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A 62-year-old man is reviewed in the medical outpatient clinic for long-standing hypertension. He has been poorly adherent to therapy. Blood pressure today is 168/98 mmHg. His serum creatinine has risen from 1.2 mg/dL to 1.9 mg/dL over the past three years (eGFR now 42 mL/min/1.73 m²), urine ACR is 210 mg/g, and the urinary sediment is bland. Renal ultrasound shows bilateral small (8.7 cm), echogenic kidneys with reduced cortical thickness, preserved in symmetry. He does not have diabetes. ECG shows Sokolow-Lyon voltage of 38 mm with lateral T-wave inversion.
Questions
a) What is the most likely diagnosis, and what two features of the presentation distinguish it from chronic glomerulonephritis and diabetic kidney disease? (2 marks)
Most likely diagnosis: benign (chronic) hypertensive nephrosclerosis — long-standing hypertension with slowly progressive CKD, sub-nephrotic proteinuria, a bland urinary sediment, and small symmetric echogenic kidneys on ultrasound (0.5 mark each for the diagnosis and each distinguishing feature). It is distinguished from chronic glomerulonephritis by the absence of haematuria, dysmorphic red cells or red-cell casts (and the small, rather than normal/large, kidneys) and from diabetic kidney disease by the absence of diabetes, the sub-nephrotic (rather than heavier) proteinuria, and the absence of diabetic retinopathy.
b) Outline his chronic pharmacological management, including first-line drug class, agent with dose, and the expected renal response. (4 marks)
- First-line agent: an ACE inhibitor or an ARB (RAAS blockade is uniquely renoprotective — it dilates the efferent arteriole, lowers intraglomerular pressure and interrupts pro-fibrotic angiotensin-II signalling); never combine the two (1 mark). Example: ramipril 2.5–10 mg OD, lisinopril 10–40 mg OD, or losartan 50–100 mg OD (0.5 mark for a correct named agent and dose).
- Add a dihydropyridine CCB (amlodipine 5–10 mg OD) and/or a thiazide-like diuretic (chlorthalidone 12.5–25 mg OD) to reach target BP (0.5 mark).
- BP target under 130/80 (ACC/AHA 2017) or SBP under 120 mmHg standardised if tolerated (KDIGO 2021) (0.5 mark).
- Add an SGLT2 inhibitor — dapagliflozin 10 mg OD or empagliflozin 10 mg OD — on top of RAAS blockade, regardless of diabetes (DAPA-CKD, EMPA-KIDNEY) (1 mark).
- Expected creatinine rise on starting the ACEi/ARB: up to 30 percent is acceptable and haemodynamic; a rise OVER 30 percent (or K over 5.6 mmol/L) should prompt stopping and screening for bilateral renal artery stenosis. Recheck creatinine and potassium at 1–2 weeks (0.5 mark).
c) The patient stops his medication and returns two years later with BP 218/130 mmHg, headache, visual disturbance, papilloedema on fundoscopy and a creatinine of 3.8 mg/dL. A blood film shows schistocytes. Describe the immediate management. (3 marks)
- Recognise this as a hypertensive emergency (malignant-phase hypertension): severe BP + grade III–IV retinopathy (papilloedema) + AKI + microangiopathic haemolytic anaemia (0.5 mark).
- Admit to HDU/ICU with a continuous arterial line and hourly neurology and urine-output monitoring (0.5 mark).
- Controlled IV BP lowering: reduce the mean arterial pressure by NO MORE than 25 percent in the first hour, then to 160/100 mmHg over 2–6 hours, then gradually to normal over 24–48 hours, using a titratable IV agent — labetalol 20–40 mg IV boluses q10 min, or 0.5–2 mg/min infusion; or nicardipine 5–15 mg/h infusion (1 mark).
- Rationale for controlled lowering: chronic hypertension shifts cerebral autoregulation to a higher range, so a precipitous fall causes ischaemic stroke, MI or AKI (0.5 mark).
- Do NOT start an ACEi/ARB in the acute emergency (the acute efferent dilation can precipitate AKI, especially with undiagnosed bilateral renovascular disease); treat pulmonary oedema and encephalopathy; search for an underlying secondary cause (0.5 mark).
d) List two complications of chronic hypertensive nephrosclerosis other than progression to end-stage kidney disease, and state which is the leading cause of death in this population. (1 mark)
Any two of: left ventricular hypertrophy and heart failure (HFpEF/HFrEF), ischaemic heart disease, atrial fibrillation, stroke, aortic dissection, acute kidney injury (acute-on-chronic) (0.5 mark). Cardiovascular disease is the leading cause of death in patients with hypertensive nephrosclerosis — more common than ESKD — which is why cardiovascular risk reduction (statin, smoking cessation, glycaemic control, antiplatelet for secondary prevention) is as important as renoprotection (0.5 mark).
References4ShowHide
- [1]Chen TK, Knicely DH, Grams ME. Chronic Kidney Disease Diagnosis and Management: A Review. JAMA, 2019.PMID 31573641
- [2]Romagnani P, Remuzzi G, Glassock R, et al. Chronic kidney disease. Nature Reviews Disease Primers, 2017.PMID 29168475
- [5]Wright JT Jr, Williamson JD, Whelton PK, et al. A Randomized Trial of Intensive versus Standard Blood-Pressure Control. New England Journal of Medicine, 2015.PMID 26551272
- [9]Heerspink HJL, Stefánsson BV, Correa-Rotter R, et al. Dapagliflozin in Patients with Chronic Kidney Disease. New England Journal of Medicine, 2020.PMID 32970396