Type 2 Diabetes Mellitus and Hepatitis C are Unlikely Contributors in a Case of Progression of Diabetic Nephropathy to End Stage Renal DiseaseNader S Bahri1*, Raafat Makary2 and Charles Heilig1
- *Corresponding Author:
- Nader S Bahri
Department of Medicine
University of Florida College of Medicine
Jacksonville, 655 W. 8th St. C-290
Jacksonville, FL. 32082, USA
Tel: (904) 244-3092
Fax: (904) 244-2165
E-mail: [email protected]
Received date: March 04, 2014; Accepted date: March 25, 2014; Published date: March 28, 2014
Citation: Bahri NS, Makary R, Heilig C (2014) Type 2 Diabetes Mellitus and Hepatitis C are Unlikely Contributors in a Case of Progression of Diabetic Nephropathy to End Stage Renal Disease. J Diabetes Metab 5:349. doi: 10.4172/2155-6156.1000349
Copyright: © 2014 Bahri NS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Progression of diabetic nephropathy to end stage renal disease can occur in the presence of minimal evidence for type 2 diabetes mellitus, and the recent literature indicates the pathology of diabetic nephropathy arises even in the absence of diabetes, suggesting other contributors like over expression of glucose transporter 1 (GLUT1) may have a similar pathogenesis. Although hepatitis C has been implicated in accelerating declines of renal function in diabetic nephropathy in some cases, evidence of hepatitis C activity cannot be assumed to contribute to the worsening renal function in this case. Here we report a case in a 61 year- old female with minimal elevation of Hemoglobin A1C (HbA1C), seropositivity for hepatitis C and anapparent rapid decline of renal function. The patient presented with a previous elevation of serum creatinine concentration from 1.4 to 4.7 mg/dl over the last 23 months. The patient had been treated with insulin and a recent HbA1C was 6.2%, correlating with an average blood glucose concentration of 130-150 mg/dl. There was no history of diabetic retinopathy or neuropathy. The patient was also taking anangiotensin converting enzyme inhibitor (ACEI) and had controlled hypertension over the 2 years prior to the current hospitalization for hematochezia. The serum creatinine then increased to nearly 6 mg/ dl after admission. Acute kidney injury work-up (super imposed on chronic kidney disease and proteinuria) beyond hematochezia, revealed hepatitis C seropositivity without liver failure. The renal biopsy was typical for established diabetic glomerulosclerosis, without evidence of another disease process. A plot of the reciprocal serum creatinine concentration versus time waned linearly as expected for progression of a single, chronic disease process, despite the appearance of promptly falling renal function on the plot of serum creatinine concentration versus time. We suggest that 1) The appearance of rapid decline ofrenal function was actually the natural progression of chronic diabetic nephropathy; 2) Other contributors rather than mild level of hyperglycemia might associated with development of substantial diabetic nephropathy despite clinical absence of other diabetic tissue complications; 3) A role for hepatitis C -persuaded acceleration of renal disease was not supported in this case.