Glomerular Structural Changes Versus Albumin Excretion

AER is an important parameter of kidney function in the early stages of nephropathy. In groups of diabetic patients representing a wide range of renal functional impairment significant correlations between glomerulopathy parameters and AER are found [1], and especially the correlation between mesangial expansion and AER has been underlined. This seems to reflect the fact that in the very advanced stages with marked proteinuria mesangial expansion is the dominant feature of the glomerulopathy. Within the range of microalbuminuria the correlation is less tight; however, positive associations have been described [6].

In a study dealing with young normoalbuminuric patients it was found that a subset exhibiting MA at the time of kidney biopsy, had more advanced changes than those patients in the lower normoalbuminuric range [35]. One of our series has been followed for six years after the baseline biopsy. It was revealed that primarily BMT, but also systolic blood pressure and mean 6-year HbA1c contributed to the variation in AER [32]. In conflict with these observations are the reports mentioned above of rather advanced glomerulopathy in cases with low grade microalbuminuria [13,40,41], and even in normoalbuminuria [13,14]. It seems that these somewhat atypical cases with concurrently rather low GFR and AER are predominantly female Type 1 diabetes patients with long duration. In one of the series [41] a high frequency of totally occluded glomeruli was found, and enlargement of the vascular pole area in the open glomeruli was marked [42]. This change may represent a compensation to falling GFR and might influence the level of AER. Diabetic patients with a slow development of nephropathy may exhibit a deviating structural pattern where changes of arterioles and arteries (diabetic macroangiopathy) play an important role.

It is still unclear whether the elevation of blood pressure observed in diabetic nephropathy precedes, develops in parallel with or follows the initial increment of AER [36]. In our prospective study none of the patients had arterial hypertension (>150/90 mmHg), but 24 hours ambulatory blood pressure was not measured [31]. No associations between blood pressure (BP) and glomerular parameters were found, neither at baseline nor at follow-up, but all patients had BP within a fairly narrow range. Thus we cannot speculate upon the role of BP on the initiation of structural lesions. However, recent findings of a Swedish group indicate such an impact [35].

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