Diabetic nephropathy in type 2 diabetes mellitus: risk factors and prevention

A nefropatia diabética (ND) é responsável pelo aumento do número de pacientes em diálise em países em desenvolvimento, e já é a principal causa de terapia de substituição renal nos países desenvolvidos. Neste manuscrito, revisamos os fatores de risco e apontamos estratégias para prevenir esta complicação microvascular nos pacientes com diabete melito tipo 2 (DM2). Alguns fatores de risco genéticos e não-genéticos estão relacionados ao desenvolvimento e à progressão da ND em pacientes DM2. Genes candidatos têm sido analisados, mas ainda há controvérsias sobre os marcadores genéticos da doença. Os fatores de risco não-genéticos reconhecidos são o mau controle glicêmico, pressórico e lipídico. Além disso, tem sido sugerido que a presença de retinopatia diabética e de neuropatia autonômica, do hábito de fumar, da alta ingestão protéica, e de níveis mais altos de albuminúria (mesmo dentro dos níveis normais) estão associados com um risco aumentado de desenvolvimento de ND. Algumas estratégias têm sido investigadas e comprovadas para prevenir ou, no mínimo, postergar o desenvolvimento da ND, tais como o controle da pressão arterial, da glicemia e da dislipidemia. Adicionalmente, os inibidores da ECA e os bloqueadores da angiotensina II apresentam efeitos independentes, não apenas explicado pelo controle da pressão arterial. Outras medidas terapêuticas são a baixa ingestão de proteínas na dieta e a suspensão do fumo.Diabetic nephropathy (DN) is responsible for the increasing number of patients on dialysis in developing countries, and is already the most common cause of renal replacement therapy in the developed ones. In this manuscript, we review the risk factors and point out strategies to prevent this microvascular complication in type 2 diabetic patients (DM2). There are some known genetic and non-genetic risk factors related to the development and progression of DN in DM2 patients. Candidate genes have been analysed, but there are still controversy about the genetic markers of the disease. Recognized non-genetic risk factors are poor glycemic, pressoric and lipidic control. Additionally, it has been suggested that the presence of diabetic retinopathy, autonomic neuropathy, smoking habit, higher protein ingestion, and higher normal levels of albuminuria (even within the normal range) are associated with an increased risk of developing DN. Some strategies have been investigated and proved to prevent or at least to postpone DN, such as to control blood pressure, glycemic levels and dyslipidemia. Furthermore, angiotensinconverting enzyme inhibitors and angiotensin-II blockers have independent effects, not explained by blood pressure control alone. Other therapeutic items are to consume a low protein diet and to quit smoking

Estimated GFR: time for a critical appraisal

Since 1957, over 70 equations based on creatinine and/or cystatin C levels have been developed to estimate glomerular filtration rate (GFR). However, whether these equations accurately reflect renal function is debated. In this Perspectives article, we discuss >70 studies that compared estimated GFR (eGFR) with measured GFR (mGFR), involving similar to 40,000 renal transplant recipients and patients with chronic kidney disease (CKD), type 2 diabetes mellitus or polycystic kidney disease. Their results show that eGFR often differed from mGFR by +/- 30% or more, that eGFR values incorrectly staged CKD in 30-60% of patients, and that eGFR and mGFR gave different rates of GFR decline. Errors were unpredictable, and comparable for equations based on creatinine and/or cystatin C. We argue, therefore, that the persistence of these errors (despite intensive research) suggests that the problem lies with using creatinine and/or cystatin C as markers of renal function, rather than with the mathematical methods used for GFR estimation.Nephrolog