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The data on plasma homocysteine and endogenous insulin in type 2 diabetes mellitus with nephropathy and relationship to body mass index (BMI) is particularly from the Indian subcontinent. A prospective study was carried out in 50 patients of type 2 diabetes mellitus with overt nephropathy (Group A). The results were compared with 25 diabetics without nephropathy (Group B), and 25 age and sex matched healthy controls (Group C). Microenzyme immunoassay and ELISA estimated the plasma homocysteine and insulin, respectively. The mean values of plasma homocysteine were significantly elevated in diabetic nephropathy (21.3+/-7.2 micromol/L) and diabetics without nephropathy (19.4+/-7.1) when compared to healthy control (11.5+/-2.3). The insulin levels and BMI were significantly higher in diabetics as compared to controls. There was no correlation between homocysteine and insulin, homocysteine and BMI, and homocysteine with the degree of renal failure.

e13537 Background: DM is the most common cause of kidney disease in the US, and it may increase the risk of CIN. In vivo studies however suggest that DM not only is not a risk factor for CIN, it may even be protective. This may be explained by dysfunction of organic cation transporter-2, the critical transporter for cisplatin uptake in proximal tubules, in diabetic kidneys. We conducted a case-control study to assess the relationship between DM and CIN. Methods: Records of all patients (pts) who received cisplatin between 1/1/00 and 12/31/06 at Oklahoma City VA Hospital were reviewed. DM was diagnosed if pt had (1) been taking anti-diabetic treatment, or (2) Hgb A1C ≥6.5%, or (3) ≥2 fasting outpatient serum glucose levels 126–199 mg/dl, or (4) ≥1 serum glucose level ≥200 mg/dl at any time, prior to receiving cisplatin. CIN was defined as increase in serum creatinine (SCr) by ≥50% above baseline and higher than upper limit of normal, after exclusion of other causes of elevated SCr, during or within 8 weeks of completion of treatment. Continuous variables are reported by means and ranges, and compared using 2-tailed student's t test. Odds ratio (OR) was calculated to compare risk of CIN between diabetics and non-diabetics. Results: Two hundred pts (2 females, 198 males) received cisplatin in the study period, 50 (25%) were diabetic. Distribution of age (years, diabetics: 62 [46–77]; non-diabetics: 60 [26–79], p = 0.18) and baseline SCr (mg/dl, diabetics: 1.0 [0.4–1.5]; non-diabetics: 1.0 [0.5–1.6], p = 0.86) were similar between the two groups. Overall 15% of pts (30 of 200) developed CIN. Risk of CIN was not different between diabetics (8 of 50 pts, 16%) and non-diabetics (22 of 150 pts, 14.7%); OR = 1.11 (95% CI = 0.46 to 2.67) (Table). Conclusions: DM was not shown to be a risk factor for development of CIN. This finding is consistent with in vivo data obtained through animal diabetic models. [Table: see text] No significant financial relationships to disclose.