This leads to renin secretion that causes the angiotensinogen conversion to angiotensin I. Angiotensin I then proceeds to the lung where it is converted to angiotensin II via angiotensin converting enzyme (ACE).In most people fibromuscular dysplasia or atherosclerosis is the reason for the occlusion of a renal artery which ultimately leads to this condition. Diagnosis
The diagnosis for renovascular hypertension is done by:
Blood test (for renal function)
Urinary test (tests for microalbuminuria)
Serology (to exclude systemic lupus erythematosus )
Lipid profile
Urinalysis (to exclude presence of red blood cells)

Treatment
In terms of treatment for renovascular hypertension surgical revascularization versus medical therapy for atherosclerosis, it is not clear if one option is better than the other according to a 2014 Cochrane review; balloon angioplasty did show a small improvement in blood pressure .Surgery can include percutaneous surgical revascularization, and also nephrectomy or autotransplantation, and the individual may be given beta-adrenergic blockers. Early therapeutic intervention is important if ischemic nephropathy is to be prevented. Inpatient care is necessary for the management of hypertensive urgencies, quick intervention is required to prevent further damage to the kidneys. Prognosis
The prognosis of individuals with renovascular hypertension is not easy to determine. Those with atherosclerotic renal artery disease have a high risk of mortality, furthermore, those who also have renal dysfunction have a higher mortality risk. However, the majority of renovascular diseases can be improved with surgery. See also
Fibromuscular dysplasia
Hypertensive nephropathy
Kidney failure
Renal artery stenosis

References
Further reading
Advances in Renal Hypertension Research and Treatment: 2012 Edition: ScholarlyPaper. ScholarlyEditions. 2012-12-26. ISBN 9781481636018. Textor, Stephen C. (2009). "Current Approaches to Renovascular Hypertension".
About half of patients recover fully. Epidemiology
While the exact incidence is unknown, estimates range from 33 - 57 percent of patients staying in the ICU for longer than 7 days. More exact data is difficult to obtain, since variation exists in defining the condition. The three main risk factors for CIP and CIM are sepsis and systemic inflammatory response syndrome (SIRS), and multi-organ failure. Reported rates of CIP/CIM in people with sepsis and SIRS range from 68 to 100 percent. Additional risk factors for developing CIP/CIM include: female gender, high blood sugar (hyperglycemia), low serum albumin, and immobility. A greater severity of illness increases the risk of CIP/CIM. Such risk factors include: multi-organ dysfunction, kidney failure, renal replacement therapy, duration of organ dysfunction, duration of ICU stay, and central neurologic failure.Certain medications are associated with CIP/CIM, such as corticosteroids, neuromuscular blocking agents, vasopressors, catecholamines, and intravenous nutrition (parenteral nutrition). Research has produced inconsistent results for the impact of hypoxia, hypotension, hyperpyrexia, and increased age on the risk of CIP/CIM. The use of aminoglycosides is not an independent risk for the development of CIP/CIM. History
CIP was first described in 1984 by Charles F. Bolton in a series of five patients. The condition used to be described as "Boltons neuropathy.". In 1996, Latronico and colleagues first described that CIP and CIM often coexist in the same patient.