A 65-Year-Old Man With Hypertension and Proteinuria

Pradeep Arora, MD; Karen Convay, NP

Disclosures

October 12, 2015

Discussion

The patient in this case has chronic kidney disease (CKD), as evidenced by a decreased eGFR for more than 3 months. The etiologies of CKD include diabetic kidney disease, hypertensive nephrosclerosis, glomerulonephritis, polycystic kidney disease, unrecovered AKI, chronic interstitial nephritis, and ischemic nephropathy. Unrecovered AKI and ischemic nephropathy are becoming important causes of CKD.

In this patient, the differential diagnoses of CKD included diabetic kidney disease; his history of long-standing diabetes mellitus along with nephrotic-range proteinuria, even in the absence of retinopathy, makes diabetic kidney disease an important consideration. Unrecovered AKI after treatment of infective endocarditis and hepatitis C-related glomerulonephritis are also among the differential diagnoses of CKD in this patient. An immunologic workup was performed and was negative.

Ideally, a kidney biopsy should be performed to confirm the diagnosis; however, the patient in this case declined. A tentative diagnosis of diabetic kidney disease was made, because the presence of diabetic retinopathy favored this diagnosis.

Once CKD is diagnosed and its etiology is determined, investigation for an acute reversible factor is paramount; these factors include volume depletion, accelerated hypertension, rapid lowering of blood pressure, treatment with nephrotoxic medications, and urinary tract obstruction. In this patient, the blood pressure was uncontrolled, but no clinically evident acute factor for deterioration was identified.

After diagnosis, identification of the etiology, and exploration for an acute reversible factor, the progression of CKD needs to be assessed. Most patients with CKD show progression of kidney disease. This may be largely due to secondary factors that are unrelated to the initial disease. These include systemic and intraglomerular hypertension, glomerular hypertrophy, intrarenal precipitation of calcium phosphate, hyperlipidemia, and altered prostanoid metabolism. The major histologic manifestation of these secondary causes of renal injury is focal segmental glomerulosclerosis.

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