PS-R04-9: REVERSIBLE ACUTE RENAL INJURY IN MALIGNANT HYPERTENSION DURING LONG-TERM FOLLOW-UP
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Background: Malignant hypertension is a disease characterized by severe hypertension and multi-organ damage. Although mortality and renal prognosis have improved with antihypertensive therapy, progression to end-stage renal disease remains a leading cause of morbidity and mortality. Case presentation: A 37-year-old man with a history of untreated hypertension and proteinuria was referred to our hospital with complaints of right paralysis. He was diagnosed with left putaminal hemorrhage and treated with conservative blood pressure reduction management. He was also complicated with severe hypertension (blood pressure 231/146 mmHg), acute renal failure (BUN 39 mg/dl, serum creatinine 4.01 mg/dl, urinary protein 2.848 g/gCre), and heart failure with preserved ejection fraction (BNP 373 pg/ml). Initial evaluation demonstrated hyperreninemia (32.6 ng/ml/hr) with hyperaldosteronism (125 pg/ml), consistent with malignant hypertension. Secondary hypertension, such as primary aldosteronism, Cushing's syndrome, pheochromocytoma, and renal artery stenosis was excluded by further examination. His renal size was mildly atrophic assessed by CT scan, suggesting a history of chronic kidney disease. At first, we gradually decreased blood pressure with antihypertensive agents except for angiotensin-converting enzyme (ACE) inhibitor and angiotensin receptor blockade (ARB) so as not to induce exacerbation of renal function via glomerular ischemia. In the long-term, he was treated to achieve a tight blood pressure control to systolic blood pressure of 100–110 mmHg with the combination of ACE inhibitor, calcium channel blocker, and alpha/beta blocker. Although his clinical course showed gradual recovery of renal function, our conservative approach successfully induced renal function recovery over six months of follow-up (BUN 27 mg/dl, serum creatinine 2.26 mg/dl, urinary protein 0.154 g/gCre). Discussion: Previous reports suggest that malignant nephrosclerosis may recover slowly if the blood pressure is tightly controlled during the follow-up. From a long-term perspective, tight blood pressure control with inhibition of the renin-angiotensin-aldosterone system, which is a critical factor of the pathogenesis in malignant hypertension, may provide beneficial effects on the renal prognosis of malignant hypertension.Keywords:
Renovascular Hypertension
The overall prevalence of renovascular hypertension is low, accounting for only 5% of all hypertensive patients in the general population and between 10 and 45% of those in a hypertension subspecialty practice (1,2). Thus, routine screening is neither cost effective nor efficient; screening should be performed only on those patients with historical and physical findings, which raise suspicion for renovascular disease. Additionally, renal artery stenosis in not synonymous with renovascular hypertension, as illustrated by multiple autopsy series (3–5). In a series of 154 randomly selected autopsies, Schwartz and White showed a strong association between renal artery stenosis and advancing age but no correlation between stenosis and increased diastolic blood pressure (DBP) (4). Similarly, Holley and coworkers (3) found that 49% of normotensive and 77% of hypertensive patients have evidence of moderate to severe renal artery stenosis.
Renovascular Hypertension
Secondary hypertension
Subspecialty
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Renovascular hypertension (RVH) is a secondary hypertension that is caused by the renal artery stenosis and is curable by surgical treatment. Sensitivity and specificity of CRS for RVH have been reported to be in exceed of 90%. Captopril-enhanced renal scintigraphy (CRS) has become an important tool in the diagnosis of RVH. In addition, the recent reports indicate that CRS is a promising means of prognostic evaluation in re-vascularization of RVH. In this report, pathophysiological considerations, methods, diagnostic criteria, diagnostic efficacy and consideration for clinical application are reviewed.
Renovascular Hypertension
Captopril
Secondary hypertension
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Renovascular Hypertension
Renal Artery Obstruction
Secondary hypertension
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Radionuclide renal scintigraphies were performed in a 24-year-old man with right renal artery branch stenosis. Captopril enhanced renal scintigraphy revealed no abnormal finding in the right kidney. But, renal scintigraphy showed regional cortical photon deficient area corresponding to the area supplied by the stenotic branch artery. The defect size increased in captopril enhanced renal scintigrphy and nearly disappeared after successful transluminal renal angioplasty. This case suggests that the captopril enhanced renal scintigraphy may be a useful method in the evaluation of renovascular hypertension, especially due to branch renal srtery stenosis.
Renovascular Hypertension
Captopril
Right Renal Artery
Renal Artery Obstruction
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Renovascular Hypertension
Secondary hypertension
Renal Artery Obstruction
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107 patients have been operated upon for atherosclerotic or fibromuscular renal artery stenosis from January 1, 1962 through December 31, 1973. At the time of last follow-up, or at 1 year 67% of patients with atherosclerotic renal artery stenosis, and 79% of patients with fibromuscular renal artery disease were considered to be improved. More recently 50 patients have been treated by surgery (24 patients) or with antihypertensive drugs. 70% (17 of 24) surgically treated patients and 61% (16 of 26) medically treated patients were improved after an average of approximately 1.5 years follow-up.
Renovascular Hypertension
Renal Artery Obstruction
Fibromuscular Dysplasia
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During a 10 year period 58 patients with renovascular hypertension due to renal artery stenosis were treated surgically. A retrospective analysis of the results was carried out. No perioperative mortalities occurred. Ten percent of the patients developed hypertension again after an average of 27 months. At follow-up (median 65 months), 85% of the patients had normal blood pressure or either no, modest or considerably reduced anti-hypertensive medication. It is concluded that surgical treatment of renovascular hypertension is a safe and effective procedure.
Renovascular Hypertension
Renal Artery Obstruction
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Detection of a renal artery stenosis (RAS) as a cause of arterial hypertension is of great practical importance because dilatation of the stenosis frequently results in an improvement or cure of the hypertension. In recent years, a number of screening procedures aimed at diagnosing renovascular hypertension have been developed, e.g., duplex sonography of the renal arteries, determination of plasma renin activity, or renal scintigraphy following administration of captopril. The possibilities and limitations of these screening procedures are described here. The best method for detecting renal artery stenosis is angiography, which can now be performed on an outpatient basis, using thin catheters.
Renovascular Hypertension
Renal Artery Obstruction
Captopril
Plasma renin activity
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Following the injection of water-soluble contrast medium and urea an increase in area of the renal shadow of less than 5 per cent was demonstrated on the affected side in 14 cases of hypertension due to renal artery stenosis (verified by operation and post-operative follow-up). On the contra-lateral side an increase of 7–20 per cent was observed in all cases. In 20 patients with hypertension and renal artery stenosis, but no surgical intervention, the same phenomenon was observed in six cases. In these patients other diagnostic criteria were also indicative of reno-vascular hypertension. It is concluded that the increase in renal size which is normally seen following the injection of water-soluble contrast medium and certain drugs is impaired in cases of significant renal artery stenosis. The underlying mechanism (also discussed in a previous paper) may in itself be responsible for the hypertension. If this be the case, measurements of variations in renal size during washout urograms would be very valuable in the diagnosis of renovascular hypertension.
Renovascular Hypertension
Renal Artery Obstruction
Washout
Right Renal Artery
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Renovascular Hypertension
Constriction
Pathophysiology of hypertension
Pathophysiology
Renal Artery Obstruction
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