Afectación trigeminal en el SUNCT / Trigeminal involvement in SUNCT syndrome

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Recomendaciones para la detección y el tratamiento del anciano con hipertensión arterial / Recommendations for diagnosis and treatment of aged hypertensives

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Role of hypertension in the progression of chronic renal disease.

Hypertension leads to renal disease through a series of mechanisms that seem to be exaggerated in African-Americans, who have a higher prevalence of both hypertension and end-stage renal disease than whites. Renal disease itself leads to hypertension, which in turn can contribute to progression of renal disease. Although there are numerous mechanisms involved in the process of renal disease progression, the renin-angiotensin system plays a major role as determined by the beneficial response to angiotensin I-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (AT II blockers) of reduced rate of progression in a variety of clinical and experimental renal diseases. Macromolecular trafficking across the glomerulus leading to proteinuria plays a significant role in progression of chronic renal disease. Reversal of this abnormality and reduced stress on capillary walls may be the major mechanisms of beneficial action of ACEIs and AT II blockers in halting renal disease progression.

Hypertension in end-stage renal disease.

Patients with moderate to severe renal disease have a very high incidence of hypertension. In end-stage renal disease (ESRD) this is true regardless of the nature of the underlying renal disease. Nevertheless, patients with glomerular diseases and autosomal dominant polycystic kidney disease are particularly vulnerable. Evidence is presented that ESRD hypertension is the result of extracellular volume expansion, increased or inappropriate response of the renin-angiotensin system and overactivity of the sympathetic system. In addition, the role of endothelin-1, nitric oxide and other vasodilators, and abnormal ion channels in generating high blood pressure, is considered.

The impact of malnutrition on kidney function.

Malnutrition is the most common cause of mortality in the world. It affects underdeveloped as well as industrialized societies, in the latter demonstrating a prevalence in hospitalized patients of between 30 and 50%. Although the prevalence has decreased in recent studies, the problem is still significant among a selected group of patients. The clinical manifestations of malnutrition may be evident on physical examination but alterations in renal function may not show up at the initial exam. Clinical and experimental models of protein-calorie malnutrition have confirmed significant alterations in renal hemodynamics, renal concentration capacity, and renal acid excretion. Children and adults with malnutrition have been shown to have a decreased glomerular filtration rate and renal plasma flow (RPF), as well as a lowered capacity to concentrate the urine and excrete an acid load. Moreover, clinical and experimental models of protein-calorie malnutrition have unravelled the roles of the renin-angiotensin system, renal prostaglandins, and urea production in the renal function changes associated with malnutrition. We have reviewed the most pertinent and recent studies from our and other laboratories which have improved our understanding of renal functional alterations in malnutrition.

Atheroembolic renal disease.

Atheroembolic renal disease is an important and often underdiagnosed cause of renal insufficiency in the elderly. Renal damage results from embolization of cholesterol crystals from atherosclerotic plaques in large vessels such as the abdominal aorta to small arteries of the kidney. The typical patient is a white man older than 60 years who has an insidious increase in serum creatinine levels after an arteriographic procedure or vascular surgery. Renal outcome ranges from partial recovery of kidney function to end stage renal disease requiring replacement therapy. Tissue injury from cholesterol crystal embolization is not restricted to the kidneys but also involves the skin, muscles, abdominal organs, and central nervous system resulting in significant morbidity and mortality. Accurate diagnosis is often made by performing a skin, muscle, or renal biopsy. Although effective therapy is lacking, heightened awareness of atheroembolic renal disease is necessary for prompt diagnosis and institution of supportive care.

Acute renal failure in the aged.

Acute renal failure (ARF) is frequent in aged individuals. In this article, we review the literature and relate our own experience in this field. It is concluded that there are no technical reasons to deny treatment for ARF using any of the available techniques based on age. Attempts to prevent the onset of ARF are important. Prophylaxis may be focused on diligent and adequate diagnosis and treatment of reversible renal hypoperfusion, by far the most common cause of pre-renal ARF in the elderly. Administration of potentially nephrotoxic drugs should be avoided, but when necessary creatinine clearance (as the marker of glomerular filtration) rather than blood creatinine levels should be used to establish the appropriate dose. In the elderly, azotemia or other consequences of ARF may induce acute behavioral changes that are almost always reversible; treatment should not be stopped on the false assumption that the patient's mental status is irreversible.

Genetic studies in a black family with autosomal dominant polycystic kidney disease and sickle-cell trait.

Autosomal dominant polycystic kidney disease (ADPKD) is caused by at least two different genes. The ADPKD1 gene is located on chromosome 16p and a second locus is at 4q. Although the ADPKD1 gene is responsible for the majority of the disease in whites, there was no information regarding the gene type in blacks. We studied a black family which presented with both ADPKD and sickle-cell trait (SA) to determine which ADPKD gene was present in this family, and to examine linkage between the ADPKD in this family and markers for the beta-hemoglobin gene on chromosome 11. The ADPKD in this family was linked to markers on chromosome 16, and no linkage was found with the beta-hemoglobin gene. Family members with SA and ADPKD had an early onset of end-stage renal disease. The hemoglobin haplotype was identified as the Central African Republic-type, which has been reported to be associated with a higher incidence of renal failure in sickle-cell anemia.

Hypertension in Hispanics. Comments on a major disease in a mix of ethnic groups.

Hypertension is a disorder that, theoretically, is easily detected and effectively treated. Unfortunately, high blood pressure is a painless cardiovascular risk factor that is associated with nonspecific symptomatology and depends--under most circumstances--on life-long treatment for amelioration or control. Paradoxically, these characteristics make hypertension susceptible to poor detection or control as a result of patient or physician idiosyncrasies. As a consequence, it remains, directly or indirectly, a leading cause of death and morbidity. Especially vulnerable are minority groups for whom a multifactorial array of impediments may retard the dissemination of information making it difficult to detect and treat hypertension. It is not clear that despite the widening of our base of knowledge in relation to hypertension in "Hispanics," we have sufficient data (or the possibility to acquire it) to help answer many of the questions that can be formulated for this amalgam of ethnic groups. Moreover, the role of acculturation in the development of high blood pressure remains largely unexplored.

Role of angiotensin II in the expression and regulation of transforming growth factor-beta in obstructive nephropathy.

Unilateral ureteral obstruction (UUO) leads to fibrosis of the obstructed kidney. We tested the hypothesis that interstitial fibrosis in UUO results, at least in part, from enhanced expression of transforming growth factor-beta (TGF-beta) which in turn is regulated by local angiotensin II (Ang II) generation. (The generic name TGF-beta is used to discuss properties shared by all isoforms, but special reference to other isoforms is made when specifically needed.) Using Northern blot and immunohistochemical analysis, we examined the expression of TGF-beta in rat kidneys after 24 hours (aUUO) and one week (cUUO) of obstruction. Obstructed kidneys from both periods had increased interstitial and perivascular TGF-beta immunoreactivity compared to contralateral and sham kidneys, in which immunostaining was confined to the inner medulla. Relative abundance of all TGF-beta mRNA isoforms were higher in the obstructed than in contralateral and sham kidneys in both aUUO and cUUO. Expression of TGF-beta isoforms varied according to site (cortex vs. medulla), segment of the nephron, type of cells and duration of the obstruction. The increase in TGF-beta immunoreactivity and mRNA levels in aUUO and cUUO was almost totally abolished by pretreatment with losartan. We conclude that in UUO: (a) TGF-beta gene expression is increased and differentially regulated; (b) Ang II, at least partially, mediates the overexpression of TGF-beta gene; and (c) Ang II may play a central role in fibrogenesis in this and other models of tubulointerstitial disease.

Sequential changes in renal expression of renin-angiotensin system genes in acute unilateral ureteral obstruction.

Unilateral ureteral obstruction (UUO) alters the expression of genes encoding for the renin-angiotensin system (RAS). We tested the hypothesis that changes in RAS genes expression occur soon after obstruction. Indeed, measurements during the first 24 hours of UUO showed up-regulation of renin mRNA in the obstructed kidney at 1 hour. UUO also led to increases in PRA and renal renin content, ACE activity and Ang II concentration in the experimental kidney. The obstructed kidney relative abundance of renin mRNA was increased compared to basal at 1, 2, 6, and 24 hours; the contralateral kidney renin mRNA expression was reduced. AT1-R mRNA expression was diminished at 6 and 24 hours in the obstructed kidney compared to contralateral and sham kidneys. ACE activity was up-regulated in the obstructed kidney and transiently down-regulated in the contralateral kidney. These findings show for the first time that activation of the RAS results from as little as 1 hour of UUO and that up-regulation of renin mRNA and ACE activity lead to increase Ang II production which down-regulates AT1-R mRNA as early as 6 hours post-UUO. These studies establish a pattern of sequential, differential regulation of the RAS genes in acute UUO that provide an explanation for the hemodynamic changes in this condition.