[Renal damage in type 2 diabetes]
- PMID: 12647281
[Renal damage in type 2 diabetes]
Abstract
Renal involvement in patients with type 2 diabetes will (probably) be one of the most important clinical problems for nephrologists to face during the next few years. Unlike type 1 diabetes, in type 2 diabetes the renal damage has not yet been well defined at both clinical and pathological levels. Pathological examination of renal biopsies has displayed different patterns of renal damage including diabetic glomerulosclerosis (Class 1), mostly chronic vascular changes (Class 2) and superimposed glomerular diseases (Class 3a) or unrelated to diabetic glomerulosclerosis (Class 3b). Despite the large number of papers published in this field, the actual prevalence and outcome of the different histological classes still remain to be established. Reported discrepancies are most likely caused by ethnic and geographic factors. However, as documented by a recent study carried out on a large number of patients, the prevalence of histological patterns is also greatly influenced by the policy for performing renal biopsies adopted at the various nephrological centers. Although the natural history of type 2 glomerulosclerosis (Class 1) still remains to be defined, those patients with clinical nephropathy and impairment of renal function have very poor outcome with a high rate of mortality and progression to uremia. Moreover, when diabetic glomerulosclerosis is complicated by superimposed glomerular diseases (Class 3a) the prognosis is much worse. On the contrary, when glomerular diseases are not associated with glomerulosclerosis lesions (Class 3b) the prognosis is markedly better. During the last ten years controlled studies have shown that the outcome in type 1 diabetic nephropathy has improved as a result of the use of drugs inhibiting the renin-angiotensin system. Although it is likely that this type of drug might also favourably influence the outcome of type 2 diabetic nephropathy, any conclusive evidence is presently still lacking.
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