A 63-year-old man, who was diagnosed with type 2 diabetes mellitus 8 years ago, comes to the office for a follow-up appointment. Over the last 2 weeks, he has noticed mild swelling in his legs, as well as fatigue. He has had no shortness of breath, orthopnea, nausea, vomiting, or diarrhea. Over the past year, the patient was found to have albuminuria on 2 separate visits. Three months ago, blood pressure was 122/78 mm Hg, serum creatinine was 1.2 mg/dL, urine albumin-to-creatinine ratio was 250 mg/g, and hemoglobin A1c was 7.2%. Lisinopril was initiated a year ago and the dose was increased 3 months ago. The patient has had no recent viral illnesses or taken any new medications. Current medications include low-dose aspirin, atorvastatin, lisinopril, and glargine insulin. The patient does not use tobacco, alcohol, or illicit drugs.
Blood pressure is 155/95 mm Hg and pulse is 85/min. Auscultation of the heart and lungs shows no abnormalities. The abdomen is nontender and no costovertebral angle tenderness. The patient has 2+ pitting edema of the bilateral lower extremities.
Laboratory results are as follows:
Hemoglobin A1c is 7.5%. A renal ultrasonogram shows symmetric, normal-sized kidneys with no evidence of hydronephrosis. Which of the following is the next most appropriate step in management of this patient?

Question

A 63-year-old man, who was diagnosed with type 2 diabetes mellitus 8 years ago, comes to the office for a follow-up appointment.  Over the last 2 weeks, he has noticed mild swelling in his legs, as well as fatigue.  He has had no shortness of breath, orthopnea, nausea, vomiting, or diarrhea.  Over the past year, the patient was found to have albuminuria on 2 separate visits.  Three months ago, blood pressure was 122/78 mm Hg, serum creatinine was 1.2 mg/dL, urine albumin-to-creatinine ratio was 250 mg/g, and hemoglobin A1c was 7.2%.  Lisinopril was initiated a year ago and the dose was increased 3 months ago.  The patient has had no recent viral illnesses or taken any new medications.  Current medications include low-dose aspirin, atorvastatin, lisinopril, and glargine insulin.  The patient does not use tobacco, alcohol, or illicit drugs.
Blood pressure is 155/95 mm Hg and pulse is 85/min.  Auscultation of the heart and lungs shows no abnormalities.  The abdomen is nontender and no costovertebral angle tenderness.  The patient has 2+ pitting edema of the bilateral lower extremities.
Laboratory results are as follows:
 Hemoglobin A1c is 7.5%.  A renal ultrasonogram shows symmetric, normal-sized kidneys with no evidence of hydronephrosis.  Which of the following is the next most appropriate step in management of this patient?

Quizplus · Accepted Answer

Diabetic nephropathy and nondiabetic glomerular diseases (eg, glomerulonephritis) can have similar presentations; however, these conditions must be differentiated from each other as their clinical course and treatment differs: Diabetic nephropathy commonly presents with albuminuria and a bland urinalysis, although hematuria and red blood cell casts can sometimes be seen. Diabetic nephropathy is slowly progressive; it typically takes years from the onset of albuminuria to the development of overt renal failure.Glomerulonephritis commonly presents with active urinary sediment (eg, hematuria, pyuria, red blood cell casts) and hypertension. It is typically rapidly progressive and may require specific anti-inflammatory therapy (eg, corticosteroids, immunosuppressants) to prevent development of end-stage renal disease. Diabetic nephropathy commonly presents with albuminuria and a bland urinalysis, although hematuria and red blood cell casts can sometimes be seen. Diabetic nephropathy is slowly progressive; it typically takes years from the onset of albuminuria to the development of overt renal failure. Diabetic nephropathy commonly presents with albuminuria and a bland urinalysis, although hematuria and red blood cell casts can sometimes be seen. Diabetic nephropathy is slowly progressive; it typically takes years from the onset of albuminuria to the development of overt renal failure. Glomerulonephritis commonly presents with active urinary sediment (eg, hematuria, pyuria, red blood cell casts) and hypertension. It is typically rapidly progressive and may require specific anti-inflammatory therapy (eg, corticosteroids, immunosuppressants) to prevent development of end-stage renal disease. Glomerulonephritis commonly presents with active urinary sediment (eg, hematuria, pyuria, red blood cell casts) and hypertension. It is typically rapidly progressive and may require specific anti-inflammatory therapy (eg, corticosteroids, immunosuppressants) to prevent development of end-stage renal disease. This patient with diabetes mellitus and a history of albuminuria now has a rapid decline in GFR, development of progressive hypertension despite an increased ACE inhibitor dose, a significant increase in proteinuria (3+ corresponds to a urine albumin-to-creatinine ratio >1,000 mg/g) with accompanying edema, and active urinary sediment; this constellation of findings makes glomerulonephritis likely. Renal biopsy is required to confirm the diagnosis. Nondiabetic glomerular diseases should also be considered in patients with marked renal dysfunction (>30% decrease in glomerular filtration rate [GFR]) after ACE inhibitor initiation or with symptoms of systemic disease. (Choice A) Excellent glucose control can cause a regression in diabetic nephropathy; however, this patient already has relatively good glycemic control (hemoglobin A1c of 7.5%), and his rapidly progressive course makes diabetic nephropathy less likely. (Choice B) Changing from an ACE inhibitor (eg, lisinopril) to an angiotensin receptor blocker (eg, valsartan) is recommended for patients who experience ACE-associated cough; it would not improve serum creatinine. (Choices C and E) Increased serum creatinine is common in patients on ACE inhibitor therapy, but the increase is usually modest (<30% decline in GFR). A more marked decline may occur with bilateral renal artery stenosis. However, renal artery stenosis should not cause active urinary sediment, and this patient tolerated an ACE inhibitor for a year without kidney injury. It is unlikely that the increased dose would cause such a rapid reduction in GFR. Educational objective: Diabetic nephropathy typically presents with bland urinalysis and albuminuria; however, hematuria and red blood cell casts may occur. Progression is slow (years); therefore, nondiabetic glomerular diseases should be considered in patients with rapidly progressive disease, unexpected reductions in glomerular filtration rates (>30%) after ACE inhibitor initiation, active urinary sediment, or symptoms of other systemic diseases. __________

A 63-Year-Old Man, Who Was Diagnosed with Type 2 Diabetes