Resistant Hypertension in a Dialysis Patient

We present a case of resistant hypertension in a patient with chronic kidney disease (CKD). The patient is a 41-year-old woman who frst presented to her general practitioner almost 20 years ago with peripheral edema and lethargy. She is a lifelong smoker and is obese. Her medical history includes asthma and cervical spondylosis. The reason for referral to the renal team was dipstick-positive proteinuria in the context of low serum albumin. As this case is from Scotland, the majority of results will be reported in SI units. In the context of a 24-hour urinary protein excretion of almost 4 g per 24 hours, hypoalbuminemia of 25 g/L, and clinical evidence of peripheral edema bilaterally to her knees, a diagnosis of nephrotic syndrome was made. The patient's renal function and blood pressure (BP) were normal at this stage. Some of her initial blood results are shown in Table 1. She was not anemic and had a normal white cell count and in?ammatory markers. However, her serum cholesterol and triglycerides were markedly elevated. An immunology screen was negative, as was blood-borne virus serology. Pictures of the patient's renal biopsy, from which she was diagnosed with primary membranous nephropathy, are shown in Figure 1. On the left, there is evidence of glomerular basement thickening; on the right, there is evidence of granular IgG deposition, which is typical for this disease. Membranous nephropathy is a cause of nephrotic syndrome in adults, and over four-ffths of cases are associated with increased levels of phospholipase A2 receptor antibodies. Hypertension is present in up to half of patients with membranous nephropathy at the time of diagnosis. At the time of presentation, 20 years ago, management of membranous nephropathy largely revolved around the treatment of BP and proteinuria. In keeping with this, the patient was commenced on an ACE (angiotensin-converting enzyme) inhibitor and loop diuretic. The patient's BP readings over the frst 12 months are shown in Figure 2A. The patient's BP increased over the frst 6 months after diagnosis, despite a doubling in doses of both the ACE inhibitor and loop diuretic. Although no longer routinely practiced in the United Kingdom, the patient also received an angiotensin receptor blocker (ARB) at 4 months to provide dual blockade of the renin-angiotensin system (RAS). The patient's excretory function remained within the reference range for the frst 6 months (Figure 2B). Despite this treatment, the patient remained heavily proteinuric and hypoalbuminemic (Figure 2C and 2D). In summary, the patient had clinical features of ongoing nephrotic syndrome, with increasing clinic BP readings.