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The purpose of this manuscript is to review the effects of sodium-glucose cotransport protein 2 inhibitors (SGLT2is) in patients with chronic kidney disease according to basic mechanisms, current recommendations, and future perspectives. Based on growing evidence from randomized, controlled trials, SGLT2is have proven their benefit on cardiac and renal adverse complications, and their indications expanded into the following five categories: glycemic control, reduction in atherosclerotic cardiovascular disease (ASCVD), heart failure, diabetic kidney disease, and nondiabetic kidney disease. Although kidney disease accelerates the progression of atherosclerosis, myocardial disease, and heart failure, so far, no specific drugs were available to protect renal function. Recently, two randomized trials, the DAPA-CKD and EMPA-Kidney, demonstrated the clinical benefit of the SGLT2is dapagliflozin and empagliflozin in improving the outcome in patients with chronic kidney disease. For the consistently positive results in cardiorenal protection, the SGLT2i represents an effective treatment to reduce the progression of kidney disease or death from cardiovascular causes in patients with and without diabetes mellitus.

Background: Renal diseases remain an increasing public health issue affecting millions of people. The kidney is a highly energetic organ that is rich in mitochondria. Numerous studies have demonstrated the important role of mitochondria in maintaining normal kidney function and in the pathogenesis of various renal diseases, including acute kidney injuries (AKIs) and chronic kidney diseases (CKDs)., Summary: Under physiological conditions, fine-tuning mitochondrial energy balance, mitochondrial dynamics (fission and fusion processes), mitophagy, and biogenesis maintain mitochondrial fitness. While under AKI and CKD conditions, disruption of mitochondrial energy metabolism leads to increased oxidative stress. In addition, mitochondrial dynamics shift to excessive mitochondrial fission, mitochondrial autophagy is impaired, and mitochondrial biogenesis is also compromised. These mitochondrial injuries regulate renal cellular functions either directly or indirectly. Mitochondria-targeted approaches, containing genetic (microRNAs) and pharmaceutical methods (mitochondria-targeting antioxidants, mitochondrial permeability pore inhibitors, mitochondrial fission inhibitors, and biogenesis activators), are emerging as important therapeutic strategies for AKIs and CKDs., Key Messages: Mitochondria play a critical role in the pathogenesis of AKIs and CKDs. This review provides an updated overview of mitochondrial homeostasis under physiological conditions and the involvement of mitochondrial dysfunction in renal diseases. Finally, we summarize the current status of mitochondria-targeted strategies in attenuating renal diseases., Competing Interests: The authors declare that they have no competing interests., (© 2023 The Author(s). Published by S. Karger AG, Basel.)

Aims: To evaluate the cost-effectiveness of glucagon-like peptide-1 receptor agonists (GLP-1RAs) versus long-acting insulins (LAIs) in patients with type 2 diabetes (T2D) using real-world data., Methods: A Markov model was utilized to estimate healthcare costs (US$) and quality-adjusted life-years (QALYs) of receiving treatments over 10 years from the healthcare sector perspective. Model inputs were derived from the analyses of Taiwan's National Health Insurance Research Database or published literature on Taiwanese T2D populations. Base-case analysis was performed for the overall study cohort and subgroup analyses were stratified by the presence or absence of established cardiovascular diseases (CVDs) or chronic kidney diseases (CKDs)., Results: Overall, using GLP-1RAs versus LAIs cost $6,053 per QALY gained. Results were robust across sensitivity and scenario analyses. Among patients with established CVDs and CKDs, GLP-1RA versus LAI therapy saved $673 (cost-saving) and cost $1,675 per QALY gained, respectively. Among patients without established CVDs and CKDs, GLP-1RA versus LAI therapy cost $9,093 and $7,659 per QALY gained, respectively., Conclusions: Using GLP-1RAs versus LAIs for T2D patients represented good economic value in real-world practice. Pronounced economic benefits of GLP-1RA therapy among those with prior CVDs or CKDs support rational treatment decisions and optimal healthcare resource allocation for these patients., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

The rising global incidence of acute and chronic kidney diseases has increased the demand for renal replacement therapy. This issue, compounded with the limited availability of viable kidneys for transplantation, has propelled the search for alternative strategies to address the growing health and economic burdens associated with these conditions. In the search for such alternatives, significant efforts have been devised to augment the current and primarily supportive management of renal injury with novel regenerative strategies. For example, gene- and cell-based approaches that utilize recombinant peptides/proteins, gene, cell, organoid, and RNAi technologies have shown promising outcomes primarily in experimental models. Supporting research has also been conducted to improve our understanding of the critical aspects that facilitate the development of efficient gene- and cell-based techniques that the complex structure of the kidney has traditionally limited. This manuscript is intended to communicate efforts that have driven the development of such therapies by identifying the vectors and delivery routes needed to drive exogenous transgene incorporation that may support the treatment of acute and chronic kidney diseases., Competing Interests: The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Corridon.)

Major advances have been made in the management of children with chronic kidney disease (CKD) over the past 30 years. However, existing epidemiological data mainly relies on registries of chronic kidney replacement therapy. The incidence and prevalence of earlier stages of CKD remain largely unknown, but rare population-based studies suggest that the prevalence of all stages CKD may be as high as 1 % of the pediatric population. Congenital disorders including renal hypodysplasia and uropathy (CAKUT) and hereditary nephropathies account for one-half to two-thirds of childhood CKD cases in high-income countries, whereas acquired nephropathies predominate in developing countries. CKD progression is slower in children with congenital disorders than in those with glomerular nephropathy, and other risk factors for progression have also been identified. Children with CKD have poorer health-related quality of life when compared to healthy children. While survival of children with CKD has continuously improved over time, mortality remains 20 to 30 times higher than in the general pediatric population., (© 2023 médecine/sciences – Inserm.)

Objective: To examine the associations of mobile phone use and its use characteristics with new-onset CKD. Methods: 408,743 participants without prior CKD in the UK Biobank were included. The primary outcome was new-onset CKD. Results: During a median follow-up of 12.1 years, 10,797 (2.6%) participants occurred CKD. Compared with mobile phone non-users, a significantly higher risk of new-onset CKD was found in mobile phone users (HR = 1.07; 95% CI: 1.02-1.13). Moreover, among mobile phone users, compared with participants with weekly usage time of mobile phone making or receiving calls <30 min, a significantly higher risk of new-onset CKD was observed in those with usage time ≥30 min (HR = 1.12; 95% CI: 1.07-1.18). Moreover, participants with both high genetic risks of CKD and longer weekly usage time of mobile phones had the highest risk of CKD. Similar results were found using the propensity score matching methods. However, there were no significant associations of length of mobile phone use, and hands-free device/speakerphone use with new-onset CKD among mobile phone users. Conclusion: Mobile phone use was significantly associated with a higher risk of new-onset CKD, especially in those with longer weekly usage time of mobile phones making or receiving calls. Our findings and the underlying mechanisms should be further investigated., Competing Interests: The authors declare that they do not have any conflicts of interest., (Copyright © 2023 Zhang, Zhang, Ye, Yang, Liu, Wu, Zhou, He and Qin.)

Background: The use of genetic testing in pediatric patients with chronic kidney diseases (CKD) has increased exponentially in the past few years, particularly with the emergence of novel sequencing techniques. However, the genetic yield remains unexpectedly low in nephrology, with an impact on diagnosis, prognosis and treatment. Moreover, the increasing diversity of genetic testing possibilities can be seen as an obstacle by clinicians, in the absence of a strong background in genetics. Here, we propose a step-by-step, multidisciplinary strategy for the diagnostic evaluation of pediatric patients with CKD, and appropriate genetic test selection to maximize the yield of genetic testing. Methods: A total of 126 pediatric patients were enrolled in a retrospective file analysis. Genetic testing techniques used included phenotype-associated next-generation panel sequencing (N = 41), Sanger and SNaPshot sequencing (N = 3) and/or whole exome sequencing (N = 2). Results: Overall genetic yield reached 63% and genetic testing significantly impacted patient management in 70%. The distribution of kidney diseases among patients was balanced and matched previously described pediatric cohorts in terms of glomerulopathies, tubulopathies and ciliopathies. Genetic analyses led to significant treatment modifications, kidney biopsy sparing and personalized nephroprotection, as well as tailored genetic counseling. Of note, the evaluation of Human Phenotype Ontology term accuracy in the cohort showed that causal mutations were precisely identified in 85% of the patients at most. Conclusion: Here we suggest a step-by-step, multidisciplinary strategy to maximize the yield of genetic testing in pediatric patients with CKD. This approach optimizes patient care while avoiding unnecessary treatments or procedures. [ABSTRACT FROM AUTHOR]

Abstract Introduction Cell-free deoxyribonucleic acid DNA (cf-DNA) in urine is promising due to the advantage of urine as an easily obtained and non-invasive sample source over tissue and blood. In clinical practice, it is important to identify non-invasive biomarkers of chronic kidney disease (CKD) in monitoring and surveillance of disease progression. Information is limited, however, regarding the relationship between urine and plasma cf-DNA and the renal outcome in CKD patients. Methods One hundred and thirty-one CKD patients were enrolled between January 2016 and September 2018. Baseline urine and plasma cell-free mitochondrial DNA (cf-mtDNA) and cell-free nuclear DNA (cf-nDNA) were isolated using quantitative real-time PCR. Estimated glomerular filtration rate (eGFR) measurement was performed at baseline and 6-month follow-up. Favorable renal outcome was defined as eGFR at 6 months minus baseline eGFR> = 0. Receiver operator characteristics (ROC) curve analysis was performed to assess different samples of cf-DNA to predict favorable renal outcomes at 6 months. A multivariate linear regression model was used to evaluate independent associations between possible predictors and different samples of cf-DNA. Results Patients with an advanced stage of CKD has significantly low plasma cf-nDNA and high plasma neutrophil gelatinase-associated lipocalin (NGAL) levels. Low urine cf-mtDNA, cf-nDNA levels and low plasma NGAL were significantly correlated with favorable renal outcomes at 6 months. The urine albumin-creatinine ratio (ACR) or urine protein-creatinine ratio (PCR) level is a robust predictor of cf-mtDNA and cf-nDNA in CKD patients. Baseline urine levels of cf-mtDNA and cf-nDNA could predict renal outcomes at 6 months. Conclusions Urinary cf-mtDNA and cf-nDNA may provide novel prognostic biomarkers for renal outcome in CKD patients. The levels of plasma cf-nDNA and plasma NGAL are significantly correlated with the severity of CKD.

Abstract Background Diabetic nephropathy (DN) affects about 40% of diabetes mellitus (DM) patients and is the leading cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) all over the world, especially in high- and middle-income countries. Most DN has been present for years before it is diagnosed. Currently, the treatment of DN is mainly to prevent or delay disease progression. Although many important molecules have been discovered in hypothesis-driven research over the past two decades, advances in DN management and new drug development have been very limited. Moreover, current animal/cell models could not replicate all the features of human DN, while the development of Epigenetics further demonstrates the complexity of the mechanism of DN progression. To capture the key pathways and molecules that actually affect DN progression from numerous published studies, we collected and analyzed human DN prognostic markers (independent risk factors for DN progression). Methods One hundred and fifty-one DN prognostic markers were collected manually by reading 2365 papers published between 01/01/2002 and 12/15/2018. One hundred and fifteen prognostic markers of other four common CKDs were also collected. GO and KEGG enrichment analysis was done using g:Profiler, and a relationship network was built based on the KEGG database. Tissue origin distribution was derived mainly from The Human Protein Atlas (HPA), and a database of these prognostic markers was constructed using PHP Version 5.5.15 and HTML5. Results Several pathways were significantly enriched corresponding to different end point events. It is shown that the TNF signaling pathway plays a role through the process of DN progression and adipocytokine signaling pathway is uniquely enriched in ESRD. Molecules, such as TNF, IL6, SOD2, etc. are very important for DN progression, among which, it seems that “AGER” plays a pivotal role in the mechanism. A database, dbPKD, was constructed containing all the collected prognostic markers. Conclusions This study developed a database for all prognostic markers of five common CKDs, offering some bioinformatics analyses of DN prognostic markers, and providing useful insights towards understanding the fundamental mechanism of human DN progression and for identifying new therapeutic targets.

Chronic kidney disease (CKD) is one of the most important noncommunicable diseases. Abnormal concentration of some tumor markers were found in a spectrum of nonmalignant diseases such as benign ovarian tumors, breast diseases, chronic hepatitis, cirrhosis, diseases of the bile duct, and in CKD. Hence, the present study was undertaken to evaluate carbohydrate antigen (CA) 15-3, carcinoembryonic antigen (CEA), CA 19-9, and human chorionic gonadotropin (HCG) concentrations in advanced stages of CKD (Stage 4 and 5) patients who are not on dialysis and with no known malignancy. Patients included 40 CKD patients and 40 healthy controls. CA 15-3, CEA, CA 19-9, and HCG in serum were estimated by enzyme-linked immunosorbent assay method. The differences in tumor marker levels between the controls and advanced stages of CKD (Stage 4 and 5) were assessed using one-way analysis of variance using the Statistical Package for the Social Sciences for Windows version 16.5. CKD patients had significantly elevated levels of CEA, HCG, CA 19-9, and CA 15-3 compared to the control group (P = 0.001). There was no difference in the tumor markers levels between CKD Stage 4 and 5. Elevation in serum tumor markers may be a possibility in patients with CKD even in the situations of the absence of a malignancy. This may be due to an alteration in their metabolism in CKD and reduction of glomerular filtration rate leading to impaired excretion. Hence, it may be prudent to exercise caution in the interpretation of serum tumor markers as a representative for underlined malignancy in patients of CKD.

Context Thyroid hormones play an important role in renal development, functioning renal mass, and early renal function. Pituitary–thyroid axis and metabolism of the peripheral thyroid hormones have been affected by chronic kidney disease (CKD). Aims The aim was to evaluate the frequency and relationship between thyroid disorders and high-sensitivity C-reactive protein (Hs-CRP) among CKD patients including hemodialysis (HD). Settings and design In Zagazig University Hospital. Participants and methods A case–control study that included 150 adult participants who were divided into: group I which included 50 patients with an estimated glomerular filtration rate (eGFR) of 41.8±23.6 ml/min/1.73 m2. Group II included 50 patients with an eGFR of 11.3±4.2 ml/min/1.73 m2.Group III included 50 participants with normal eGFR. All participants were evaluated for serum creatinine and albumin, complete blood count, estimation of GFR by modification of diet in renal disease (MDRD) equation, and serum thyroid-stimulating hormone (TSH), free T3, free T4, and Hs-CRP. Statistical analysis Using the Statistical Package for the Social Sciences under windows version 20. Qualitative variables were expressed by frequency and percentage, mean±SD, χ2-test, Student’s t-test, analysis of variance (F-test), and correlation analysis. Results The frequency of subclinical hypothyroidism (46%) and overt hypothyroid (42%) in groups I and II, respectively, has been much higher in CKD patients. There was a strong significant negative correlation of Hs-CRP with eGFR, FT3, FT4 (P

Preterm birth interrupts the development and maturation of the kidneys during the critical growth period. The kidneys can also exhibit structural defects and functional impairment due to hyperoxia, as demonstrated by various animal studies. Furthermore, hyperoxia during nephrogenesis impairs renal tubular development and induces glomerular and tubular injuries, which manifest as renal corpuscle enlargement, renal tubular necrosis, interstitial inflammation, and kidney fibrosis. Preterm birth along with hyperoxia exposure induces a pathological predisposition to chronic kidney disease. Hyperoxia-induced kidney injuries are influenced by several molecular factors, including hypoxia-inducible factor-1α and interleukin-6/Smad2/transforming growth factor-β, and Wnt/β-catenin signaling pathways; these are key to cell proliferation, tissue inflammation, and cell membrane repair. Hyperoxia-induced oxidative stress is characterized by the attenuation or the induction of multiple molecular factors associated with kidney damage. This review focuses on the molecular pathways involved in the pathogenesis of hyperoxia-induced kidney injuries to establish a framework for potential interventions.

Background: secondary hyperparathyroidism (SHPT) is an early complication of chronic kidney disease (CKD). Maintaining the level of 25(OH)D and parathyroid hormone concentrations in the target range reduce its associated complications (fractures and cardiovascular calcification). Aims: to examine the effectiveness of vitamin D supplementation and selective vitamin D receptor agonists treatment on SHPT in CKD. Material and methods: prospective observational study to evaluate the efficacy and safety of vitamin D therapy SHPT in 54 in patients with CKD. The first phase (24 weeks) treatment of suboptimal 25-hydroxycalciferol (25(OH)D) levels. The second (16 weeks) treatment colecalciferol-resistant SHPT by combination of cholecalciferol with paricalcitol. Blood samples were taken to assess parathyroid hormone (PTH), 25(OH)D, creatinine, calcium, phosphorus levels and calcium excretion. Results: After 8 weeks of cholecalciferol treatment all patients achieved 25(OH)D levels above 20 ng/ml, however 78% of patients still had SHPT. After 16 weeks, the decrease of PTH was achieved in all patients, but significantly only in patients with CKD 2 (19.2%, p 0.01) and 3 (31%, p 0.05), compared with CKD 4 (17%, p 0.05). After 24 weeks of therapy, PTH normalized in all patients with CKD 2, in 15 (79%) with CKD 3 and in 9 (50%) patients with CKD 4. Cholecalciferol treatment resulted in a substantial increase in 25(OH)D levels with minimal or no impact on calcium, phosphorus levels and kidney function. After 24 weeks we initiated combination therapy (cholecalciferol and paricalcitol) for patients with colecalciferol-resistant SHPT (n=13). PTH levels decreased from 149.113.4 to 118.214.1 pg/ml at 8 weeks, and to 93.19.7 pg/ml (p 0.05) at 16 weeks of treatment. No significant differences in serum calcium, phosphorus or urinary calcium levels. Normalization of PTH was achieved in all patients with CKD 3 and in 8 patients with stage 4. One patient with CKD 4 needed an increase in paricalcitol dose. Conclusion: Cholecalciferol can be used in correcting vitamin D deficiency in patients with all stages of CKD, however, its effectiveness in reducing PTH in stage 4 is limited. Selective analogs, such as paricalcitol, were well-tolerated and effectively decreased PTH levels.

Abstract Background Urinary mitochondrial DNA (mtDNA) fragment level has been proposed as a biomarker of chronic kidney disease (CKD). In this study, we determine the relation between urinary mtDNA level and rate of renal function deterioration in non-diabetic CKD. Methods We recruited 102 non-diabetic CKD patients (43 with kidney biopsy that showed non-specific nephrosclerosis). Urinary mtDNA level was measured and compared to baseline clinical and pathological parameters. The patients were followed 48.3 ± 31.8 months for renal events (need of dialysis or over 30% reduction in estimated glomerular filtration rate [eGFR]). Results The median urinary mtDNA level was 1519.42 (inter-quartile range 511.81–3073.03) million copy/mmol creatinine. There were significant correlations between urinary mtDNA level and baseline eGFR (r = 0.429, p

INTRODUCTION: Chronic kidney disease is an important risk factor for cardiovascular-related morbidity and death. In Ghana, relatively little is known about the prevalence of chronic kidney disease (CKD) in homeless and slum dwellers in the major cities of the country. This study aimed at determining the prevalence of CKD among homeless people in Nima and Agbogbloshie, Accra, Ghana, and to evaluate the association between socio demographic characteristics and CKD. METHODS: we recorded information on individuals´ socio-demographic characteristics and anthropometric indices, and took blood samples from a total of 512 homeless participants for serum creatinine measurement. Renal function was estimated according to the 4-variable Modification of Diet in Renal Disease (MDRD) and Cockcroft–Gault (C-G) equations. RESULTS: participants with normal serum creatinine (SCr), made up of 232 males and 280 females totaling 512 took part in the study. Those with normal glomerular filtration rate (GFR) were 86% and 84.6% by means of the C-G and MDRD equations respectively. According to the C-G formula, kidney damage and mild to severe renal insufficiency was found in 13.2% of the participants and 4 participants (0.8%) had renal failure. On the other hand, 15.4% of the participants were found to have some kidney damage and mild to severe renal insufficiency according to the MDRD formula with no participant suffering from kidney failure. CONCLUSION: the prevalence of CKD among the homeless Ghanaians was significant, especially among those with hypertension, diabetes and human immunodeficiency syndrome virus (HIV) infection.

Introduction: After worldwide closures due to the COVID-19 pandemic, schools have reopened in most European countries in late 2020. Consequently, for children with chronic diseases the risks of COVID-19 have to be weighed against the long-time risks of missing school.Methods: To evaluate the impact of chronic diseases on school attendance for children in Europe during the COVID-19 pandemic we conducted a survey among members of the European Society for Pediatric Nephrology (ESPN) between September and November 2020. We asked for current forms of schooling, the existence of national guidelines, parental concerns, and the pediatric nephrologists recommendations for school attendance for specific virtual patients with chronic kidney disease (CKD).Results: Recommendations varied widely among pediatric nephrologists. A minority stated that specific recommendations for COVID-19 risk in children with kidney diseases existed in their country from local health authorities (9 of 29 countries; 31%) and/or national pediatric nephrology societies (9 of 29 countries; 31%). Over 90% of physicians have experienced parents keeping their children out of school against medical advice of their health providers and about 50% have experienced their patients being refused by school authorities. Consequently, 25% of all pediatric nephrologists estimated that more than 10% of their patients will not attend school regularly.Conclusion: COVID-19 causes educational deficits in the already vulnerable population of children with CKD. As the evidence for the course of COVID-19 in children with chronic diseases grows, rapidly adapted recommendations from pediatric societies could help reduce uncertainty among doctors, patients, and parents.

Chronic renal failure is the loss of the ability of kidneys to excrete waste products, concentrate urine, electrolytes and fluid balance leading to retention of creatinine, urea and other metabolic waste products in the body. The present study was planned to evaluate and correlate Symmetric Dimethylarginine (SDMA) with the severity of chronic kidney disease (CKD) and with BUN and creatinine in dogs. Twenty four dogs presented at Veterinary Clinical Complex of LLUVAS, Hisar (India), diagnosed to be suffering from renal failure on the basis of history, clinical signs and ultrasonographic findings were included in the study. The dogs were divided into three categories (atypical, mild and severe) based on the duration of presentation of cases after emergence of the clinical signs. Six apparently healthy dogs were taken for comparsion with affected ones. Serum from all the affected and apparently healthy animals was used to evaluate SDMA using ELISA kits, whereas BUN and creatinine were determined using biochemistry autoanalyzer. SDMA was significantly (20-fold) elevated in dogs suffering from renal failure as compared to the control group. Significant (p<0.01) positive correlations of SDMA with BUN and serum creatinine were found in all three categories of dogs indicating that serum SDMA can be a biomarker for detection of CKD earlier than does measurement of serum creatinine in dogs. [ABSTRACT FROM AUTHOR]

Chronic kidney disease (CKD) is a major cause of morbidity and mortality worldwide, imposing a great burden on the healthcare system. Regrettably, effective CKD therapeutic strategies are yet available due to their elusive pathogenic mechanisms. CKD is featured by progressive inflammation and fibrosis associated with immune cell dysfunction, leading to the formation of an inflammatory microenvironment, which ultimately exacerbating renal fibrosis. Transforming growth factor β1 (TGF-β1) is an indispensable immunoregulator promoting CKD progression by controlling the activation, proliferation, and apoptosis of immunocytes via both canonical and non-canonical pathways. More importantly, recent studies have uncovered a new mechanism of TGF-β1 for de novo generation of myofibroblast via macrophage-myofibroblast transition (MMT). This review will update the versatile roles of TGF-β signaling in the dynamics of renal immunity, a better understanding may facilitate the discovery of novel therapeutic strategies against CKD.

Aims. The prevalence of CKD in patients with diabetes mellitus in the Middle East region is unknown. Therefore, we aimed to understand the pooled prevalence of CKD in patients with diabetes mellitus in the Middle East region. Methods. PubMed, Embase, and Cochrane databases were searched for relevant studies up to October 2020. The search strategy was conducted using both keywords and MeSH terms. Randomised controlled trials (RCTs) and observational studies that included patients from all age groups and any study design that reported on the prevalence of CKD in patients with diabetes mellitus were included. The pooled estimate for the prevalence of CKD in patients with diabetes was calculated using random-effect models with 95% confidence intervals (CIs). Results. A total of 489 citations were identified, of which only nine studies matched our inclusion criteria and were included in the meta-analysis. All of the studies used an observational study design covering a total of 59,395 patients with type 2 diabetes mellitus. The pooled estimate of the prevalence of CKD in patients with diabetes mellitus was 28.96% (95% CI: 19.80–38.11). Conclusions. A high prevalence of CKD in patients with diabetes mellitus in the Middle East region was found. Further epidemiological studies are warranted in this area to have a better estimate of the prevalence of CKD among DM in the Middle East region.