Corneal Endothelial Alterations in Chronic Renal Failure

Sati, Alok; Jha, Ashok Kumar; Moulick, P.S.; Shankar, Sandeep; Gupta, Sandeep; Khan, M. A.; Dogra, PN; Sangwan, Veena

doi:10.1097/ico.0000000000000922

Cited by 37 publications

(29 citation statements)

References 10 publications

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“…[2][3][4] Beyond the deterioration of renal capillary endothelium, diminished endothelial repair systems and decreased number of endothelial progenitor cells were also reported in DM by previous studies. 4,5 Consequently, microalbuminuria is accepted as a critical marker of generalised endothelial dysfunction, which is involved in pathogenesis of many systemic conditions such as heart disease, stroke, venous thrombosis, tumour growth, metastasis and various infections. [4][5][6] However, it is not clear whether corneal endothelium is also affected by similar pathological mechanisms in patients with microalbuminuria.…”

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confidence: 56%

“…1,2 In DM, hyperglycaemia-induced various mediators (inflammatory cytokines, advanced glycation end products, reactive oxygen species and vascular endothelial growth factor) trigger renal capillary endothelial damage that result in glomerular hyperfiltration and microalbuminuria. [1][2][3][4] Capillary rarefaction, glomerular fibrosis and renal failure are the major findings of end-stage diabetic nephropathy. [2][3][4] Beyond the deterioration of renal capillary endothelium, diminished endothelial repair systems and decreased number of endothelial progenitor cells were also reported in DM by previous studies.…”

mentioning

confidence: 99%

“…[1][2][3][4] Capillary rarefaction, glomerular fibrosis and renal failure are the major findings of end-stage diabetic nephropathy. [2][3][4] Beyond the deterioration of renal capillary endothelium, diminished endothelial repair systems and decreased number of endothelial progenitor cells were also reported in DM by previous studies. 4,5 Consequently, microalbuminuria is accepted as a critical marker of generalised endothelial dysfunction, which is involved in pathogenesis of many systemic conditions such as heart disease, stroke, venous thrombosis, tumour growth, metastasis and various infections.…”

mentioning

confidence: 99%

“…4,5 Consequently, microalbuminuria is accepted as a critical marker of generalised endothelial dysfunction, which is involved in pathogenesis of many systemic conditions such as heart disease, stroke, venous thrombosis, tumour growth, metastasis and various infections. [4][5][6] However, it is not clear whether corneal endothelium is also affected by similar pathological mechanisms in patients with microalbuminuria.…”

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confidence: 99%

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Effect of microalbuminuria on corneal endothelium in patients with diabetes without retinopathy

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Fenkci

Yaylalı

et al. 2020

Clinical and Experimental Optometry

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Background The aim of this study was to investigate the effect of microalbuminuria on corneal endothelium in patients with diabetes without retinopathy. Methods This cross‐sectional study comprised 100 patients with type 2 diabetes mellitus (DM) without diabetic retinopathy and 92 control subjects without diabetes. Forty‐five patients had microalbuminuria and 55 subjects were microalbuminuria negative. Endothelial measurements were obtained using specular microscopy. Endothelial cell density, average area, co‐efficient of variation, maximum area, minimum area, hexagonality and corneal thickness were compared between the groups on the basis of microalbuminuria, DM duration and medication, HbA1c, body mass index, serum lipid and protein profiles, hypertension and hyperlipidaemia diagnosis. Results There were no significant differences in age, gender, endothelial cell density, average area, co‐efficients of variation, maximum area, minimum area, hexagonality or corneal thickness among the microalbuminuria positive, microalbuminuria negative and control groups (p > 0.05). However, microalbuminuria positive patients had lower high‐density lipoprotein levels than the microalbuminuria negative patients (p = 0.042). DM and control groups showed similar endothelial measurements (p > 0.05). Patients with a HbA1c > 7 per cent (53 mmol/mol) had lower hexagonality value (p = 0.039) than in the subjects with a HbA1c ≤ 7 per cent. No significant differences were found in endothelial parameters when groups were compared based on DM duration, medication and co‐morbidities. Conclusions Microalbuminuria positive and negative patients with DM without retinopathy seem to have similar corneal endothelial measurements with controls. However, patients with a HbA1c > 7 per cent should be monitored for deterioration in corneal endothelial cell morphology even without diabetic retinopathy, which might be critical prior to anterior segment surgery.

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confidence: 56%

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confidence: 99%

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confidence: 99%

mentioning

confidence: 99%

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Effect of microalbuminuria on corneal endothelium in patients with diabetes without retinopathy

Toprak

Fenkci

Yaylalı

et al. 2020

Clinical and Experimental Optometry

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“…Systemic hemodynamic parameters, as well as eye fluid volume and composition, can change with HD. There are many studies examining the anterior and posterior segment showed significant changes in IOP and CCT (8)(9)(10)(11)(12). Given the contradictory reports of HD affecting IOP, precise and mechanistic insights of HD on IOP are not well-established (11,13,14).…”

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confidence: 99%

Evaluation Of Intraocular Pressure and Central Corneal Thickness Changes After Hemodıalysis in Patıents With Chronic Renal Failure

Erdem¹,

Güneş²

2019

Eastern J Med

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Substance P inhibits high urea‐induced apoptosis through the AKT/GSK‐3β pathway in human corneal epithelial cells

Wang

Yuan

et al. 2019

J of Cellular Biochemistry

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To investigate the effect of substance P (SP) on human corneal epithelial cells (HCECs) that have been stressed by a high urea environment and to determine the relationship between SP and the protein kinase B (AKT)/glycogen synthase kinase-3β (GSK-3β) signaling pathway. An in vitro model of chronic renal failure (CRF)-related dry eye was used to study HCECs that were treated with high urea concentrations. Cell proliferation was assayed using a cell counting kit-8 test.Besides, cell apoptosis was evaluated by flow cytometry. Furthermore, the effects of SP and the AKT inhibitor perifosine on the urea-treated HCECs were examined using immunofluorescence, quantitative real time polymerase chain reaction (qRT-PCR), and Western blot analysis. SP markedly reduced the number of apoptotic HCECs and decreased the cleaved caspase-3 expression levels while contributing to increased cellular proliferation (P < 0.05). The Western blot analysis and qRT-PCR experiments revealed that SP significantly increased the expression of p-AKT and p-GSK-3β (P < 0.05); additionally, these increases were attenuated after the perifosine inhibition of the AKT signaling pathway (P < 0.05). These in vitro experiments demonstrated that SP may protect against the apoptotic damage of HCECs caused by the high urea condition. The underlying mechanism may be related to the activation of the AKT/GSK-3β signaling pathway. K E Y W O R D SAKT, glycogen synthase kinase-3β, human corneal epithelial cells, high urea, substance P

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Corneal Endothelial Alterations in Chronic Renal Failure

Abstract: Corneal endothelial alteration is present in patients with chronic renal failure, more marked in patients undergoing hemodialysis and with raised blood urea level.

Cited by 37 publications

References 10 publications

Effect of microalbuminuria on corneal endothelium in patients with diabetes without retinopathy

Effect of microalbuminuria on corneal endothelium in patients with diabetes without retinopathy

Evaluation Of Intraocular Pressure and Central Corneal Thickness Changes After Hemodıalysis in Patıents With Chronic Renal Failure

Substance P inhibits high urea‐induced apoptosis through the AKT/GSK‐3β pathway in human corneal epithelial cells

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