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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
ORIGINAL ARTICLE  
Year : 2021  |  Volume : 32  |  Issue : 5  |  Page : 1300-1309
Insulin resistance in nondiabetic chronic kidney disease patients


1 Department of Nephrology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India
2 Department of Biochemistry, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India
3 Department of Endocrinology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India

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Date of Web Publication4-May-2022
 

   Abstract 


Chronic kidney disease (CKD) is accompanied by numerous metabolic derangements due to risk factors such as oxidative stress, chronic inflammation, and endothelial dysfunction. Insulin resistance (IR) has been reported as an independent risk factor for cardiovascular morbidity and mortality in patients with CKD. As reported from previous studies, it has been shown that IR is also seen in mild-to-moderate stages of CKD. Hence, the present study aimed to study IR in nondiabetic CKD patients and correlated with different stages of CKD. A two-year cross-sectional study was conducted in 175 patients among whom 25 healthy controls and 150 nondiabetic CKD patients in different stages are included. In the present study, fasting insulin and homeostatic model assessment for IR (HOMA-IR) levels were found to be higher in all nondiabetic CKD patients when compared to controls which was found to be statistically significant (P <0.05). In the present study, IR, as evidenced by HOMA-IR, is noted in patients on predialysis, continuous ambulatory peritoneal dialysis (CAPD), and postrenal transplant patients. Hence, periodic monitoring of IR by HOMA-IR might be prudent in CKD patients on predialysis, CAPD and in postrenal transplant patients. Interventions targeting IR in this patient population can also decrease cardiovascular morbidity and mortality.

How to cite this article:
Nallamothu P, Nimmanapalli HD, Sachan A, Srinivasa Rao P V, Vishnubotla S. Insulin resistance in nondiabetic chronic kidney disease patients. Saudi J Kidney Dis Transpl 2021;32:1300-9

How to cite this URL:
Nallamothu P, Nimmanapalli HD, Sachan A, Srinivasa Rao P V, Vishnubotla S. Insulin resistance in nondiabetic chronic kidney disease patients. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 May 25];32:1300-9. Available from: https://www.sjkdt.org/text.asp?2021/32/5/1300/344749



   Introduction Top


Chronic kidney disease (CKD) is one of the most important chronic, noncommunicable disease globally. CKD is a major risk factor for end-stage renal disease (ESRD) and cardiovascular disease leading to mortality in patients with uremia.[1] In addition to the traditional risk factors, certain nontraditional risk factors were found to have a major role in cardiovascular mortality in patients with CKD. Insulin resistance (IR) is recognized as one of the nontraditional risk factors and also as an independent predictor of cardiovascular mortality in patients with CKD.[2] IR is a common and early alteration which is being apparent even at normal glomerular filtration rate (GFR) levels and also in mild-to-moderate stages of CKD. However, IR was found to increase progressively as the GFR levels decline and also with different stages of CKD and henceforth considered as an important predictor of CKD. Due to the abnormal insulin action, it was found that the nutritional, metabolic, and cardiovascular complications of renal disease might occur.[3] Identifying and treating risk factors for early CKD might be the best approach to prevent and delay the adverse outcomes. Therefore, IR might be an important therapeutic target for the reduction of cardiovascular mortality in patients with CKD.[4] The etiology of IR is multifactorial and is secondary to disturbances such as chronic inflammation, oxidative stress, Vitamin D deficiency, secondary hyperparathyroidism, anemia, and malnutrition.[5] These factors are associated with increased cytokines and adipokine levels, sodium retention, and down-regulation of then natriuretic peptide system. Recent reports also indicated that these different conditions impair insulin-initiated intracellular signaling leading to the development of IR. The insulin-signaling cascade is a sequence of phosphorylation/dephosphorylation events dueto redox-sensitive enzymatic activities. Following insulin binding to its receptor, autophosphorylation of the insulin receptor is followed by kinase reactions. Consequently, IRS-1 degradation suppresses insulin-induced intracellular signaling causing IR. Further, IR contributes to the progression of renal disease due to the worsening insulin receptor-signaling pathways.[6],[7] Understanding mechanisms of IR could lead to therapeutic strategies that improve the metabolism in patients with CKD. There is an abundant evidence that IR complicates CKD by interfering with processes that contribute to abnormalities in the metabolism of lipids and carbohydrates and loss of protein stores.[8] IR and hyperinsulinemia further contribute to diabetes mellitus (DM), hypertension (HTN), and dyslipidemia in patients with CKD. Efforts for new cardiovascular risk factors is required as the measurement of individual lipids is not sufficient to improve cardiovascular disease prediction. Hence, it is emphasized that lipoprotein ratios or “atherogenic indices” have been identified to optimize the predictive capacity of the lipid profile. These ratios were found to have a better predictive role in assessing risk than isolated lipids.[9] Prospective data showing the association between impaired insulin sensitivity and mortality in patients with CKD are scarce and conflicting. Two surveys on non-diabetic elderly Caucasians showed that oral glucose test is inversely associated with the eGFR.[10] Inline with these findings, in a study of nondiabetic US middle-aged CKD adults, showed progressively increase levels of insulin with the increase in homeostatic model assessment for IR (HOMA-IR).[11] Similarly, in the Health, Aging, and Body Composition study, individuals with nondiabetic CKD found an inverse relation between HOMA-IR and eGFR.[12] The recent study in nondiabetic patients with moderate to severe CKD compared with controls also has confirmed that glucose intolerance and hyperinsulinemia are quite common in patients with CKD. Adequate hemodialysis (HD) has shown to have a positive effect on IR, but there is little clinical data regarding the effect of peritoneal dialysis (PD) on insulin sensitivity. In a small Japanese cohort of 170 nondiabetic dialysis patients IR, as measured by the HOMA-IR, predicted mortality independently of other risk factors such as body mass index and inflammation.[13] However, weak associations between HOMA-IR and cardiovascular events were reported in small studies in HD and PD patients. In a recent study in dialysis patients, IR was associated with non-CV death but not with CV mortality.[14] With this background, the present study aimed to evaluate IR in non-diabetic CKD patients and correlate with different stages of CKD.


   Materials and Methods Top


A two-year cross-sectional study was conducted on 175 subjects among whom 25 healthy controls and 150 nondiabetic CKD patients in different stages as per National Kidney Foundation Kidney Disease Outcomes Quality Initiative staging attending the nephrology outpatient department at Sri Venkateswara Institute of Medical Sciences, Tirupati were included.[1] One hundred and fifty nondiabetic CKD patients were divided into six groups based on the stages of the disease consisting of 25 patients in each group were included. One hundred and seventy-five non-diabetic subjects were classified as follows: Group I: age- and gender-matched healthy individuals as controls, Group II: nondiabetic CKD patients with Stages 1, 2, and 3, Group III: nondiabetic CKD patients with Stages 4 and 5, Group IV: nondiabetic CKD patients on HD, Group Va: nondiabetic CKD patients on PD with only dextrose solution (3 bags), Group Vb: nondiabetic CKD patients on PD with dextrose and icodextrin (2 bags and 1 × 7.5%), Group VI: Renal transplant recipients. A written informed consent before study enrolment was taken from all the study subjects. The study was conducted after obtaining approval from the institutional ethics committee. Patients with DM, acute renal failure, acute on CKD, active infection, autoimmune disease, pediatric age group (<18 years), pregnant women, and unwilling patients were excluded from the study.

Sample collection

Five milliliters of fasting venous blood were collected from all the subjects. From that 2 mL of blood was transferred into fluoride bottle for fasting plasma glucose estimation and the remaining blood was collected in additive-free tubes for other laboratory investigations. The blood samples were allowed to stand for 30 min, centrifuged at 3000 rpm for 15 min. Separated serum was stored at −80°C until further analysis. Serum urea, creatinine, total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), calcium, and phosphorus were estimated using commercial kits. All the above parameters were analyzed on clinical chemistry Auto analyser Beckman Coulter DXC 600 Synchron, USA. Low-density lipoprotein (LDL) and very LDL (VLDL) were calculated by Freidewalds equation.[15] Further, atherogenic ratios were calculated by using the indices as follows: Castelli index 1: TC/HDL-c, Castelli index 2: LDL-c/HDL-c, TG/HDL-c, Atherogenic coefficient: non-HDL-c/HDL-c, non-HDL-c = TC - HDL-c and Atherogenic index of plasma: log TG/HDL-c. Parathyroid hormone was estimated by chemiluminescence assay and vitamin D was estimated by immunoradiometric assay (IRMA) on Beckman analyzer. eGFR was calculated using modification of diet in renal disease formula. Height, weight, body mass index, and blood pressure were recorded. IR was assessed by HOMA-IR.[16]

HOMA-IR (mg/dL × mIU/L) = fasting glucose (mg/dL) × fasting insulin (mIU/L)/405


   Statistical Analysis Top


All continuous variables were tested for normal distribution with Kolmogorov–Smirnov test. As the data are normally distributed values were presented as mean ± standard deviation. Categorical values were presented as numbers and percent using Chi-square test. Unpaired student’s t-test was used for comparison of means between cases and controls. Comparison of means across the groups was done by the analysis of variance (ANOVA) followed by post-hoc analysis. Statistical analysis was performed using Microsoft Excel spreadsheets and IBM SPSS Statistics version 22.0 (IBM Corp., Armonk, NY, USA). A P <0.05 was considered significant.


   Results Top


IR is common among individuals with CKD even in the early stages of CKD. IR is prevalent in CKD diabetic and nondiabetic patients and it worsens with the decline in e GFR. All the nondiabetic CKD patients are from the department of nephrology at the Sri Venkateswara Institute of Medical Sciences, Tirupati. One hundred and fifty CKD non-diabetic patients and 25 nondiabetic controls were included in the study. In the present study mean age of the nondiabetic CKD patients was found to be higher than the controls but was not statistically significant (P = 0.140). However, in the present study among nondiabetic CKD patients, the mean age of the predialysis CKD patients (43.2 ± 14.12) were found to be younger than the dialysis CKD patients (50.4 ± 10.18). On the whole CKD patients with renal transplant recipients were found to be the youngest (33.1 ± 8.18) as compared with other nondiabetic CKD groups. In the present study, male-to-female ratio in all the nondiabetic CKD patients and controls was observed to have male preponderance. Body mass index was found to be higher in all nondiabetic CKD patients when compared to controls which were found to be statistically significant (P = 0.001). Waist circumference was also found to be higher in all nondiabetic CKD patients when compared to controls but was found to be not statistically significant (P = 0.926). eGFR was found to be lower in all nondiabetic CKD patients when compared to controls which was found to be statistically significant (P <0.001). There is a falling trend in the mean value of eGFR with increase in the severity of CKD from stage 1 to 5 and it was least among HD and PD nondiabetic CKD patients but showed an increasing trend in renal transplant nondiabetic CKD patients due to adequate graft function. The mean ± SD of the biochemical parameters of the 25 controls and 150 nondiabetic CKD patients by using unpaired t-test was shown in [Table 1]. The present study observed that FBS and PPBS levels were found to be increased in all groups of CKD patients when compared to controls but were within the normal limits which were found to be statistically significant (P = 0.001). In the present study, fasting insulin and HOMA-IR levels were found to be higher in all nondiabetic CKD patients when compared to controls which was found to be statistically significant (P <0.05) [Figure 1]a and [Figure 1]b. The present study also found that HbA1c levels were within normal levels in all CKD patients and controls and was not statistically significant (P = 0.892). Serum lipids levels were found to be within the normal limits in all CKD patients and controls but was also found to be not statistically significant (P >0.05). But when atherogenic ratios were compared in between the two groups, it was found that except for LDL-c/HDL-c all the atherogenic ratios were found to be statistically increased in non-diabetic CKD patients when compared to controls (P <0.05). In the present study, serum 25(OH) vitamin D3 levels were found to be decreased in all CKD patients and control group but was found to be not statistically significant (P = 0.892) whereas serum parathormone levels were found to be increased in all nondiabetic CKD patients when compared to controls and were found to be statistically significant (P = 0.010). Serum calcium and phosphorus levels were found to be increased in all nondiabetic CKD patients when compared to controls but were within the normal limits which were found to be not statistically significant (P >0.05). However, calcium and phosphorus product was found to be increased in all CKD patients when compared to controls and was found to be statistically significant (P <0.001). Significance of difference across the study groups by using one-way ANOVA was done and is shown in [Table 2]. In the present study, various demographic and biochemical parameters between predialysis, dialysis, and postrenal transplant CKD patients were evaluated and compared them with controls. There was a statistically significant difference between the study groups for fasting insulin levels, HOMA-IR, Serum TG, VLDL-c LDL-c, TC, atherogenic indices, phosphorous and Vitamin D3 was observed (P <0.05). Comparison of means between the study groups by using post hoc analysis is shown in [Table 3]. Fasting insulin, HOMA-IR levels showed a statistically significant difference in mild-to-moderate stage of predialysis CKD group as compared to the control group. None of the parameters showed a statistically significant change in the levels in both the dialysis groups. IR in renal transplant group when compared to control group showed a similar pattern as same as in mild-to-moderate stage of predialysis CKD group.
Figure 1 a and b: Fasting insulin and HOMA-IR levels among control and non-diabetic chronic kidney disease groups.
Group I: Apparently healthy controls, Group II: Nondiabetic chronic kidney disease patients.


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Table 1: Comparison of biochemical parameters in control and non-diabetic chronic kidney disease groups.

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Table 2: Comparison of means across the study groups by using ANOVA analysis.

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Table 3: Level of significance between thestudy groupsfor insulin resistance by using post hoc analysis.

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   Discussion Top


IR refers to the reduced sensitivity of organs to insulin-initiated biologic processes that could result in metabolic defects. A complex relationship exists between uremia and insulin function. IR might play a key role in the development of cardiometabolic complications and is associated with increased cardiovascular risk and premature death.[17] Prospective data concerning the association between IR and clinical outcomes in CKD patients are few and contradictory. IR is found to be common in patients with CKD even when the serum creatinine is minimally increased. Only a few clinical studies have reported IR in nondia-betic patients with mild renal dysfunction.[18],[19] Hence, the present study evaluated IR in non-diabetic patients with CKD and correlated with the different stages of CKD.

In the present study, body mass index (BMI) and waist circumference were found to be increased in all CKD patients when compared to controls which might be explained due to male predominance in CKD patients when compared to the control group. These findings suggest that IR is primarily determined by BMI and waist circumference. BMI and waist circumference are the relevant indicators of IR (HOMA-IR) as reported in other studies.[20],[21] Studies in the general population have revealed that abdominal fat is associated with IR, hyperinsulinemia, and dyslipidemia in Asian Indians. Hyperinsulinemia is associated with IR in the nondiabetic state which plays a role in kidney function by inducing glomerular hyper-filtration and increased vascular permeability. Measurement of fasting insulin level is the most practical approach for the measurement of IR.[22] It correlates well with IR. In the present study, the mean fasting insulin and HOMA-IR levels were found to be significantly higher in CKD patients as compared to controls (P = 0.040, P = 0.050 respectively). IR results from a defective uptake, metabolism,or storage of glucose in skeletal muscles, liver, and adipose tissue because of alterations in insulin signaling at the receptor or postreceptor level. A high serum insulin value in individuals with normal glucose tolerance reflects IR which might lead to the development of DM.[23] Defronzo et al first studied IR in patients with ESRD undergoing dialysis, using euglycemic insulin clamp techniques.[24] Very few Indian studies have been conducted on IR in nondiabetic CKD patients and majority were conducted in diabetic CKD patients. An Indian study on IR in patients with diabetic kidney disease, reported positive correlation between increasing IR and worsening GFR. Most studies describing relationships between IR and cardiovascular disease were based on HOMA-IR index. As reported by few Indian studies found a higher HOMA-IR value in nondiabetic CKD population.[25],[26] In a study on dialysis patients who compared 33 HD patients with controls observed that mean fasting plasma glucose concentrations were lower in MHD patients than in healthy persons. They also reported fasting serum insulin concentrations were similar in both groups and HOMA-IR values were not significant suggesting the HOMA-IR index as an imperfect biomarker of IR in CKD.[27] This is in contrast to present study findings in which high IR was observed in nondiabetic CKD patients and the highest HOMA-IR value in renal transplant recipients as compared to controls. The reason might be that in renal transplant recipients, the major risk factor for impaired glucose tolerance was immunosuppressive therapy leading to IR. 1,25 Vitamin D deficiency is common in CKD patients, particularly when the GFR is below 30 mL/min/1.73 m2. In the present study, serum 1,25(OH) vitamin D3 levels were found to be decreased in all nondiabetic CKD patients and serum parathormone levels were found to be increased in all nondiabetic CKD patients. Meta-analysis data from 17 clinical trials in CKD dialysis patients showed that short-term Vitamin D therapy (4–12 weeks) improves insulin secretion and insulin sensitivity. Vitamin D stimulates insulin release by modulating intracellular free calcium as well as by increasing the expression of the insulin receptor and by enhancing glucose transport. However, CKD stage 3 and 4 patients, therapy with an active form of Vitamin D or with cholecalciferol did not found to have an effect in IR suggesting that Vitamin D has no major impact on insulin response.[28],[29] verall, the mechanism(s) by which Vitamin D improves insulin sensitivity in advanced CKD remain unclear. Vitamin D deficiency triggers secondary hyperparathyroidism and high parathyroid hormone which can per se inhibit insulin secretion.

HTN, diabetes,and dyslipidemia are the most important consequences of IR and hyper-insulinemia and therefore, IR might contribute to the high risk of CVD through these risk factors.[19] In the present study, all the lipids levelswere found to be within normal limits in all CKD patients and controls which was also found to be not statistically significant (P >0.05). The correlation between renal insufficiency and lipid parameters in the current study implies that dyslipidemia is associated with adverse cardiovascular events in patients with CKD. However, the atherogenic ratios were found to be elevated in all nondiabetic CKD patients as compared to controls in the present study. Hence, atherogenic indices are better predictors of cardiovascular risk rather than individual lipids. IR favors a pro-coagulant state due to inhibition of plasminogen activator inhibitor-1 reduced conversion of plasminogen to plasmin occurs. Due to decreased lipoprotein lipase (LPL) and increased LPL inhibitor apolipoprotein C-III levels, TG-rich lipoproteins such as VLDL, chylomicrons, and chylomicron remnants increase in early stages of CKD. Further these remnant lipoproteins can penetrate the vascular endothelium leading to atherosclerotic risk.[30] IR is a well-known complication in HD and PD patients because of marked metabolic disorders observed in them as well as the exposure to glucose-based PD fluids.[31] In the present study, higher BMI and waist circumference were observed in both the PD groups when compared to the control group. The explanation for this is could be due to the absorption of large quantities of glucose that contribute to changes in body composition and obesity in patients undergoing CAPD. In the present study, among the PD groups, the PD dextrose patients were found to have higher BMI and waist circumference than the Icodextrin-based PD patients. Our study results were supported by the study done in CAPD patients with three dextrose-based PD bag prescription by Moncrief et al who found that dialysate glucose could constitute a considerably greater fraction of total energy intake.[13] The most widely available non-glucose PD solution is 7.5% icodextrin solution. The substitution of icodextrin for glucose-based solution during long dwell has been consistently associated with improvement in markers of glucose and lipid metabolism.[32] Icodextrin did not improve insulin sensitivity, but instead reduced IR related to glucose exposure in the long PD dwell. Icodextrin is a mixture of high molecular weight glucose polymers isolated from hydrolyzed corn starch. Icodextrin provides a colloidal rather than a crystalloid osmotic force, thereby inducing a slower but more sustained removal of fluid via peritoneal ultrafiltrate for the long dwell in PD.[32] The present study findings were also in favor to the positive metabolic effects of icodextrin in reducing the atherogenic lipids which can reduce the incidence of metabolic syndrome among CAPD patients.


   Conclusion Top


IR prevails in non-diabetic CKD patients and contributes to the progression of ESRD and high cardiovascular risk. The severity of IR as assessed by HOMA-IR could predict the progression of CKD. In the present study among all the CKD groups IR as assessed by HOMA-IR was highest in predialysis CKD patients in stages 4 and 5, whereas HD patients had the lowest HOMA-IR. IR is higher in PD dextrose in comparison to PD icodextrin group. Hence, icodextrin can be recommended in additionto conventional PD prescription in nondiabetic CKD patients at risk of developing metabolic syndrome and DM. Since IR is a modifiable risk factor and its reduction might decrease CV morbidity and mortality, unraveling the precise molecular mechanisms responsible for the pathogenesis of CKD-related IR is of importance for the identification of novel therapeutic targets aimed at reducing renal and cardiovascular damage in non diabetic CKD patients.

Source(s) of support: SBAVP scheme for financial assistance.

Conflict of interest: None declared.



 
   References Top

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Correspondence Address:
Harini Devi Nimmanapalli
Department of Biochemistry, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1319-2442.344749

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