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Although patients with secondary hypertension comprise only a small percentage of those with elevated blood pressure, this subgroup should not be ignored. In many cases, correcting the cause of secondary hypertension can lead to a cure, thus avoiding the need for long-term medical therapy, with its attendant risks and economic toll. Moreover, effective treatment of secondary hypertension can prevent chronic complications, such as left ventricular hypertrophy and coronary artery disease, which markedly increase morbidity and mortality. Nearly all forms of secondary hypertension are related to decreased renal function and/or derangement of hormonal balance or secretion. If hypertension is secondary to chronic renal failure of any etiology, it can be recognized from biochemical assays for blood urea nitrogen and creatinine.

Many primary renal diseases are associated with marked proteinuria resistant to immunosuppressive therapy. Short-term treatment with angiotensin converting enzyme (ACE) inhibitors may decrease proteinuria in these patients, but the long-term effect of these agents on urinary protein excretion is not known. We conducted a double-blind, parallel-design, placebo-controlled study of 1 year duration to evaluate the efficacy of the new ACE inhibitor, perindopril, in reducing proteinuria in patients with nephrotic syndrome due to histologically proven membranous and membranoproliferative glomerulonephritis and focal segmental glomerulosclerosis. Half of the patients treated with perindopril displayed a decrease in urinary protein excretion from 6.1 +/- 1.0 to 1.2 +/- 0.5 g/24 h, and a rise in serum albumin levels. In the placebo group, protein excretion increased modestly and serum albumin level did not change. There was no difference between the responders and nonresponders to perindopril in age, blood pressure, level of creatinine clearance or urinary sodium excretion. However, the degree of proteinuria before treatment with perindopril was significantly (p0.01) higher in the nonresponders. In 3 patients in whom the treatment with perindopril was extended for 18-24 months, urinary protein excretion remained below 1 g/24 h. The data show that perindopril: (1) is an effective agent in the treatment of proteinuria of primary renal diseases; (2) the effect is sustained for up to 2 years if the administration of the drugs is maintained, and (3) this action of perindopril does not depend on the level of sodium intake.

Background Cocaine abuse has been known to have detrimental effects on the cardiovascular system. Its toxicity has been associated with myocardial ischemia, cerebrovascular accidents and mesenteric ischemia. The pathophysiology of cocaine-related renal injury is multifactorial and involves renal hemodynamic changes, alterations in glomerular matrix synthesis, degradation and oxidative stress, and possibly induction of renal atherogenesis. Renal infarction as a result of cocaine exposure, however, is rarely reported in the literature. Case presentation A 48 year-old male presented with a four-day history of severe right flank pain following cocaine use. On presentation, he was tachycardic, febrile and had severe right costovertebral angle tenderness. He had significant proteinuria, leukocytosis and elevated serum creatinine and lactate dehydrogenase. Radiographic imaging studies as well as other screening tests for thromboembolic events, hypercoagulability states, collagen vascular diseases and lipid disorders were suggestive of Cocaine-Induced Renal Infarction (CIRI) by exclusion. Conclusion In a patient with a history of cocaine abuse presenting with fevers and flank pain suggestive of urinary tract infection or nephrolithiasis, cocaine-induced renal infarction must be considered in the differential diagnosis. In this article, we discuss the prior reported cases of CIRI and thoroughly review the literature available on this disorder. This is important for several reasons. First, it will allow us to discuss and elaborate on the mechanism of renal injury caused by cocaine. In addition, this review will demonstrate the importance of considering the diagnosis of CIRI in a patient with documented cocaine use and an atypical presentation of acute renal injury. Finally, we will emphasize the need for a consensus on optimal treatment of this disease, for which therapy is not yet standardized.

We examined the efficacy of low daily dose (1.25 mg/day) of indapamide in the treatment of high blood pressure in patients with diabetes mellitus with normal renal function and those with moderate renal insufficiency (serum creatinine

Increased sympathetic nervous system (SNS) activity plays a role in the genesis of hypertension in rats with chronic renal failure (CRF). Because nitric oxide (NO) modulates the activity of the SNS, a deficit of NO synthesis could be responsible for the increased SNS activity in these animals. In the present study, we evaluated the effects of L-arginine and L-NAME on blood pressure and SNS activity-in Sprague Dawley 5/6 nephrectomized or sham-operated rats. SNS activity was determined by measuring norepinephrine turnover rate in several brain nuclei involved in the regulation of blood pressure. In the same brain nuclei, we measured NO content and nitric oxide synthase (NOS) gene expression by semiquantitative measurements of NOS mRNA reverse transcription polymerase chain reaction. In CRF rats, norepinephrine turnover rate was increased in the posterior hypothalamic nuclei, locus coeruleus, paraventricular nuclei, and the rostral ventral medulla, whereas NOS mRNA gene expression and NO2/NO3 content were increased in all brain nuclei tested. L-NAME increased blood pressure and NE turnover rate in several brain nuclei of both control and 5/6 nephrectomized rats. In CRF rats, a significant relationship was present between the percent increment in NOS mRNA gene expression related to the renal failure, and the percent increase in norepinephrine turnover rate caused by L-NAME. This suggests that endogenous NO may partially inhibit the activity of the SNS in brain nuclei involved in the neurogenic regulation of blood pressure, and this inhibition is enhanced in CRF rats. In summary, the increase in SNS activity in the posterior hypothalamic nuclei and in the locus coeruleus of CRF rats is partially mitigated by increased local expression of NOS m-RNA.