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160 NODULAR GLOMERULOSCLEROSIS UNMASKING IMPAIRED FASTING GLUCOSE.
  1. A. Sequeira1,
  2. N. Koshy1,
  3. P. Isaac1,
  4. P. Meka1,
  5. B. Sachdeva1,
  6. J. Blondin1
  1. 1Louisiana State University Health Sciences Center, Shreveport, LA.

Abstract

Introduction Nodular glomerulosclerosis is a recognized complication of diabetes. We report a case with a similar pathology in a patient with impaired fasting glucose.

Case A 46-year-old female with a 5-year history of hypertension was admitted with a 1-month history of gradually worsening pedal edema and weight gain. She had a family history of diabetes but denied symptoms of hyperglycemia. On physical examination, she had a blood pressure of 180/90 mm Hg with pitting pedal edema. Her BMI was 35. Pertinent laboratory data: hemoglobin 8.5 g/dL, serum albumin 1.9 g/dL, BUN 14 mg/dL, creatinine 1.3 mg/dL (MDRD GFR 46 mL/min), cholesterol 182 mg/dL, triglycerides 128 mg/dL, LDL 105 mg/dL, and HDL 51 mg/dL. Her fasting glucose readings ranged from 90 to 112 mg/dL, suggesting impaired fasting glucose. Glycosylated hemoglobin was 6.4%. Urinalysis was remarkable for proteinuria (quantified at 14 g) and glucosuria. Normal-sized kidneys were noted on ultrasonography. A kidney biopsy performed to ascertain the etiology of the proteinuria revealed nodular glomerulosclerosis with arterial hyalinosis. Secondary causes of nodular glomerulosclerosis such as multiple myeloma, light-chain deposition disease, and amyloidosis were ruled out. Fundoscopy revealed features suggestive of diabetic retinopathy.

Discussion Rare accounts of nodular glomerulosclerosis occurring in the absence of overt diabetes have been reported. Patients with such a presentation are predominantly middle-aged, hypertensive men who have a history of obesity. A family history of diabetes is often present. Additionally, renal failure at presentation and retinal changes consistent with diabetic retinopathy have also been noted. This has led to speculation that factors other than hyperglycemia may be responsible for end-organ damage. These include genetic susceptibility, hypertension, and smoking. A number of other reasons may explain the apparent lack of hyperglycemia. Delayed insulin catabolism and poor appetite, which often accompanies renal failure, may mask the hyperglycemic state, whereas insulin resistance decreases as weight is lost. If hypertension coexists, it contributes to the acceleration of the underlying nephropathy.

Conclusion Impaired fasting glucose should be considered as an etiology of nodular glomerulosclerosis, especially in individuals with the above characteristics

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