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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aging and hypertension are associated with a progressive decline in renal blood flow and renal function. As a result, physicians planning therapeutic strategies to control blood pressure need to consider these changes and how they relate to potassium homeostasis, particularly in elderly patients. Commonly used antihypertensive drugs such as beta-blockers, angiotensin converting enzyme inhibitors and potassium-sparing diuretics need to be used with increasing caution in patients with declining renal function. This is especially important in patients with diabetes who may also have type IV renal tubular acidosis, and in patients given concomitant therapy with non-steroidal anti-inflammatory drugs. Other therapies such as calcium channel blockers, particularly those that gate atrioventricular nodal conduction, also need to be used with care in people with significant renal insufficiency and hyperkalemia, as this clinical scenario may result in a greater risk of complete heart block.
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PMID:Non-diuretic-based antihypertensive therapy and potassium homeostasis in elderly patients. 943 77

Alagille syndrome (AS) is characterized by the association of at least three of the following five abnormalities: chronic cholestasis, peripheral pulmonary artery stenosis, vertebral arch defects, embryotoxon, and typical facies. In addition to urological abnormalities, tubulointerstitial nephritis, renal tubular acidosis, and mesangiolipidosis have been noted in AS. The usual manifestations of such renal pathologies rarely include hypertension. We report five patients with at least four of the five major features of AS who developed secondary hypertension of renovascular origin 3.5-28 years after the initial diagnosis of AS. Angiography demonstrated uni- or bilateral renal artery stenosis and various other abnormalities of the main arteries in all five patients: aorta (3 cases), celiac artery (4 cases), superior mesenteric artery (1 case), subclavian artery (1 case). Our findings underscore the value of arterial blood pressure monitoring in patients with AS. If hypertension occurs, a renovascular origin should be sought. The diffuse vascular abnormalities which appeared to be a feature of AS in these patients should prompt larger studies of vascular abnormalities in AS.
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PMID:Renovascular hypertension and vascular anomalies in Alagille syndrome. 954 69

Fibronectin glomerulopathy (GFND) is a newly recognized autosomal dominant disease of the kidney that results in albuminuria, microscopic hematuria, hypertension, renal tubular acidosis type IV, and end-stage renal disease in the 2d to 6th decade of life. The disease is characterized histologically by massive deposits of fibronectin (Fn) present in the subendothelial spaces of renal glomerular capillaries. The cause of human GFND is unknown. In order to localize a candidate gene for GFND, we performed linkage analysis of a large, 193-member pedigree containing 13 affected individuals. Since we had previously excluded the genes for Fn and uteroglobin as candidate genes for GFND, a total-genome search for linkage was performed. Examination of 306 microsatellite markers resulted in a maximum two-point LOD score of 4.17 at a recombination fraction of. 00 for marker D1S249, and a maximum multipoint LOD score of 4.41 for neighboring marker D1S2782. By detection of recombination events, a critical genetic interval of 4.1 cM was identified, which was flanked by markers D1S2872 and D1S2891. These findings confirm that GFND is a distinct disease entity among the fibrillary glomerulopathies. Gene identification will provide insights into the molecular interactions of Fn in GFND, as well as in genetically unaltered conditions.
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PMID:The gene for human fibronectin glomerulopathy maps to 1q32, in the region of the regulation of complement activation gene cluster. 983 25

Renal tubular acidosis (RTA) is uncommonly encountered in pregnancy. The risk for these women to develop pregnancy-induced hypertension has not been previously described. The renal defect noted in these women, aggravated by the normal hypervolemia of pregnancy, may predispose to hypertension. Three pregnancies in two women with RTA type 1 developed persistent diastolic hypertension in the third trimester. Mild renal insufficiency was noted in each woman as defined by serum creatinine of 0.9-1.1 and 1.4-1.6 mg/dL, respectively. Vaginal delivery was achieved in each without complications. Blood pressures returned to normal following each pregnancy. Pregnancy-induced hypertension developed in each of three pregnancies in two patients with RTA type 1. The risk for these women to develop pregnancy-induced hypertension may be associated with the higher reported risk in women with underlying renal disease.
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PMID:Pregnancy and renal tubular acidosis. 1045 32

The carbon dioxide (CO2) pneumoperitoneum of laparoscopic surgery is a complex physiologic event associated with neuroendocrine, respiratory, cardiovascular, and renal disturbances, as well as compromised organ blood flow. A case is presented of a 67-year-old man with a history of chronic renal failure, renal tubular acidosis, and hypertension, who underwent an uneventful elective laparoscopic cholecystectomy that included 75 minutes of CO2 pneumoperitoneum of 15 mmHg pressure. Postoperatively, the patient developed acute renal failure from which he recovered within 2 weeks. In the absence of other evident precipitating factors, we suspect that the CO2 pneumoperitoneum played a causal role in the development of his acute renal failure. The potential seriousness of the physiologic insult of conventional CO2 pneumoperitoneum suggests that "minimal access" surgery is not necessarily "minimally invasive."
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PMID:Acute renal failure following laparoscopic cholecystectomy: a case report. 1052 28

Mutations in WNK1 and WNK4, genes encoding members of a novel family of serine-threonine kinases, have recently been shown to cause pseudohypoaldosteronism type II (PHAII), an autosomal dominant disorder featuring hypertension, hyperkalemia, and renal tubular acidosis. The localization of these kinases in the distal nephron and the Cl(-) dependence of these phenotypes suggest that these mutations increase renal Cl(-) reabsorption. Although WNK4 expression is limited to the kidney, WNK1 is expressed in many tissues. We have examined the distribution of WNK1 in these extrarenal tissues. Immunostaining using WNK1-specific antibodies demonstrated that WNK1 is not present in all cell types; rather, it is predominantly localized in polarized epithelia, including those lining the lumen of the hepatic biliary ducts, pancreatic ducts, epididymis, sweat ducts, colonic crypts, and gallbladder. WNK1 is also found in the basal layers of epidermis and throughout the esophageal epithelium. The subcellular localization of WNK1 varies among these epithelia. WNK1 is cytoplasmic in kidney, colon, gallbladder, sweat duct, skin, and esophagus; in contrast, it localizes to the lateral membrane in bile ducts, pancreatic ducts, and epididymis. These epithelia are all notable for their prominent role in Cl(-) flux. Moreover, these sites largely coincide with those involved in the pathology of cystic fibrosis, a disease characterized by deranged epithelial Cl(-) flux. Together with the known pathophysiology of PHAII, these findings suggest that WNK1 plays a general role in the regulation of epithelial Cl(-) flux, a finding that suggests the potential of new approaches to the selective modulation of these processes.
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PMID:WNK1, a kinase mutated in inherited hypertension with hyperkalemia, localizes to diverse Cl- -transporting epithelia. 1252 52

The fetotoxic effects of angiotensin converting enzyme inhibitors when used during the second half of pregnancy are well known. The more recently developed angiotensin II receptor antagonists appear to yield similar fetal abnormalities. We report a premature infant born to a 41-year-old mother with a long history of infertility who had received losartan therapy for hypertension throughout an undetected pregnancy. Ultrasound examination 2 days prior to delivery identified a single fetus at 29 weeks gestation, anhydramnios, and an empty fetal bladder. The neonatal course was complicated by oliguria, hyperkalemia, marked renal dysfunction, respiratory failure, joint contractures, and a large anterior fontanelle with widely separated sutures. Hypotension (mean arterial pressure<25 torr) on day 1 responded to volume expansion, dopamine, and hydrocortisone. Serum creatinine reached a maximum of 2.7 mg/dL on day 6 and decreased to 0.4 by day 56. No formal urinalysis was performed, but the urine was reported to be visually clear throughout the course. Although a renal ultrasound on day 2 was normal, a follow-up study at 7 months revealed bilateral generalized parenchymal echogenicity, consistent with medical renal disease. Since then, weight and length have been at the 5th percentile or less, with apparent renal tubular acidosis necessitating the addition of sodium citrate supplements. This case emphasizes the importance of maintaining a high index of suspicion for potential pregnancy when contemplating the use of a drug of this class, and considering serial testing for pregnancy when using such drugs, even in patients with a longstanding history of infertility.
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PMID:Gestational therapy with an angiotensin II receptor antagonist and transient renal failure in a premature infant. 1679 14

Hypokalemia is a common and important finding in hospitalized patients because it may provoke cardiac arrhythmias and/or respiratory arrest. Our aim is to suggest better diagnostic tools and therapeutic principles, and summarize new molecular advances that are linked to hypokalemia. Measurements in freshly-voided urine to evaluate potassium (K+) excretion and an assessment of the acid-base status in blood can help differentiate between the various causes of hypokalemia. In patients with a low rate of K+ excretion, hypokalemia can be explained by an acute shift of K+ into cells, intestinal K+ loss, or prior renal K+ excretion. Patients with a high rate of K+ excretion usually have metabolic acid-base disorders. In patients with hyperchloremic metabolic acidosis, an assessment of the rate of excretion of ammonium (NH4+) in the urine separates those with renal tubular acidosis (RTA) (low NH4+ excretion) from those with causes other than RTA. In patients with metabolic alkalosis, a high blood pressure helps to distinguish between a state with high mineralocorticoid activity from others with extracellular fluid (ECF) volume contraction. Measurement of renin activity, aldosterone, and cortisol levels in plasma help to differentiate between the causes with mineralocorticoid excess whereas the urine chloride (Cl-) concentration may reveal the basis for renal Na+ wasting and distinguish it from non-renal Na+ loss. The treatment of hypokalemia is guided by the risk imposed by hypokalemia, magnitude of the K+ deficit, route of the K+ administration, available K+ preparations, adjuncts to therapy, and special associated conditions. Recent molecular advances in inherited hypokalemic disorders affecting transcellular K+ shift, gastrointestinal and renal K+ excretion are also discussed.
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PMID:Hypokalemia: a practical approach to diagnosis and its genetic basis. 1758 63

In situations where the cause of hypokalemia is not obvious, measurement of urinary potassium excretion and blood pressure and assessment of acid-base balance are often helpful. A random urine potassium-creatinine ratio (K/C) less than 1.5 suggests poor intake, gastrointestinal losses, or a shift of potassium into cells. If hypokalemia is associated with paralysis, we should consider hyperthyroidism, familial or sporadic periodic paralysis. Metabolic acidosis with a urine K/C ratio less than 1.5 suggests lower gastrointestinal losses due to diarrhea or laxative abuse. Metabolic acidosis with K/C ratio of 1.5 higher is often due to diabetic ketoacidosis or type 1 or type 2 distal renal tubular acidosis. Metabolic alkalosis with a K/C ratio less than 1.5 and a normal blood pressure is often due to surreptitious vomiting. Metabolic alkalosis with a higher K/C ratio and a normal blood pressure suggests diuretic use, Bartter syndrome, or Gitelman syndrome. Metabolic alkalosis with a high urine K/C ratio and hypertension suggests primary hyperaldosteronism, Cushing syndrome, congenital adrenal hyperplasia, renal artery stenosis, apparent mineralocorticoid excess, or Liddle syndrome. Hypomagnesemia can lead to increased urinary potassium losses and hypokalemia. The differential rests upon measurement of blood magnesium, aldosterone and renin levels, diuretic screen in urine, response to spironolactone and amiloride, measurement of plasma cortisol level and the urinary cortisol-cortisone ratio, and genetic testing.
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PMID:Diagnosis of hypokalemia: a problem-solving approach to clinical cases. 1937 23

The kidney maintains systemic acid-base homeostasis through proximal tubular reclamation of filtered bicarbonate, and excretion of the daily mineral acid load by collecting duct type A intercalated cells. Impairment of either process produces renal tubular acidosis (RTA). This article will provide an overview of familial forms of proximal and distal renal tubular acidosis (pRTA and dRTA). Recessive pRTA with ocular and central nervous system abnormalities is caused by loss-of-function mutations in basolateral membrane Na-HCO3- cotransporter NBCe1/ SLC4A4. Recessive dRTA with deafness is caused by loss-of-function mutations in either of 2 subunits of the vacuolar H+-ATPase (V-ATPase) of intercalated cells; the B1 subunit of the V1 cytoplasmic ATPase complex, and the a4 subunit of the V0 transmembrane pore complex. Dominant and recessive forms of dRTA are also caused by loss-of-function mutations in the basolateral membrane AE1 Cl-/HCO3- exchanger of the type A intercalated cell. The dominant AE1 dRTA mutations are accompanied by mild or asymptomatic erythroid changes, while the erythroid dyscrasias accompanying recessive AE1 dRTA mutations can be mild or severe. Recessive mixed proximal-distal RTA is caused by loss-of-function mutations of the cytoplasmic carbonic anhydrase II. Hyperkalemic RTA accompanied by hypertension (pseudohypoaldosteronism type 2 [PHA2]) is caused by dominant gain-of-function mutations in the kinases WNK1 and WNK4. Hyperkalemic RTA accompanied by volume depletion is caused by loss-of-function mutations in genes encoding the mineralocorticoid receptor or the epithelial Na+ channel (ENaC) subunits. Additional RTA genes identified in knockout mice may lead to identification of additional human RTA genes.
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PMID:Familial renal tubular acidosis. 2117 Aug 90


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