Clinical and cellular markers of diabetic nephropathy.

initiated at that time because the patient was reluctant to start this treatment in the event that she became pregnant. When the patient was evaluated in our office at the age of 21, we did not elicit a family history of renal disease. Her social history was negative for tobacco, alcohol, and recreational drug use. Her medications included insulin, 10–15 units of NPH and 20–25 units of regular insulin in the morning and 8 units of NPH insulin and 10–15 units of regular insulin before dinner. Her blood pressure was 121/68 mm Hg in the seated position and 120/68 mm Hg in the standing position. Her heart rate was 70 beats/min and 75 beats/min in the seated and standing positions, respectively. Her fundi showed mild proliferative changes. No hemorrhages were seen. Her abdomen was soft, and no masses were felt. Her pulses in the lower extremities were 2 bilaterally. At that time the BUN and serum creatinine were 15 mg/dL CASE PRESENTATION and 1.1 mg/dL, respectively. Her blood glucose was 160 mg/dL A 21-year-old white woman was referred for evaluation of and HbA1c was 9.9%. Her serum electrolytes were: sodium, microalbuminuria. She stated that at the age of 11 a diagnosis 138 mmol/L; potassium, 4.1 mmol/L; calcium, 8.5 mg/dL (2.2 of diabetes was made because of polyuria and polydipsia, and mmol/L); and chloride, 103 mmol/L. Total cholesterol was 190 she was begun on a regimen of insulin. Two months later, mg/dL; fasting triglycerides, 140 mg/dL. Dipstick urinalysis was she was hospitalized with an episode of diabetic ketoacidosis. negative for protein; a 24-hour urine collection indicated a Review of her medical records revealed no further episodes of glomerular filtration rate (GFR) (creatinine clearance) of 115 ketoacidosis. During her adolescence, compliance with insulin mL/min, and an albumin excretion rate of 250 mg/24 hours therapy was problematic despite frequent counseling and ad(Fig. 1). justment of her insulin dose. On one evaluation at the age of 18, A 24-hour ambulatory blood pressure monitoring was done her blood glucose was 200 mg/dL, and her plasma electrolytes, at this time (Fig. 2). Mean systolic and diastolic blood pressures blood urea nitrogen (BUN), and serum creatinine were in the were 122 mm Hg and 70 mm Hg, respectively. Mean systolic normal range. Her blood pressure while seated was 122/70 and diastolic blood pressures during the sleep period were 121 mm Hg, and her heart rate was 86 beats/min. A urinalysis was mm Hg and 69 mm Hg, respectively. Mean systolic and diastolic normal with a negative dipstick for protein; a 24-hour urine blood pressures during daily activities were 123 mm Hg and collection revealed a creatinine clearance of 125 mL/min, and a 71 mm Hg, respectively. At that time, renoprotective therapy urine albumin excretion (UAE) rate of 20 mg/24 hours (normal, with an ACE inhibitor, captopril at a dose of 25 mg orally twice 0–30 mg/24 hours) (Fig. 1). daily, was initiated. She also was referred to the Endocrinology Over the following years, her glycemic control was poor, as revealed by glycosylated hemoglobin (HbA1c) ranging between Clinic to optimize her glycemic control. 9% and 11%. When she was 20 years old, her pediatrician found that the urine albumin excretion had increased to 200 DISCUSSION mg/24 hours and referred the patient to us for nephrologic evaluation. Therapy with an angiotensin-converting enzyme Dr. Daniel Batlle (Chief, Division of Nephrology; (ACE) inhibitor was considered by her pediatrician but not and Professor of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA): Diabetic nephropathy is a microvascular complication of both The Nephrology Forum is funded in part by grants from Amgen, Incorporated; Merck & Co., Incorporated; Dialysis Clinic, Incorpotype 1 and type 2 diabetes, which is associated with endrated; and Bristol-Myers Squibb Company. stage renal disease (ESRD) and premature death from cardiovascular disease [1, 2]. The development of clinical