Pseudo Renal Artery Stenosis (PRAS) Syndrome

Pettinger, William A.; Mitchell, Helen C.; Lee, Hing-Chung; Redman, Helen C.

doi:10.1093/ajh/2.5.349

Cited by 12 publications

(7 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Despite this, the aldosterone secretion from the right adrenal is clearly unsuppressed as the level of aldosterone in the blood taken from around the right adrenal vein is higher than surrounding areas reflecting activation of the renin angiotensin system similar to that seen in unilateral renal artery stenosis. The same results can occur in hypertensive nephrosclerosis and Pettinger et al 21 have used the term pseudo renal artery stenosis to describe this occurrence on a background of hypertensive nephrosclerosis.…”

Section: Discussionmentioning

confidence: 75%

See 1 more Smart Citation

High and non-suppressible plasma renin activity in a patient with aldosterone producing adenoma: pathophysiologic and diagnostic implications

Tai

Eng

1999

J Hum Hypertens

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 75%

“…This can occur in bilateral renal artery stenosis, renal artery stenosis to a single kidney or in those with severe arteriolar disease. 21,22 This patient had a normal captopril renogram, which although is not the gold standard for diagnosis of renal artery stenosis (sensitivity 71-92%, [23][24][25][26], makes this diagnosis unlikely.…”

Section: Discussionmentioning

confidence: 99%

High and non-suppressible plasma renin activity in a patient with aldosterone producing adenoma: pathophysiologic and diagnostic implications

Tai

Eng

1999

J Hum Hypertens

View full text Add to dashboard Cite

show abstract

“…However, renal arteriographic studies were negative, suggesting a syndrome of pseudo renal artery stenosis. 29 We were unable to maintain the mean DBP at proposed levels in both groups of randomized patients after 2 years of good BP control. A similar observation was noted in the Framingham study 30 and other previous studies.…”

Section: Figure 2 P/o/ Of Changes In Quantity Of Antihypertensive Drmentioning

confidence: 85%

Long-term improvement in renal function after short-term strict blood pressure control in hypertensive nephrosclerosis.

et al. 1989

View full text Add to dashboard Cite

Seventy-nine hypertensive nephrosclerosis patients i entered a prospective randomized singleblind study to 1) establish the pattern of decay of renal function in this population and the variability therein and 2) to determine if strict diastolic blood pressure (DBP) control (<80 mm Hg) is more effective than conventional levels (90-95 mm Hg) in conserving renal function. Because of unexpected significant improvement in renal function in patients from both groups, which changed the perspectives on the course of this disease as described herein, this report is being published before completion of the trial. The selection criteria were 1) serum creatinine concentration of 1.6-7.0 mg/dl, 2) glomerular filtration rate of less than 70 ml/min/1.73 m 2 , and 3) absence of diseases (other than hypertension) known to destroy renal function. Renal function was assessed by glomerular filtration rate ([ l2S I]iothalamate clearance) and serum creatinine concentration. Before randomization, DBP was aggressively treated to reduce it to less than 80 mm Hg. Twenty-two subjects (14 in the strict DBP control group and eight in the conventional DBP control group) have been enrolled in the study for 36 months. In contrast to results from previous studies in humans and rats, renal function improved in both patient groups. Thus, irrevocable progression of renal damage after onset of renal failure from high blood pressure does not necessarily occur, and in fact, long-term improvement of renal function resulted from the effects of the study itself. The study design involving the 2-4-month initial period of aggressive DBP control at 80 mm Hg or less followed by control of DBP at less than 90 mm Hg was associated with long-term improvement in renal function. (Hypertension 1989; 13:766-772)

show abstract

“…Thus, hyper-filtration cannot be a major mechanism of destroying kidney function in our patients as suggested by studies in rats (41,42). Minoxidil-induced hyper-filtration may, in fact, explain why hemodialysis may be discontinued in some minoxidil treated patients (44) and should be systematically studied for delay of, or reducing hemodialysis.Discovery of, and understanding of the mechanism of the PRAS Syndrome originally described for minoxidil (6) but subsequently found to be related to severe reversible loss of renal function with other antihypertensive drugs (43,44). (See below)…”

Section: Minoxidil and Saving The Kidneys In Refractory Hypertensionmentioning

confidence: 99%

“…It soon became apparent that far better blood pressure control was needed to “save-the-kidneys” and that more understanding of drug interactions with minoxidil and blood pressure support mechanisms might enable us to achieve better blood pressure control. These interactions extend to fascinating intra-renal mechanisms involving arteriolar hypertrophy, adrenergic receptors, renin-angiotensin and the increasingly recognized cause of reversible renal failure from drugs, the Pseudo Renal Artery Stenosis Syndrome (PRASS) (6). Interestingly, mechanisms of PRASS (to be discussed) were the cause of poor kidney outcomes in the SPRINT trial in the Elderly (2) in the Strict Blood Pressure Control Group (37 events) vs Conventional (13 events) blood pressure control group.…”

Section: Introductionmentioning

confidence: 99%

Hypertension's 3 Dilemmas and 3 Solutions: Pharmacology of the Kidney in Hypertension

Pettinger

2017

Journal of Cardiovascular Pharmacology

Self Cite

View full text Add to dashboard Cite

SUMMARY The Hypertension Community has three conflicting dilemmas, a goal systolic pressure of 120 mmHg or less (The SPRINT Trials), 40% of our 60,000,000 hypertensives still sustain blood pressures above 140/90 mmHg and our most potent antihypertensive drug minoxidil sits on the side-lines, imprisoned in the FDA’s Black Box Designation. My solutions to these dilemmas are: #1. Review of the facts of our most potent antihypertensive drug minoxidil which is essentially free of toxicity, #2. Treatment focus on the fundamental cause of High Blood Pressure, excess dietary sodium and, #3. Prevention of, and/or reversal of, the fundamental mechanism of worsening hypertension, arteriolar hypertrophy. My focus at U.T. Southwestern in Dallas was on extremely severely hypertensive patients with a quantifiable, measurable complication of high blood pressure, progression of nephrosclerotic damage to kidneys. This model had the greatest likelihood of exposing fundamental dis-regulatory mechanisms in hypertensive patients (which it did) and the potential for study of the most relevant antihypertensive drug interactions to achieve optimal blood pressure control (which it did). By maintaining diastolic pressures at 80 mmHg or less in the first NIH supported, long term randomized clinical trial to save the kidneys, the bases for a fundamental blood pressure support mechanism (arteriolar hypertrophy) was illuminated but not fully described until now. This fundamental hypertensinogenic mechanism results from HBP but with time and severity, becomes its own raison d’être. I am now 84 years of age. As a result of a stroke 20 years ago which caused permanent double vision and because of poor blood pressure control with triple therapy I started using minoxidil 5 mg/day along with atenolol and occasional furosemide. Now, along with some dietary salt restriction, my resting blood pressure is 110/65–125/75 and, in spite of > 30 year history of HBP, I have no retinal arteriolar hypertrophy nor arcus senilis (Dr. Schwartz-U. of Miami) which is almost universally present at this age. YES, prevention of, or reversal of, arteriolar hypertrophy should be a central focus of HBP treatment. I simply wish to share a bit of accumulated wisdom that might be of use to others.

show abstract

Pseudo Renal Artery Stenosis (PRAS) Syndrome

Cited by 12 publications

References 0 publications

High and non-suppressible plasma renin activity in a patient with aldosterone producing adenoma: pathophysiologic and diagnostic implications

High and non-suppressible plasma renin activity in a patient with aldosterone producing adenoma: pathophysiologic and diagnostic implications

Long-term improvement in renal function after short-term strict blood pressure control in hypertensive nephrosclerosis.

Hypertension's 3 Dilemmas and 3 Solutions: Pharmacology of the Kidney in Hypertension

Contact Info

Product

Resources

About