Diabetic Retinopathy, Nephropathy, and Neuropathy with Normal Glucose Tolerance

Diabetic Retinopathy, Nephropathy, and Neuropathy with Normal Glucose Tolerance I read with interest a recent report of a patient with diabetic nephropathy and retinopathy but no abnormality of glucose tolerance. I describe in this letter a similar patient who was referred to a diabetes clinic a year ago by an ophthalmologist because gross diabetic retinopathy was noted during the eye examination for evaluation of bilateral cataracts. I admitted this 76-yr-old man to a diabetes ward for further evaluation. The only symptoms he related to on inquiry were recurrent edema of the ankles, lightheadedness on awakening in the morning, and lack of sustained penile erection. Past history was remarkable for prostatectomy for cancer 4 yr previously, with no sign of recurrence, and varicose vein stripping in right lower extremity several years previously. History of alcohol abuse and smoking was denied. He also denied previous knowledge of his being diabetic as well as family history of diabetes mellitus. Physical examination revealed an elderly white gentleman in no acute distress. Systemic examination was unremarkable except for ankle edema, orthostasis from 140/90 mm Hg during recumbency to 110/70 mm Hg on standing, with no significant alteration in heart rate and diminished vibration sensation in both lower extremities below both knees. Laboratory profile showed normochromic, normocytic anemia (Hb 10.5 g/dl) and the following blood chemistries: BUN 54 mg/dl, creatinine 4-5 mg/dl, albumin 2.9 g/dl with total protein 5.5 g/dl, and normal serum calcium, phosphorus, uric acid, and liver enzymes. Serum electrolytes showed mild, hyperchloremic hyperkalemic acidosis with chloride 116 meq/ L, HCO3 20 meq/L, and K 5.2 meq/L. Arterial blood gases revealed pH 7.37, PCO2 33%, and PO2 88%, thus confirming mild metabolic acidosis. Throughout hospitalization for 10 days, fasting plasma glucose was < 110 mg/dl and mean fasting blood sugar, 94 ± 2 mg/dl. Similarly, HbA! concentration ranged from 6.0% to 6.9% (normal <8.2% in our laboratory). Several random plasma glucose values, including several 2-h postprandial levels were <160 mg/dl. A glucose tolerance test was not performed because of lack of symptoms of hyperglycemia as well as persistently normal fasting plasma glucose and HbA^ as per the criteria established by the National Diabetes Data Group. Urinalysis revealed 4+ proteinuria. Twenty-four-hour urinary protein was 3.8 g and creatinine clearance was 16 ml/min. The patient was treated with furosemide 40 mg/day and a 60-g protein diet. With this regimen, the patient's edema resolved and acidosis and serum K+ improved toward normalcy. Orthostasis improved, as well, and therefore the patient was discharged from the hospital. Renal biopsy was deferred because of the patient's age since it did not appear to alter the nature of treatment. The etiology of the nephrotic syndrome was presumed to be diabetic in origin because of the presence of diabetic retinopathy and peripheral neuropathy. During the 6 mo after discharge, fasting plasma glucose has remained <110 mg/dl on several visits, despite progression of the patient's uremia with a rise in BUN up to 80 mg/dl and creatinine up to 8 mg/dl. Thus, although it is common to observe the occurrence of microangiopathic complications several years after onset of diabetes and the severity of those complications to correlate with the duration of clinical diabetes,' it may not be unusual for those complications to be present in the absence of clinical diabetes, as illustrated by this patient and the patient in the recent report. Finally, these observerations may question the importance of adequate metabolic control in delaying the onset or retarding the progress of microangiopathic complications in diabetes mellitus.