A 60-year-old man comes to the office for follow-up of hypertension and type 2 diabetes mellitus. The patient reports that his blood pressure is usually 110-130/70-85 mm Hg and his fasting glucose 85-95 mg/dL when he measures them at home. He has had no headaches, chest pain, or vision changes but reports increased urinary frequency and nocturia 2-3 times per night over the past 3 months. The patient has had no dysuria but says it takes him longer to finish urinating and he often urinates again within 1-2 hours. His current medications are metformin and lisinopril. Temperature is 37 C (98.6 F), blood pressure is 122/78 mm Hg, and pulse is 68/min. BMI is 23 kg/m². Physical examination shows normal funduscopy findings, normal heart and lung sounds, and a soft and nontender abdomen with a palpable bladder. Rectal examination reveals a smooth, enlarged prostate with no induration. Today's and previous laboratory results are as follows: Urine studies reveal no significant albuminuria, hematuria, or pyuria. Which of the following is the best next step in management of this patient?

Question

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This patient with lower urinary tract symptoms (eg, urinary frequency, nocturia, impaired flow) consistent with benign prostatic hyperplasia (BPH) has a slowly rising creatinine level; urinalysis does not show evidence of albuminuria, hematuria, or pyuria, making intrinsic kidney disease less likely. This presentation raises suspicion for BPH-induced obstructive uropathy (eg, enlarged prostate, palpable bladder), which may result in permanent kidney damage due to blockage of free flow of urine. With obstructive uropathy, a renal ultrasound examination (which should be performed in all patients being evaluated for creatinine elevation or chronic kidney disease) typically reveals hydronephrosis; it can also help assess the extent of kidney injury. If irreversible kidney damage (eg, cortical atrophy on sonogram due to increased pressure) has not yet occurred, management of BPH may improve creatinine levels. In this patient, other possible causes of the rising creatinine level are diabetic and hypertensive nephropathies. However, his hemoglobin A1c and blood pressure measurements are within goal, and he has no evidence of albuminuria or retinopathy. Therefore, his creatinine elevation is not likely caused by diabetes or hypertension, and additional antihypertensive therapy and stricter glycemic control are not indicated (Choices A and E). (Choice B) ACE inhibitors (eg, lisinopril) often cause an elevation in creatinine level, but this elevation would be rapid and would occur within 3-5 days of starting the medication, not over 12-24 months, as seen in this patient. (Choice C) A kidney biopsy would be appropriate to evaluate glomerular hematuria (eg, red cell casts and dysmorphia), nephrotic syndrome (eg, heavy proteinuria), or other acute kidney damage that has not been explained by less invasive testing. It can be considered in this patient if renal ultrasonography is unrevealing. However, skipping an ultrasound examination and performing a biopsy to determine the cause of a rising serum creatinine level in the absence of any additional laboratory abnormalities would not be appropriate. Educational objective: Benign prostatic hyperplasia can cause an obstructive uropathy that presents as a slowly rising creatinine level. A renal ultrasound examination, which should be performed in all patients being evaluated for creatinine elevation or chronic kidney disease, typically reveals hydronephrosis and may help assess the extent and reversibility of kidney injury. References: Approach to managing elevated creatinine. (http://www.ncbi.nlm.nih.gov/pubmed/15171676) Diagnosis and management of non-dialysis chronic kidney disease in ambulatory care: a systematic review of clinical practice guidelines. (http://www.ncbi.nlm.nih.gov/pubmed/30305035)

A 60-Year-Old Man Comes to the Office for Follow-Up of Hypertension