Clinical and therapeutic aspects of diabetic nephropathy.
The prognosis of renal survival in both type 1 and type 2 diabetes mellitus is not benign. Several factors characterize the increase in the risk of developing renal damage in diabetic patients, distinguished in diabetes-related factors, genetic factors and other factors.


METHODS
Diagnosis requires standard annual urinalysis and dipstick for albumin. In patients with negative urine dipstick, the routine approach is to evaluate the albumin/creatinine ratio (ACR) in the first voided urine. The degree of renal impairment is assessed by an annual evaluation of the glomerular filtration rate (GFR) by the Cockroft/Gault formula in normoalbuminuric patients. In patients with overt nephropathy this evaluation needs to be more frequent.


METHODS
A thorough therapeutic approach, in both the early and later stages of diabetic nephropathy, is fundamental because of the increased risk of morbidity and mortality. Renal damage (and the natural history of the disease) is approached on three different levels. Primary prevention, in patients with no clinical and biochemical signs of renal damage, is a strict glycemic control by oral antidiabetic agents or insulin, as required, together with the maintenance of blood pressure (BP) levels < 130/85 mmHg, preferably using ACE-inhibitors. Secondary prevention aims to prevent or slow the progresssion from micro- to macroalbuminuria. BP control is the first-line approach, along with a strict glycemic control. At this stage, it is necessary to use other anti-hypertensive agents besides ACE-inhibitors to achieve optimal BP levels of 130/85 mmHg. Tertiary prevention addresses the reduction in the rate of renal failure progression by optimal BP control, a slightly hypoproteic diet and the control of dyslipidemia, in the presence of a (non-fundamental) euglycemic state.
a pharmacological blockade of endothelin and/or sympathetic system, an amelioration of hypoxia by correcting reduced hemoglobin levels, an interference with the formation and accumulation of advanced glycosilation end-products (AGE). Finally, the manipulation of the sex hormone balance, genetic screening for a predisposition to progressive renal dysfunction and, eventually, gene therapy complete the scenario for future approaches to this major complication of diabetic disease.
Strippoli
Giovanni F
GF
Department of Emergency and Organ Transplantation (DETO), Section of Nephrology, University of Bari, Italy.
Di Paolo
Salvatore
S
Cincione
Raffaele
R
Di Palma
Anna M
AM
Teutonico
Annalisa
A
Grandaliano
Giuseppe
G
Schena
Francesco P
FP
Gesualdo
Loreto
L
D000419:Albuminuria / Q000517:prevention & control; D003131:Combined Modality Therapy; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000188:drug therapy; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000188:drug therapy; D003928:Diabetic Nephropathies / Q000175:diagnosis / Q000401:mortality / Q000517:prevention & control* / Q000628:therapy*; D004032:Diet; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000175:diagnosis / Q000188:drug therapy; D007677:Kidney Function Tests; D008019:Life Style; D008297:Male; D009765:Obesity / Q000175:diagnosis / Q000628:therapy; D011322:Primary Prevention / Q000379:methods*; D011379:Prognosis; D006435:Renal Dialysis / Q000379:methods; D018570:Risk Assessment; D012720:Severity of Illness Index; D016019:Survival Analysis; D016896:Treatment Outcome