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Ecase #19-B
Kay English, M.D.
October 22-26, 2001
67 y/o hx type II DM, HTN, Hyperlipidemia, CAD s/p MI, PTCA, prior resolved
nephrotic syndrome presumed secondary to NSAIDs, knee DJD with recent
steroid injection. Patient of provider A seen by provider B c/o chronic
headache, edema and 12# weight gain, some DOE, and BP noted to be 200/116.
Lasix and hydralazine added to lisinopril. CBC, BMP normal (Cr 0.8),
U/A positive for protein. BP next day 166/102 and hydralazine dose doubled.
Seen 5 days later by provider C (also seen in Overlake ER where Toprol
added.) Patient had mistakenly stopped Lisinopril, BP 173/110, Lisinopril
restarted, Lasix increased, and nephrology consult urgently requested.
Medics called clinic next day after patient had called 911 - reported
multiple ER visits. Patient seen urgently in clinic. Wonders if steroid
knee injection has raised her blood pressure since prior prednisone therapy
was associated with high BP. BP 190/110, mild edema and puffy face noted.
Nitropaste and higher dose of Lisinopril ordered (not purchased by patient
secondary to financial constraints). The following day, rather than keep
her clinic appointment, she went to the Swedish ER where CR 2.6 and patient
admitted. She progressed to oliguria, ARF requiring dialysis, and underwent
a kidney biopsy. She was started presumptively on prednisone and biopsy
showed minimal change disease.
- This case is full of red herrings.
- A diabetic with hx of nephrotic syndrome with an apparent recurrence
after stopping ACEI.
- HTN out of control with an assumption of noncompliance.
- Question of steroid injection as precipitant.
- Lack of adequate medical records (clinic change, poor historian, multiple
locations for visits)
- History of vascular disease and possible renal artery stenosis.
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How common is secondary hypertension and what are the causes?
Secondary Hypertension: Detection and Management
for the Primary Care Provider. Wofford MR, King DS, Wyatt SB,
Jones MS
J Clin Hypertens (Greenwich) 2000 Mar;2(2):124-131
Of hypertensive patients, 95% have primary hypertension. Secondary
causes of hypertension include renal disease, such as chronic parenchymal
disease and renovascular hypertension, a number of endocrinopathies
(primary aldosteronism, pheo, thyroid disease, hypercalcemia) and
miscellaneous causes such as sleep apnea and substance abuse.
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What can be expected with minimal change disease?
Minimal change glomerulopathy of adulthood. Korbet
SM, Schwartz MM, Lewis EJ.
Am J Nephrol 1988;8(4):291-7
Of 80 adult patients, 18% presented with creatinine greater than 1.3
mg/dl. All had nephrotic range proteinuria. Microscopic hematuria
and hypertension were present in 21%. In patients treated with prednisone,
91% had complete remission. 65% of patients initially responding
to prednisone relapsed, 70% within 3 months.
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How likely is it that "resistant" hypertension is due to noncompliance?
Relation between insufficient response to antihypertensive
treatment and poor compliance with treatment: a prospective case-control
study. Nuesch R, Schroeder K, Dieterle T, Martina B, Battegay
E.
BMJ 2001 Jul 21;323(7305)142-6
Of 110 outpatients followed, 49 developed resistant hypertension.
Compliance (taking more than 80% of prescribed medication) was measured.
Non-compliance with treatment was equally prevalent in patients with
treatment resistant hypertension and in treatment responsive patients.
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