Effects of glycaemic management on diabetic kidney disease

Abstract

Hyperglycaemia contributes to the onset and progression of diabetic kidney disease (DKD). Observational studies have not consistently demonstrated a glucose threshold, in terms of HbA1c levels, for the onset of DKD. Tight glucose control has clearly been shown to reduce the incidence of micro- or macroalbuminuria. However, evidence is now also emerging to suggest that intensive glucose control can slow glomerular filtration rate loss and possibly progression to end stage kidney disease. Achieving tight glucose control needs to be balanced against the increasing appreciation that glucose targets for the prevention of diabetes related complications need be individualised for each patient. Recently, empagliflozin which is an oral glucose lowering agent of the sodium glucose cotransporter-2 inhibitor class has been shown to have renal protective effects. However, the magnitude of empagliflozin’s reno-protective properties are over and above that expected from its glucose lowering effects and most likely largely result from mechanisms involving alterations in intra-renal haemodynamics. Liraglutide and semaglutide, both injectable glucose lowering agents which are analogues of human glucagon like peptide-1 have also been shown to reduce progression to macroalbuminuria through mechanisms that remain to be fully elucidated. Here we review the evidence from observational and interventional studies that link good glucose control with improved renal outcomes. We also briefly review the potential reno-protective effects of newer glucose lowering agents.

The association between dietetic consultation and time to dialysis for patients attending a pre‐dialysis clinic: A retrospective cohort study

“…In larger observational studies, diabetes has also been found as a predictor of progression to CKD Stage 5. 29 Thus, in the wider NSW CKD population that has lower rates of diabetes, DC may potentially delay TTD further compared to the results obtained in this study. Based on the study results, a post-analysis sample size calculation found the study to be adequately powered.…”

“…In this study, diabetes was found to be negatively associated with TTD (HR 1.81), with these patients commencing dialysis quicker than those without diabetes. In larger observational studies, diabetes has also been found as a predictor of progression to CKD Stage 5 . Thus, in the wider NSW CKD population that has lower rates of diabetes, DC may potentially delay TTD further compared to the results obtained in this study.…”

Clinical Factors and Anticoagulation Level That Determine the Sudden Loss of Kidney Function in Patients Long-Taking Warfarin (A 5-Year Prospective, Observational Study)

“…Среди них процент больных, имевших и не имевших диагноз СД (вне зави-симости от типа терапии), был сопоставим в группах с физиологической и быстрой потерей почечной функции. Надо отметить, что, несмотря на прямую зависимость раз-вития и прогрессирования ХБП от степени компенсации СД, четкая связь выявляется при уровне гликированного гемоглобина >7 % [40][41][42]. Среди участников нашего исследо-вания с установленным диагнозом СД были больные, у которых гликемия была компенси-рована на протяжении всего периода наблю-дения, в т. ч. и на фоне соблюдения диеты, без гипогликемической терапии.…”

“…Негативное влияние протеинурии на ухуд-шение функции почек подтверждено резуль-татами многочисленных исследований и в настоящее время не подвергается сомнению [40,[42][43][44][45]. Так, по данным [46], для пациен-тов с СД, имеющих протеинурию, средняя динамика СКФ за 4 года наблюдения соста-вила -8,42 мл / мин, что было вдвое больше по сравнению с пациентами без протеинурии.…”

The privileged position of glp-1 in diabetic nephropathy

“…[8][9][10][11][12] Diabetic kidney disease occurs in patients with T2DM as a consequence of reduced kidney function, triggered by hypertensive nephrosclerosis and unresolved acute renal failure as the main culminating reasons. [13][14][15][16][17][18][19] Diabetic nephropathy is a diagnosis that refers to specific pathologic structural and functional changes seen in kidneys of patients with T2DM. These changes result in a clinical presentation that is characterized by proteinuria, hypertension, and progressive reductions in kidney function.…”