Nodular glomerulosclerosis, which is one of the major pathological findings of diabetic glomerulosclerosis, is a glomerular change characterized by nodular mesangial sclerosis and accentuated glomerular lobularity [9, 10]. Numerous glomerulopathies resemble these morphological alterations when viewed under light microscopy: hypertensive renal disease, light chain deposition induced by a plasma cell dyscrasia, MPGN, and occasionally, amyloidosis . In our case, no etiological linkages between these diseases and the glomerular injuries, except that between hypertension and glomerular damage, were confirmed. Indeed, two glomeruli that were detected on low magnification of renal biopsy specimens obtained from the patient showed collapsed glomerular tufts with wrinkling of the capillary walls and urinary space filled with acellular material, which seemed to be compatible with the features of ischemic glomeruli in hypertensive patients .
Apart from the diagnosis of type 2 diabetes eleven years prior to admission and the results of the ophthalmologic analysis, one may argue that there may have been no clear clinical evidence of diabetes in this patient, since normal values of FBS and HbA1c were noted on admission. However, a transient improvement in glucose metabolism is not exceptional in diabetics with eating disorders . This was the case with this patient, as psychosomatic care for anorexia initiated after the renal biopsy resulted in the gradual deterioration of the patient’s glycemic control, thus necessitating the administration of insulin. The most characteristic immunofluorescent change in diabetic glomerulosclerosis is shown in diffuse linear staining of the glomerular and tubular basement membranes, although this is not necessarily true for all cases with diabetic glomerulopathy and the intensity of such staining varies between individual diabetics. Hyalinosis or exudative lesions often stain brightly with IgM and C3, as demonstrated in our patient [7, 14, 15]. Although the precise process underlying the development of such lesions remains to be delineated, it has been suggested that the development of lesions is associated with endothelial injury and possible hemodynamic alterations . Consequently, it is reasonable to consider that the patient’s low compliance with the overall management of his diabetes and associated complications, such as hypertension, for the long time period prior to his admission may have played a pivotal role in the acceleration of microvascular and endothelial injuries, thus resulting in the various degrees of sclerotic changes compatible with diabetic glomerulosclerosis.
The presence of glomerular electron-dense material and the absence of various serological disorders associated with the development of crescentic glomerulonephritis may indicate the contribution of latent immune-based processes to the development of crescentic glomerular injuries in this patient . However, the hyalinosis or exudative lesions seen in diabetic glomerulosclerosis are also known to be part of an accumulation of homogenous electron dense material . Therefore, it may be difficult to distinguish non-immune hyaline accumulations from granular, electron-dense immune deposits . Nevertheless, the correlations with the clinical, laboratory, and light and immunofluorescence microscopic findings in the current patient do not seem to support the possibility of a superimposed immune-mediated glomerular injury. Instead, the fact that there were varying stages of crescents with exudative lesions compatible with diabetic glomerular injuries shown in the renal biopsy of this patient finally led us to consider that the diabetic glomerular damage could be linked to the formation of crescents, which has been mentioned by a previous study .
In diabetics with overt proteinuria, a diagnosis of diabetic kidney disease can be made in the appropriate clinical setting without pathological confirmation in cases with diabetic retinopathy, a long duration of diabetes, and hypertension . On the other hand, performing a renal biopsy on diabetics has usually been considered when the presence of renal disease other than diabetic kidney disease is suggested by clinical signs, such as the rapid deterioration of renal function, the detection of microscopic or macroscopic hematuria, or the presence of proteinuria in newly diagnosed diabetics without any retinopathy or neuropathy [6, 7]. In this context, the information available concerning the qualitative and quantitative renal morphology of diabetic glomerular injuries seem to involve an intrinsic selection bias [6, 7, 17], and the presence of crescents within the glomeruli damaged by diabetes may therefore sometimes be overlooked especially in the diabetics with potentially advanced diabetic glomerular injuries as demonstrated in the current report. Subsequently, it is not surprising that the etiological linkage between diabetic glomerulosclerosis and the development of crescents has been barely mentioned in previous literature. Nevertheless, such a relationship may not be exceptional [2, 8, 18]. Apparently, the diagnostic and clinical impact of glomerular crescents in patients with diabetic glomerulosclerosis should therefore be evaluated more carefully.