Diabetic Nephropathy – Pathophysiology: An Overview
Saxena Tarun, Khichi Garima, Saxena Ashutosh, Goyal Ramakant, Salem Nitasha
Archives of Clinical Nephrology
Diabetic nephropathy (DN) is one of the commonest etiologies for ESRD. Various studies suggest that diabetic nephropathy occurs due to the accumulation of advanced glycosylated end products (AGEs), the activation of isoforms of protein C kinase, etc. Correlation of renal arterial fl ow resistance, GFR, and progression towards ESRD in DN is not well narrated in literature. Therefore, the main object of the study was to assess renal arterial fl ow resistance in patients with DN and to compare it
... ith patients having non-evident diabetic nephropathy. Methods: This is a case control study done in a retrospective manner in the central part of Rajasthan, India, based upon data collection of admitted patients. Arbitrarily, a record of 40 cases (all males) consisting of poorly controlled diabetic cases (Hba1C >10 %) without nephropathy (n=20, group A) was compared with records of diabetic cases with nephropathy (n=20, group B). Group B had been further subdivided according to CKD (chronic kidney disease) staging. Data were examined for vital parameters, Serum creatinine, e-GFR, R.I. (resistive index) in renal arterial Doppler, urine albumin. Results: Group A and group B were characteristically the same. In group B 7 cases had CKD 1(B1), 2 cases had CKD 2 (B2), 4 cases had CKD 3 (B3) and 7 cases had CKD 5(B5) stage. In group B there was a progressive rise in R.I. index parallel to decline in GFR, rise in albuminuria from B1 to B5 stage (p<0.001). These parameters were normal in group A. Conclusion: It is concluded that DN begins from an increase in resistance to fl ow in renal arteries primarily resulting from resistance in afferent arterioles due to the reduction in size. This reduction may be because of increased ACE/ basal sympathetic activity at the beginning. Later on, there is a further increase in resistance due to progressive deposition of AGE end products in afferent arterioles further reducing the size and hydrostatic pressure at the afferent arteriolar end, resulting in a progressive decrease in GFR. Simultaneously hypo-perfusion of kidney tissue activates the renin-angiotensin system further reduces fl ow and progresses the DN.