Displaying publications 1 - 20 of 70 in total

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  1. Liew A, Bavanandan S, Prasad N, Wong MG, Chang JM, Eiam-Ong S, et al.
    Nephrology (Carlton), 2020 Nov;25(11):809-817.
    PMID: 33111435 DOI: 10.1111/nep.13804
    Matched MeSH terms: Diabetic Nephropathies/diagnosis; Diabetic Nephropathies/etiology; Diabetic Nephropathies/therapy*
  2. Zhang X, Seman NA, Falhammar H, Brismar K, Gu HF
    J Diabetes Res, 2020;2020:8305460.
    PMID: 32626783 DOI: 10.1155/2020/8305460
    Diabetic kidney disease (DKD) is a complex disease, in which local inflammatory stress results from both metabolic and hemodynamic derangements. Intercellular adhesion molecule 1 (ICAM-1) is an acute-phase protein marker of inflammation. In the recent years, clinical observations have reported that increased serum/plasma ICAM-1 levels are positively correlated with albuminuria in the patients with type 1 (T1D) and type 2 diabetes (T2D). Genetic association studies have demonstrated that genetic polymorphisms, including SNP rs5498 (E469K, G/A), in the ICAM1 gene is associated with DKD. rs5498 is a nonsynonymous SNP and caused by substitution between E (Glu) and K (Lys) for ICAM-1 protein. In this review, we first summarized the genetic effects of ICAM1 E469K polymorphism in DKD and then demonstrated the possible changes of ICAM-1 protein crystal structures according to the genotypes of this polymorphism. Finally, we discussed the genetic effects of the ICAM1 E469K polymorphism and the biological role of increased circulating ICAM-1 protein and its formation changes in DKD.
    Matched MeSH terms: Diabetic Nephropathies/genetics*; Diabetic Nephropathies/metabolism
  3. A/L B Vasanth Rao VR, Tan SH, Candasamy M, Bhattamisra SK
    Diabetes Metab Syndr, 2018 11 30;13(1):754-762.
    PMID: 30641802 DOI: 10.1016/j.dsx.2018.11.054
    Diabetic nephropathy (DN) is a major cause of end-stage renal disease and affects a large number of individuals with diabetes. However, the development of specific treatments for DN has not yet been identified. Hence, this review is concisely designed to understand the molecular pathways leading to DN in order to develop suitable therapeutic strategies. Extensive literature search have been carried in regard with the pathogenesis and pathophysiology of DN, drug targets and updates on clinical trials, the consequences associated with DN and the potential biomarkers for diagnosis and prediction of DN are discussed in this review. DN is characterised by microalbuminuria and macroalbuminuria, and morphological changes such as glomerular thickening, interstitial fibrosis, formation of nodular glomerulosclerosis and decreased endothelial cell fenestration. Besides, the involvement of renin-angiotensin-aldosterone system, inflammation and genetic factors are the key pathways in the progression of DN. In regard with drug development drugs targeted to epidermal growth factor, inflammatory cytokines, ACTH receptor and TGFβ1 receptors are in pipeline for clinical trials whereas, several drugs have also failed in phase III and phase IV of clinical trials due to lack of efficacy and severe adverse effect. The research on DN is limited with respect to its pathogenesis and drug development. Thus, a more detailed understanding of the pathogenesis of DN is very essential to progress in the drug development process.
    Matched MeSH terms: Diabetic Nephropathies/diagnosis*; Diabetic Nephropathies/drug therapy*; Diabetic Nephropathies/metabolism
  4. Suleiman AB, Jeyaindran S, Morad Z, Kong CT
    Med J Malaysia, 1984 Sep;39(3):225-8.
    PMID: 6544924
    More than half of 174 patients with end stage renal disease (ESRD) treated by the Department of Nephrology, General Hospital Kuala Lumpur in 1982 presented for the first time in uraemia, with no known renal disease in the past. Although about half of all patients seen in 1982 were treated by dialysis or transplantation, the great majority of the estimated number of patients developing ESRD in Malaysia in 1982 did not receive definitive treatment.
    Matched MeSH terms: Diabetic Nephropathies/complications
  5. Wong JS
    Med J Malaysia, 2005 Jun;60(2):146-50.
    PMID: 16114154 MyJurnal
    Diabetic nephropathy is now the number one cause of end stage renal failure in Malaysia. This places a huge burden on patients and the health care system especially in developing countries with limited health care resources, such as in Sarawak in East Malaysia. This study describes the prevalence of proteinuria/microalbuminuria in diabetic patients treated in Klinik Kesihatan Tanah Puteh. Early detection of proteinuria/microalbuminuria allows remedial measures to be taken to retard the progression of nephropathy. Forty-eight percent of the cases had proteinuria and microalbuminuria was found in 16%. Seventy-eight percent of cases with proteinuria were on treatment with angiotensin-converting-enzyme inhibitors or angiotensin-receptor blockers. Seventy-five percent of patients had hypertension but only 6% achieved the targeted BP of < 130/80 mmHg.
    Study site: Diabetic clinic of Klinik Kesihatan Tanah Puteh, Kuching, Sarawak, Malaysia
    Matched MeSH terms: Diabetic Nephropathies/complications*; Diabetic Nephropathies/epidemiology
  6. Ahmad FU, Sattar MA, Rathore HA, Abdullah MH, Tan S, Abdullah NA, et al.
    Ren Fail, 2012;34(2):203-10.
    PMID: 22229751 DOI: 10.3109/0886022X.2011.643365
    The coexistence of hypertension and diabetes results in the rapid development of nephropathy. Hydrogen sulfide (H2S) is claimed to control the vascular and renal functions. This study tested the hypothesis that exogenous H2S lowers the blood pressure and decreases the progression of nephropathy in spontaneously hypertensive rats (SHR) that were diabetic. Eighteen SHR were divided into three groups: SHR, SHR diabetic, and SHR diabetic treated with a group of Wistar-Kyoto rats serving as normotensive nondiabetic control. Diabetes was induced with streptozotocin (STZ) in two groups and one diabetic group received sodium hydrosulfide (NaHS), a H2S donor for 5 weeks. Blood pressure was measured in conscious and anesthetized states and renal cortical blood perfusion in acute studies. Plasma and urinary H2S levels, creatinine concentrations, and electrolytes were measured on three different occasions throughout the 35-day period. Diabetic SHR had higher blood pressure, lower plasma and urinary H2S levels, and renal dysfunction as evidenced by increased plasma creatinine, creatinine clearance, and decreased urinary sodium-to-potassium ratio and renal cortical blood perfusion. NaHS reduced blood pressure, increased H2S levels in plasma and urinary excretion, and reversed the STZ-induced renal dysfunction. The findings of this study suggest that the administration of exogenous H2S lowers the blood pressure and confers protection against the progression of STZ-induced nephropathy in SHR.
    Matched MeSH terms: Diabetic Nephropathies/etiology; Diabetic Nephropathies/prevention & control*
  7. Abbasi SH, Aftab RA, Chua SS
    PLoS One, 2020;15(6):e0234376.
    PMID: 32569265 DOI: 10.1371/journal.pone.0234376
    BACKGROUND: Profound healthcare challenges confront societies with an increase in prevalence of end-stage renal disease (ESRD), which is one of the leading causes of morbidity and mortality worldwide. Due to several facility and patient related factors, ESRD is significantly associated with increased morbidity and mortality attributed to infections.

    AIMS AND OBJECTIVE: The aim of this study was to assess systematically the characteristics of patients and risk factors associated with nosocomial infections among ESRD patients undergoing hemodialysis.

    METHODS: A systematic literature search was performed to identify eligible studies published during the period from inception to December 2018 pertaining to risk factors associated with nosocomial infections among hemodialysis patients. The relevant studies were generated through a computerized search on five databases (PubMed, EBSCOhost, Google Scholar, ScienceDirect and Scopus) using the Mesh Words: nosocomial infections, hospital acquired infections, healthcare associated infections, end stage renal disease, end stage renal failure, hemodialysis, and risk factors. The complete protocol has been registered under PROSPERO (CRD42019124099).

    RESULTS: Initially, 1411 articles were retrieved. Out of these, 24 were duplicates and hence were removed. Out of 1387 remaining articles, 1337 were removed based on irrelevant titles and/or abstracts. Subsequently, the full texts of 50 articles were reviewed and 41 studies were excluded at this stage due to lack of relevant information. Finally, nine articles were selected for this review. Longer hospital stay, longer duration on hemodialysis, multiple catheter sites, longer catheterization, age group, lower white blood cell count, history of blood transfusion, and diabetes were identified as the major risk factors for nosocomial infections among hemodialysis patients.

    CONCLUSION: The results of this review indicate an information gap and potential benefits of additional preventive measures to further reduce the risk of infections in hemodialysis population. Moreover, several patient-related and facility-related risk factors were consistently observed in the studies included in this review, which require optimal control measures.

    Matched MeSH terms: Diabetic Nephropathies/complications; Diabetic Nephropathies/therapy
  8. Selvarajah S, Uiterwaal CS, Haniff J, van der Graaf Y, Visseren FL, Bots ML, et al.
    Eur J Clin Invest, 2013 Feb;43(2):198-207.
    PMID: 23301500 DOI: 10.1111/eci.12035
    BACKGROUND:
    Renal impairment and type 2 diabetes mellitus (DM) are well-known independent risk factors for mortality. The evidence of their combined effects on mortality is unclear, but of importance because it may determine aggressiveness of treatment. This study sought to assess and quantify the effect modification of diabetes on renal impairment in its association with mortality.

    MATERIALS AND METHODS:
    Patients with cardiovascular disease or at high risk, recruited in the Second Manifestations of ARTerial disease cohort study, were selected. A total of 7135 patients were enrolled with 33 198 person-years of follow-up. Renal impairment was defined by albuminuria status and estimated glomerular filtration rate (eGFR). Outcome was all-cause mortality.

    RESULTS:
    Mortality increased progressively with each stage of renal impairment, for both albuminuria status and eGFR, for diabetics and non-diabetics. There was no effect modification by diabetes on mortality risk due to renal impairment. The relative excess risk due to interaction (RERI) for DM and microalbuminuria was 0·21 (-0·11, 0·52), for overt proteinuria -1·12 (-2·83, 0·59) and for end-stage renal failure (ESRF) 0·32 (-3·65, 4·29). The RERI for DM with eGFR of 60-89 mL/min/1·73 m(2) was -0·31(-0·92, 0·32), for eGFR of 30-59 mL/min/1·73 m(2) -0·07 (-0·76, 0·62) and for eGFR of < 30 mL/min/1·73 m(2) 0·38 (-0·85, 1·61).

    CONCLUSIONS:
    Type 2 diabetes mellitus does not modify nor increase the risk relation between all-cause mortality and renal impairment. These findings suggest that the hallmark for survival is the prevention and delay in progression of renal impairment in patients with cardiovascular disease.
    Matched MeSH terms: Diabetic Nephropathies/complications; Diabetic Nephropathies/mortality*
  9. Chong YB, Keng TC, Tan LP, Ng KP, Kong WY, Wong CM, et al.
    Ren Fail, 2012;34(3):323-8.
    PMID: 22250665 DOI: 10.3109/0886022X.2011.647302
    BACKGROUND:
    Type 2 diabetes mellitus (T2DM) is reportedly the leading cause of end-stage renal disease (ESRD) worldwide. However, non-diabetic renal diseases (NDRD) are not uncommon among T2DM patients with renal involvement. Our study aimed to examine the prevalence of NDRD in T2DM and clinical markers for diabetic nephropathy (DN) and NDRD and to determine the role of renal biopsy in T2DM patients and its impact on clinical practice.

    METHODS:
    We conducted a retrospective analysis of T2DM patients in whom renal biopsies were performed from January 2004 to March 2008 (n = 110).

    RESULTS:
    Biopsy results were divided into three groups: group I/pure DN (62.7%), group II/isolated NDRD (18.2%), and group III/mixed lesions (19.1%). The causes of NDRD in decreasing order of frequency were acute interstitial nephritis, glomerulonephritides, hypertensive renal disease, and acute tubular necrosis. Significant clinical markers for DN are presence of diabetic retinopathy and longer duration of diabetes. For NDRD, useful clinical markers include the presence of acute renal failure and microscopic hematuria. In the DN subgroup, Indians had significantly shorter duration of diabetes on biopsy compared with Malays and Chinese.

    CONCLUSIONS:
    NDRD is prevalent in T2DM patients, and given its potentially treatable nature, renal biopsy should be considered in T2DM patients with nephropathy, especially in those with atypical features.
    Matched MeSH terms: Diabetic Nephropathies/etiology; Diabetic Nephropathies/epidemiology; Diabetic Nephropathies/pathology
  10. Lokman FE, Seman NA, Ismail AA, Yaacob NA, Mustafa N, Khir AS, et al.
    J Nephrol, 2011;24(6):778-89.
    PMID: 21360476 DOI: 10.5301/JN.2011.6382
    BACKGROUND: Diabetic nephropathy (DN) is the most common cause of end-stage renal disease (ESRD) among type 2 diabetes mellitus patients (DM) in Malaysia. This study used microarray analysis to determine the gene expression profiling in ethnic Malay patients with type 2 DM.
    METHODS: A total of 312 patients were recruited; 25 were on dialysis due to ESRD, 128 were classified as normoalbuminuric, 93 as microalbuminuric and 66 as macroalbuminuric, based on urine albumin to creatinine ratio of <3.5, between 3.5 and 35 and =35 mg/mmol, respectively.
    RESULTS: Microalbuminuria was associated with up- and down-regulation of 2,694 and 2,538 genes, respectively, while macroalbuminuria was associated with up-regulation of 2,520 genes and down-regulation of 2,920 genes. There was significant up-regulation of 1,135 genes and down-regulation of 908 genes in the ESRD samples. Thirty-seven significantly up-regulated genes and 40 down-regulated genes were commonly expressed in all 3 groups of patients with worsening of renal functions. Up-regulated genes included major histocompatibility complex (HLA-C), complement component 3a receptor 1 (C3AR1), solute carrier family 16, member 3 (SLC16A3) and solute carrier family 9 (sodium/hydrogen exchanger) (SLC9A8). Consistently down-regulated genes included were bone morphogenetic phosphatase kinase (BMP2K), solute carrier family 12, member 1 (SLC12A1), solute carrier family 7 (SLC7A2), paternally expressed 10 (PEG10) and protein phosphatase 1 regulatory (inhibitor unit) (PPP1R1C).
    CONCLUSION: This study has identified several genes of interest, such as HLA-C, SLC16A3, SLC9A8, SLC12A1 and SLC7A2, that require verification of their roles as susceptibility genes for diabetic nephropathy in ethnic Malays with type 2 DM.
    Matched MeSH terms: Diabetic Nephropathies/ethnology*; Diabetic Nephropathies/genetics*; Diabetic Nephropathies/epidemiology
  11. Cheong I
    Family Practitioner, 1988;11:92-93.
    5% of hospital admissions in Malaysia each year consist of patients suffering from renal diseases; from these 600 new cases of chronic renal failure will be diagnosed. The common causes of chronic renal failure in Malaysia in order of frequency are chronic glomerulonephritis, diabetic nephropathy, obstructive uropathy, malignant hypertension, chronic pyelonephritis, SLE nephritis and gouty nephropathy. Prevention of renal diseases require good control of the underlying conditions.
    Matched MeSH terms: Diabetic Nephropathies
  12. Abu Seman N, Anderstam B, Wan Mohamud WN, Östenson CG, Brismar K, Gu HF
    J Diabetes Complications, 2015 Nov-Dec;29(8):1234-9.
    PMID: 26255081 DOI: 10.1016/j.jdiacomp.2015.07.004
    Recent research has implicated that the inflammation may be a key pathophysiological mechanism in diabetic nephropathy (DN). Intercellular adhesion molecule 1 (ICAM-1) is an acute phase marker of inflammation. In the present study, we carried out genetic, epigenetic and protein analyses of ICAM-1 in a Malaysian population, including normal glucose tolerance (NGT) subjects and type 2 diabetes (T2D) patients with or without DN in order to evaluate its role in DN.
    Matched MeSH terms: Diabetic Nephropathies
  13. Salman IM, Ameer OZ, Sattar MA, Abdullah NA, Yam MF, Abdullah GZ, et al.
    Neurourol Urodyn, 2011 Mar;30(3):438-46.
    PMID: 21284025 DOI: 10.1002/nau.21007
    We assessed the role of renal sympathetic nervous system in the deterioration of renal hemodynamic and excretory functions in rats with streptozotocin (STZ)-induced diabetic kidney disease (DKD).
    Matched MeSH terms: Diabetic Nephropathies/blood; Diabetic Nephropathies/etiology*; Diabetic Nephropathies/physiopathology
  14. Salman IM, Ameer OZ, Sattar MA, Abdullah NA, Yam MF, Najim HS, et al.
    J Nephrol, 2010 5 4;24(1):68-77.
    PMID: 20437405 DOI: 10.5301/jn.2010.6
    BACKGROUND: Renal sympathetic innervation plays an important role in the control of renal hemodynamics and may therefore contribute to the pathophysiology of many disease states affecting the kidney. Thus, the present study aimed to investigate the role of the renal sympathetic nervous system in the early deteriorations of renal hemodynamics and structure in rats with pathophysiological states of renal impairment.

    METHODS: Anesthetized Sprague Dawley (SD) rats with cisplatin-induced acute renal failure (ARF) or streptozotocin (STZ)-induced diabetes mellitus (DM) were subjected to a renal hemodynamic study 7 days after cisplatin and STZ administration. During the acute study, renal nerves were electrically stimulated, and responses in renal blood flow (RBF) and renal vascular resistance (RVR) were recorded in the presence and absence of renal denervation. Post mortem kidney collection was performed for histopathological assessment.

    RESULTS: In innervated ARF or DM rats, renal nerve stimulation produced significantly lower (all p<0.05, vs. innervated control) renal vasoconstrictor responses. These responses were markedly abolished when renal denervation was performed (all p<0.05); however, they appeared significantly higher compared with denervated controls (all p<0.05). Kidney injury was suppressed in denervated ARF, while, irrespective of renal denervation, renal specimens from DM rats were comparable to controls.

    CONCLUSIONS: Renal sympathoexcitation is involved in the pathogenesis of the renal impairment accompanying ARF and DM, and may even precede the establishment of an observable renal injury. There is a possible enhancement in the renal sensitivity to intrarenal norepinephrine following renal denervation in ARF and DM rats.
    Matched MeSH terms: Diabetic Nephropathies/etiology; Diabetic Nephropathies/pathology; Diabetic Nephropathies/physiopathology*
  15. Zainordin NA, Eddy Warman NA, Mohamad AF, Abu Yazid FA, Ismail NH, Chen XW, et al.
    PLoS One, 2021;16(10):e0258507.
    PMID: 34644368 DOI: 10.1371/journal.pone.0258507
    INTRODUCTION: There is limited data on the effects of low carbohydrate diets on renal outcomes particularly in patients with underlying diabetic kidney disease. Therefore, this study determined the safety and effects of very low carbohydrate (VLCBD) in addition to low protein diet (LPD) on renal outcomes, anthropometric, metabolic and inflammatory parameters in patients with T2DM and underlying mild to moderate kidney disease (DKD).

    MATERIALS AND METHODS: This was an investigator-initiated, single-center, randomized, controlled, clinical trial in patients with T2DM and DKD, comparing 12-weeks of low carbohydrate diet (<20g daily intake) versus standard low protein (0.8g/kg/day) and low salt diet. Patients in the VLCBD group underwent 2-weekly monitoring including their 3-day food diaries. In addition, Dual-energy x-ray absorptiometry (DEXA) was performed to estimate body fat percentages.

    RESULTS: The study population (n = 30) had a median age of 57 years old and a BMI of 30.68kg/m2. Both groups showed similar total calorie intake, i.e. 739.33 (IQR288.48) vs 789.92 (IQR522.4) kcal, by the end of the study. The VLCBD group showed significantly lower daily carbohydrate intake 27 (IQR25) g vs 89.33 (IQR77.4) g, p<0.001, significantly higher protein intake per day 44.08 (IQR21.98) g vs 29.63 (IQR16.35) g, p<0.05 and no difference in in daily fat intake. Both groups showed no worsening of serum creatinine at study end, with consistent declines in HbA1c (1.3(1.1) vs 0.7(1.25) %) and fasting blood glucose (1.5(3.37) vs 1.3(5.7) mmol/L). The VLCBD group showed significant reductions in total daily insulin dose (39(22) vs 0 IU, p<0.001), increased LDL-C and HDL-C, decline in IL-6 levels; with contrasting results in the control group. This was associated with significant weight reduction (-4.0(3.9) vs 0.2(4.2) kg, p = <0.001) and improvements in body fat percentages. WC was significantly reduced in the VLCBD group, even after adjustments to age, HbA1c, weight and creatinine changes. Both dietary interventions were well received with no reported adverse events.

    CONCLUSION: This study demonstrated that dietary intervention of very low carbohydrate diet in patients with underlying diabetic kidney disease was safe and associated with significant improvements in glycemic control, anthropometric measurements including weight, abdominal adiposity and IL-6. Renal outcomes remained unchanged. These findings would strengthen the importance of this dietary intervention as part of the management of patients with diabetic kidney disease.

    Matched MeSH terms: Diabetic Nephropathies/complications; Diabetic Nephropathies/diet therapy*; Diabetic Nephropathies/pathology
  16. Das RR, Rahman MA, Al-Araby SQ, Islam MS, Rashid MM, Babteen NA, et al.
    Oxid Med Cell Longev, 2021;2021:9711176.
    PMID: 34367469 DOI: 10.1155/2021/9711176
    The purpose of this study was to look into the effects of green coconut mesocarp juice extract (CMJE) on diabetes-related problems in streptozotocin- (STZ-) induced type 2 diabetes, as well as the antioxidative functions of its natural compounds in regulating the associated genes and biochemical markers. CMJE's antioxidative properties were evaluated by the standard antioxidant assays of 1,1-diphenyl-2-picrylhydrazyl (DPPH), superoxide radical, nitric oxide, and ferrous ions along with the total phenolic and flavonoids content. The α-amylase inhibitory effect was measured by an established method. The antidiabetic effect of CMJE was assayed by fructose-fed STZ-induced diabetic models in albino rats. The obtained results were verified by bioinformatics-based network pharmacological tools: STITCH, STRING, GSEA, and Cytoscape plugin cytoHubba bioinformatics tools. The results showed that GC-MS-characterized compounds from CMJE displayed a very promising antioxidative potential. In an animal model study, CMJE significantly (P < 0.05) decreased blood glucose, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine, uric acid, and lipid levels and increased glucose tolerance as well as glucose homeostasis (HOMA-IR and HOMA-b scores). The animal's body weights and relative organ weights were found to be partially restored. Tissue architectures of the pancreas and the kidney were remarkably improved by low doses of CMJE. Compound-protein interactions showed that thymine, catechol, and 5-hydroxymethylfurfural of CMJE interacted with 84 target proteins. Of the top 15 proteins found by Cytoscape 3.6.1, 8, CAT and OGG1 (downregulated) and CASP3, COMT, CYP1B1, DPYD, NQO1, and PTGS1 (upregulated), were dysregulated in diabetes-related kidney disease. The data demonstrate the highly prospective use of CMJE in the regulation of tubulointerstitial tissues of patients with diabetic nephropathy.
    Matched MeSH terms: Diabetic Nephropathies/etiology; Diabetic Nephropathies/pathology; Diabetic Nephropathies/prevention & control*
  17. Alomari G, Al-Trad B, Hamdan S, Aljabali A, Al-Zoubi M, Bataineh N, et al.
    Drug Deliv Transl Res, 2020 Feb;10(1):216-226.
    PMID: 31637677 DOI: 10.1007/s13346-019-00675-6
    Several recent studies have reported that gold nanoparticles (AuNPs) attenuate hyperglycemia in diabetic animal models without any observed side effects. The present study was intended to provide insight into the effects of 50-nm AuNPs on diabetic kidney disease. Adult male rats were divided into three groups (n = 7/group): control (non-diabetic, ND), diabetic (D), and diabetic treated intraperitoneally with 50-nm AuNPs (AuNPs + D; 2.5 mg/kg/day) for 7 weeks. Diabetes was induced by a single-dose injection of 55 mg/kg streptozotocin. The result showed that AuNP treatment prevented diabetes-associated increases in the blood glucose level. Reduction in 24-h urinary albumin excretion rate, glomerular basement membrane thickness, foot process width, and renal oxidative stress markers was also demonstrated in the AuNP-treated group. In addition, the results showed downregulation effect of AuNPs in renal mRNA or protein expression of transforming growth factor β1 (TGF-β1), fibronectin, collagen IV, tumor necrosis factor-α (TNF-α), and vascular endothelial growth factor-A (VEGF-A). Moreover, the protein expression of nephrin and podocin, podocyte markers, in glomeruli was increased in the AuNPs + D group compared with the D group. These results provide evidence that 50-nm AuNPs can ameliorate renal damage in experimental models of diabetic nephropathy through improving the renal function and downregulating extracellular matrix protein accumulation, along with inhibiting renal oxidative stress and amelioration of podocyte injury.
    Matched MeSH terms: Diabetic Nephropathies/drug therapy*; Diabetic Nephropathies/etiology; Diabetic Nephropathies/metabolism
  18. Sthaneshwar P, Chan SP
    Malays J Pathol, 2010 Jun;32(1):43-7.
    PMID: 20614725 MyJurnal
    Type IV collagen is the principal component of glomerular basement membrane and messangial matrix. Studies have shown increased levels of urinary type IV collagen (uIV) in diabetic patients compared to healthy controls. The concentration of uIV increases gradually as diabetic nephropathy progresses.
    AIM AND METHOD: This study was carried out to determine whether urinary type IV collagen (uIV) can serve as an indicator of diabetic nephropathy. Using a sandwich enzyme immunoassay technique, uIV excretion was determined in 30 type 2 diabetic patients with normoalbuminuria and 20 patients with microalbuminuria.
    RESULTS: uIV excretion was significantly increased in type 2 diabetics, in both normoalbuminuric and microalbuminuric patients, compared with healthy controls. The increase in urinary type IV collagen was well correlated with the amount of urinary albumin but not with HbA1C.
    CONCLUSION: Our findings that uIV is higher in those with microalbuminuria and correlates with albuminuria, support uIV as an indicator of diabetic nephropathy. Whether the increased uIV excretion would predict the impending renal failure needs further confirmation.
    Matched MeSH terms: Diabetic Nephropathies/urine*
  19. Wiart C
    Nutr Res, 2015 Jun;35(6):545.
    PMID: 25957969 DOI: 10.1016/j.nutres.2015.04.014
    Matched MeSH terms: Diabetic Nephropathies/prevention & control*
  20. Ho YL, Ng PF, Krishinan S, Abdul Kareem BA
    J Cardiothorac Surg, 2021 May 29;16(1):151.
    PMID: 34051789 DOI: 10.1186/s13019-021-01526-7
    BACKGROUND: Papillary fibroelastomas are rare but benign cardiac tumour that are often found on cardiac valvular surfaces. Their clinical manifestations ranging from clinically asymptomatic to substantial complications that are usually secondary to systemic embolism. Multiple theories have been proposed to explain the pathophysiology of its formation.

    CASE PRESENTATION: We reported a rare case of large papillary fibroelastoma in the right atrium of a young gentleman which was complicated with pulmonary embolism. Transthoracic echocardiography identified a large pedunculated mass measuring 3.4cmX3.4cmX2cm in right atrium with stalk attached to interatrial septum. The intracardiac mass was resected surgically, which revealed papillary fibroelastoma in histology examination.

    CONCLUSION: Differential diagnosis of intracardiac masses requires clinical information, laboratory tests and imaging modalities including echocardiography. Incidentally discovered papillary fibroelastomas are treated on the basis of their sizes, site, mobility and potential embolic complications. Due to the embolic risk inherent to intraacardiac masses, surgical resection represents an effective curative protocol in treating both symptomatic and asymptomatic right sided and left sided papillary fibroelastomas, with excellent long term postoperative prognosis.

    Matched MeSH terms: Diabetic Nephropathies/complications
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