating patients with no predialysis cardiac history, 57 underwent coronary angiography, whereas the other 55 underwent stress thallium-201 single-photon emission computed tomography within 1 month of beginning hemodialysis to detect asymptomatic coronary artery disease (CAD). In subsequent follow-up for a median of 24 months, subjects experiencing an initial MACE were compared with those who did not have such an event based on several clinical parameters at the end of predialysis phase. Asymptomatic CAD was present in 47 patients (42%), who had a higher cumulative MACE rate, than subjects without CAD (49 vs 3%, P<0.001). Multivariate Cox's regression analysis showed that three variables independently predicted initial MACE: asymptomatic CAD (hazard ratio or HR, 611.31; 95% confidence interval or CI, 14.07-26549.23; P<0.001), diabetes (HR, 20.41; 95% CI, 2.07-200.00; P=0.010), and each 1 mg/l increment in C-reactive protein (CRP) (HR, 1.94; 95% CI, 1.27-2.94; P=0.002). In conclusion, detection of asymptomatic CAD, presence of diabetes, or elevated CRP at the end of the predialysis phase were significantly associated with occurrence of an initial MACE in CKD patients starting hemodialysis who had no CAD symptoms.

Aged↗
PubMed2006

Gender differences in renal nuclear receptors and aryl hydrocarbon receptor in 5/6 nephrectomized rats.

This study was aimed at delineating molecular pathways essential in gender-different pathogenesis of chronic kidney diseases (CKD). Renal transcripts of nuclear receptors and metabolic enzymes in male and female kidneys from 5/6 nephrectomized (Nx) rats 7 weeks post-Nx were examined using branched DNA signal amplification assay. Nx-males had marked kidney injury coupled with anemia and malnutrition. Nx-females had moderate renal injury, and were free of albuminuria, anemia, and malnutrition. Nx-males had systemic and renal inflammation, which were largely absent in Nx-females. Blood 17beta-estradiol, testosterone, and corticosterone did not change, whereas urinary testosterone decreased in both genders. Compared to males, female kidneys had higher androgen receptor (AR) and aryl hydrocarbon receptor (AhR) but lower estrogen receptor alpha (ERalpha). Compared to Nx-males, female remnant kidneys had less decreases in ERalpha and peroxisome proliferator-activated receptor alpha (PPARalpha), had no induction of AR and decrease of acyl-CoA oxidase, whereas had induction of cytochrome P450 4a1 (Cyp4a1) but decrease of AhR. Renal protein expression of a 52-kDa isoform of Wilm's tumor 1 (WT1), transcription factor critical in nephrogenesis, decreased dramatically in Nx-males but largely preserved in Nx-females. In conclusion, gender divergences in basal expression and alteration of ERalpha, AR, AhR, WT1, and PPARalpha/Cyp4a1 during CKD may explain gender differences in CKD progression and outcome of renal transplantation.

Acyl-CoA Oxidase↗
PubMed2006

Very low protein diet supplemented with ketoanalogs improves blood pressure control in chronic kidney disease.

Blood pressure (BP) is hardly controlled in chronic kidney disease (CKD). We compared the effect of very low protein diet (VLPD) supplemented with ketoanalogs of essential amino acids (0.35 g/kg/day), low protein diet (LPD, 0.60 g/kg/day), and free diet (FD) on BP in patients with CKD stages 4 and 5. Vegetable proteins were higher in VLPD (66%) than in LPD (48%). LPD was prescribed to 110 consecutive patients; after run-in, they were invited to start VLPD. Thirty subjects accepted; 57 decided to continue LPD; 23 refused either diet (FD group). At baseline, protein intake (g/kg/day) was 0.79+/-0.09 in VLPD, 0.78+/-0.11 in LPD, and 1.11+/-0.18 in FD (P<0.0001). After 6 months, protein intake was lower in VLPD than LPD and FD (0.54+/-0.11, 0.78+/-0.10, and 1.04+/-0.21 g/kg/day, respectively; P<0.0001). BP diminished only in VLPD, from 143+/-19/84+/-10 to 128+/-16/78+/-7 mm Hg (P<0.0001), despite reduction of antihypertensive drugs (from 2.6+/-1.1 to 1.8+/-1.2; P<0.001). Urinary urea excretion directly correlated with urinary sodium excretion, which diminished in VLPD (from 181+/-32 to 131+/-36 mEq/day; P<0.001). At multiple regression analysis (R2=0.270, P<0.0001), BP results independently related to urinary sodium excretion (P=0.023) and VLPD prescription (P=0.003), but not to the level of protein intake. Thus, in moderate to advanced CKD, VLPD has an antihypertensive effect likely due to reduction of salt intake, type of proteins, and ketoanalogs supplementation, independent of actual protein intake.

Aged↗
PubMed2006

25-Hydroxyvitamin D, insulin resistance, and kidney function in the Third National Health and Nutrition Examination Survey.

Previous research has reported reduced serum 25-hydroxyvitamin D levels in patients with chronic kidney disease (CKD), although the relationship between vitamin D status and insulin resistance (IR) in patients with CKD has not been examined in the general population. We examined the association that kidney function, based on glomerular filtration rate (eGFR) estimated from serum creatinine, has with serum levels of 25-hydroxyvitamin D and components of the metabolic syndrome among 14 679 participants in the Third National Health and Nutrition Examination Survey (NHANES III). In this analysis, adjusted mean serum 25-hydroxyvitamin D was significantly lower only in the participants with a severe (15-29 ml/min/1.73 m(2)) decrease in eGFR compared to those with normal kidney function (61.6 vs 73.3 nmol/l, P=0.0063). Serum 25-hydroxyvitamnin D (P=0.0018) and level of kidney function (P=0.0003) were inversely associated, independent of each other, with homeostasis model assessment of insulin resistance (HOMA-IR), adjusting for confounders. Participants with high 25-hydroxyvitamin D levels (>81 nmol/l) had lower HOMA-IR. We conclude that 25-hydroxyvitamin D deficiency is not as prevalent in the US general population with decreased eGFR as previously reported in patients with CKD; and that vitamin D and kidney function have independent inverse associations with IR.

Adult↗
PubMed2007

Insulin resistance and protein catabolism in non-diabetic hemodialysis patients.

Chronic kidney disease (CKD) is associated with complex metabolic changes including insulin resistance. Siew et al. have highlighted an important relationship between insulin resistance and skeletal muscle protein turnover. If insulin resistance is implicated in sarcopenia of CKD, further research will be required to determine whether interventions that improve insulin sensitivity improve clinical outcomes and cardiovascular risk in CKD.

Cardiovascular Diseases↗