Diabetes mellitus is one of the most prevalent chronic diseases worldwide. Diabetic patients are at risk of developing cataract and present for surgery at an earlier age than non-diabetics. The aim of this study was to review the problems associated with cataract surgery in a diabetic patient. Corneal complications in diabetic patients include delayed wound healing, risk of developing epithelial defects or recurrent erosions due to the impairment of epithelial basement membranes and epithelial–stromal interactions. Diabetic patients present lower endothelial cell density and their endothelium is more susceptible to trauma associated with cataract surgery. A small pupil is common in diabetic patients making cataract surgery technically challenging. Finally diabetic patients have an increased risk for developing postoperative pseudophakic cystoid macular edema, posterior capsule opacification or endophthalmitis. In patients with pre-proliferative or proliferative diabetic retinopathy, diabetic macular edema or iris neovascularization adjunctive therapy such as an intravitreal anti-vascular endothelial growth factor injection, can inhibit exacerbation related to cataract surgery.

Most studies evaluating cataract surgery focus on the primary outcome of early, central, best-corrected visual acuity. However, cataract surgery and intraocular lens (IOL) design have other secondary visual outcomes as well as impacts on various ocular tissues, the visual function, and quality of life. Some of these aspects are more difficult to quantify, or are historically neglected, but might be extremely important to patients. One important development was the addition of blue-light filtering to IOL design. Whether these IOLs truly have the retinal protective qualities they were designed for is disputed, yet other inadvertent desirable and possibly detrimental influences are being examined. Risk of falls, driving accidents, and other injuries decrease following cataract surgery, especially in the elderly, the importance of which cannot be overemphasized. Cataract formation contributes to social isolation and decreases cognitive stimulation in the elderly population, while cataract extraction can reduce the risk of dementia and cognitive decline. Diffractive multifocal and extended depth-of-focus IOLs improve spectacle independence and patient reported outcomes, but positive and negative dysphotopsia may be persistent. Future directions such as using the IOL enabling clear spectacle-free vision at all distances, or intraoperative drug delivery systems show promising preliminary results. It seems inevitable that a higher focus on the secondary outcomes of surgery will increase. We believe that these aspects will become more and more relevant when considering new IOL designs and surgical techniques, a fact that will benefit both the patients and the surgeons.

Objective— Chronic rejection is the main reason for the poor long-term survival of heart transplant recipients and is characterized by cardiac allograft inflammation, fibrosis, and arteriosclerosis. We examined the specific roles of different platelet-derived growth factor (PDGF) ligands (A–D)—potent mesenchymal cell mitogens—in rat cardiac allografts. Methods and Results— PDGFR-α mRNA was upregulated in acutely-rejecting, and PDGF-A and PDGF-C mRNA in chronically-rejecting cardiac¢hatn allografts. In acute rejection, PDGFR-α immunoreactivity increased in the media of arteries. In chronically-rejecting allografts, immunoreactivity of all PDGF ligands and receptors—except that of PDGF-B ligand—was found in the intima of arteries, and the expression of PDGF-A and PDGF-C was seen in cardiomyocytes. Intracoronary adeno-associated virus-2 (AAV2)-mediated PDGF-A and -D gene transfer enhanced cardiac allograft inflammation. AAV2-PDGF-A, AAV2-PDGF-C, and AAV2-PDGF-D significantly upregulated profibrotic TGF-β1 mRNA and accelerated cardiac fibrosis and arteriosclerosis. In contrast, AAV2-PDGF-B did not aggravate chronic rejection. Conclusions— We found that alloimmune response induces PDGF-A, PDGF-C, and PDGF-D expression in the graft vasculature. PDGF-A, PDGF-C, and PDGF-D mediated profibrotic and proarteriosclerotic effects in transplanted hearts involving the TGF-β1 pathway. Inhibition of signaling of all PDGF-ligands except that of PDGF-B may thus be needed to inhibit chronic rejection in cardiac allografts.

Ischemia-reperfusion injury (IRI) after kidney transplantation may result in delayed graft function. We used rat renal artery clamping and transplantation models to investigate cholesterol-independent effects of clinically relevant single-dose peroral simvastatin treatment 2 h before renal ischemia on microvascular injury. The expression of HMG-CoA reductase was abundant in glomerular and peritubular microvasculature of normal kidneys. In renal artery clamping model with 30-min warm ischemia, simvastatin treatment prevented peritubular microvascular permeability and perfusion disturbances, glomerular barrier disruption, tubular dysfunction and acute kidney injury. In fully MHC-mismatched kidney allografts with 16-h cold and 1-h warm ischemia, donor simvastatin treatment increased the expression of flow-regulated transcription factor KLF2 and vasculoprotective eNOS and HO-1, and preserved glomerular and peritubular capillary barrier integrity during preservation. In vitro EC Weibel–Palade body exocytosis assays showed that simvastatin inhibited ischemia-induced release of vasoactive angiopoietin-2 and endothelin-1. After reperfusion, donor simvastatin treatment prevented microvascular permeability, danger-associated ligand hyaluronan induction, tubulointerstitial injury marker Kim-1 immunoreactivity and serum creatinine and NGAL levels, and activation of innate and adaptive immune responses. In conclusion, donor simvastatin treatment prevented renal microvascular dysfunction and IRI with beneficial effects on adaptive immune and early fibroproliferative responses. Further studies may determine potential benefits in clinical cadaveric kidney transplantation.