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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2013  |  Volume : 24  |  Issue : 1  |  Page : 86-88
Florid diabetic complications in impaired glucose tolerance

1 Department of Nephrology, AIIMS, Delhi, India
2 Department of Neurology, AIIMS, Delhi, India
3 Department of Pathology, AIIMS, Delhi, India

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Date of Web Publication22-Jan-2013


We report a 56-year-old gentleman who had a history of impaired fasting glucose 4 years earlier but spontaneously reverted to normoglycemia. He subsequently presented with impaired glucose tolerance and proteinuria. Detailed evaluation revealed florid complications of diabetes, including nodular glomerulosclerosis of the kidney. Such complications in pre-diabetes have rarely been reported. We need to search for them early to prevent further morbidity.

How to cite this article:
Bhatt AP, Gupta A, Vibha D, Sharma A, Mahajan S. Florid diabetic complications in impaired glucose tolerance. Saudi J Kidney Dis Transpl 2013;24:86-8

How to cite this URL:
Bhatt AP, Gupta A, Vibha D, Sharma A, Mahajan S. Florid diabetic complications in impaired glucose tolerance. Saudi J Kidney Dis Transpl [serial online] 2013 [cited 2022 Jan 21];24:86-8. Available from: https://www.sjkdt.org/text.asp?2013/24/1/86/106251

   Case Report Top

A 56-year-old non-smoker, non-hypertensive gentleman was referred to the renal clinic with complaints of generalized fatigue and weakness. He was diagnosed to have impaired fasting glucose (IFG) four years back (fasting plasma glucose - 112 mg/dL). Subsequent fasting plasma glucose levels were normal on regular intervals and diabetes was ruled out by a 2-h oral glucose tolerance test and two glycated hemoglobin (HbA1c) measurements done at that time. He denied any dietary, life-style or pharmacological intervention. There was no family history of diabetes.

On examination, there was pallor with mild bilateral pitting edema. His blood pressure was 120/76 mmHg. His waist circumference was 96 cm and the waist-hip ratio was 0.87, with a body mass index of 22 kg/m 2 .

Investigations revealed hemoglobin of 11.9 g/dL, normocytic normochromic anemia, leukocyte count of 6600/mm 3 , blood urea of 54 mg/dL, serum creatinine of 1.2 mg/dL, serum total protein of 7.5 g/dL, albumin of 3.8 g/dL, total cholesterol of 135 mg/dL, high-density lipoprotein of 48 mg/dL and triglycerides of 148 mg/dL. His fasting and post-prandial plasma glucose levels were 88 and 164 mg/dL, respectively. HbA1c was 5.8%. Urine examination revealed proteinuria 3+, sugar nil and bland sediments. Twenty-four hour proteinuria was 2.4 gm.

The thyroid stimulating hormone level was 4.06 μIU/mL and the B 12 level was 178 pg/ mL, and he had a negative M band on serum and urine electrophoresis. Serum iron studies were normal. Ultrasound of the abdomen showed normal-sized kidneys with preserved cortico-medullary differentiation. He was sero-negative for hepatitis B surface antigen as well as anti-hepatitis C virus and human immunodeficiency virus antibodies. Antinuclear anti-bodies and complement levels were normal.

Fundoscopy showed changes suggestive of non-proliferative diabetic retinopathy and nerve conduction studies revealed symmetric sensory motor neuropathy.

Renal biopsy showed classical nodular glomerulosclerosis. Stains for amyloid and immunoflourescene for light chains were negative.

   Discussion Top

Our case describes the florid complications of diabetes mellitus in a patient with impaired glucose tolerance (IGT), although presently non-diabetic. Non-diabetics with IFG/IGT often have complications normally associated with diabetes. [1] Microvascular and macro-vascular complications of hyperglycemia often predate the diagnosis of diabetes. Greater prevalence of retinopathy and nephropathy has been associated with increasing hyperglycemia below the threshold for diagnosis of diabetes. [2]

The relationship between glycemic control and occurrence of diabetic complications remains unclear. Epidemiological studies reveal that approximately 25% of diabetic individuals do not develop complications, irrespective of the degree of glycemic control. Studies of genetic factors, including HLA type, capillary basement membrane thickness, genetic predisposition to hypertension and familial clustering of diabetic complications, suggest that there is a genetic component to developing the complications of diabetes. On the other hand, clinical trials have demonstrated that progression of early, mild background retinopathy, microalbuminuria and parameters of nervous system function are stabilized with improved glycemic control. The degree of glycemic control required to have an impact on diabetic complications is unknown. [3] Further investigation is needed to address the probable inter-relationship of genetic factors and glycemic control on the development of diabetic complications.

Two large studies have suggested that significant differences in HbA1c concentration might not confer substantial benefits to macro-vascular events. [4],[5] A case report has highlighted the development of Charcot's arthropathy in a patient 11 years after undergoing kidney and pancreas transplantation and having normal allograft function. [6] Although it is clear that genetic factors modulate the risk for developing diabetic nephropathy (DN), and that some patients escape this complication despite decades of poor glycemic control, [7],[8],[9] it is also clear that hyperglycemia is a necessary pre-condition for the development of lesions of DN and renal functional disturbances. Indeed, the two major early glomerular lesions, glomerular basement membrane thickening and mesangial expansion, are not present at diagnosis of diabetes but are found two to five years after the onset of hyperglycemia. [7]

Nodular glomerulosclerosis has also been seen in a patient with the metabolic syndrome without diabetes. [10] Our case did not have most of the criteria for metabolic syndrome. [11]

Our present case defies the notion that DN develops only in well-established diabetes mellitus, as our patient had only IGT with normal HbA1c levels. Our case further suggests that IGT is another new cause of nodular glomerulosclerosis. A high index of suspicion is required to diagnose these diabetic complications early to prevent progressive morbidity even in non-diabetics.

   References Top

1.Nichols GA, Arondekar B, Herman WH. Complications of dysglycemia and medical costs associated with nondiabetic hyperglycemia. Am J Manag Care 2008;14:791-8.   Back to cited text no. 1
2.Gabir MM, Hanson RL, Dabelea D, et al. Plasma glucose and prediction of microvascular disease and mortality: Evaluation of 1997 American Diabetes Association and 1999 World Health Organization criteria for diagnosis of diabetes. Diabetes Care 2000;23:1113-8.  Back to cited text no. 2
3.Strowig S, Raskin P. Glycemic control and diabetic complications. Diabetes Care 1992;15: 1126-40.  Back to cited text no. 3
4.ADVANCE Collaborative Group, Patel A, MacMahon S, et al. Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes. N Engl J Med 2008;358:2560-72.  Back to cited text no. 4
5.Action to Control Cardiovascular Risk in Diabetes Study Group, Gerstein HC, Miller ME, et al. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med 2008;358:2545-59.  Back to cited text no. 5
6.Caldara R, Grispigni C, La Rocca E, et al. Acute charcot's arthropathy despite 11 years of normoglycemia after successful kidney and pancreas transplantation. Diabetes Care 2001; 24:1690.  Back to cited text no. 6
7.Parving HH, Mauer M, Ritz E: Diabetic nephropathy. In: Brenner and Rector's the Kidney, 7 th ed., Brenner BM, ed. Philadelphia: WB Saunders; 2004. p. 1777-818.  Back to cited text no. 7
8.Pirart J. Diabetes mellitus and its degenerative complications: A prospective study of 4,400 patients observed between 1947 and 1973. Diabetes Metab 1977;3:173-82.  Back to cited text no. 8
9.The EURODIAB IDDM Complications Study Group: Microvascular and acute complications in insulin dependent diabetes mellitus: The EURODIAB IDDM Complications Study. Diabetologia 1994;37:278-85.  Back to cited text no. 9
10.Souraty P, Nast CC, Mehrotra R, Barba L, Martina J, Adler SG. Nodular glomerulosclerosis in a patient with metabolic syndrome without diabetes. Nat Clin Pract Nephrol 2008; 4:639-42.  Back to cited text no. 10
11.Alberti KG, Zimmet P, Shaw J. The metabolic syndrome--a new worldwide definition. Lancet 2005;366:1059-62.  Back to cited text no. 11

Correspondence Address:
Ankur Gupta
Department of Nephrology, AIIMS, Delhi - 110 029
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DOI: 10.4103/1319-2442.106251

PMID: 23354198

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