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

Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited disorder frequently associated with renal failure, hypertension, and other abnormalities. The present study determined whether chronic caffeine intake in an animal model of this disease would affect renal structure and function and blood pressure. Heterozygous male Han:Sprague-Dawley rats with ADPKD and normal littermates were provided with either tap water or solutions of caffeine to drink, starting at 1 month of age. When rats were aged 6 months, glomerular filtration rate (GFR) and mean arterial blood pressure (MAP) were measured under Inactin (Byk Gulden, Konstanz, Germany) anesthesia. Caffeine intake had no effect on GFR or cyst development in rats with PKD. MAP was greater in rats with PKD than normal rats and was increased more by caffeine. The hypertensive effect of chronic caffeine intake could not be ascribed to direct pressor effects of angiotensin II. Based on our finding that caffeine exacerbates hypertension in rats with PKD, it may be prudent for patients with ADPKD to limit coffee consumption to four or fewer cups of caffeinated coffee per day, pending studies of humans.
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PMID:Chronic caffeine consumption exacerbates hypertension in rats with polycystic kidney disease. 1168 64

Autosomal dominant polycystic kidney disease (ADPKD) has aroused great interest these last years, especially after the discovery of the genes responsible for this disease. It remains a frequent cause of chronic renal failure (CRF). In this work we report the results of a multi-centre retrospective study. The data relates to 41 centres of nephrology and dialysis in Morocco, 308 Moroccan families and 420 observations. We have tried to determine the frequency of this pathology in Morocco, its complications and difficulties in taking care of it. The average age of the discovery of ADPKD was 46 +/- 3 years and the sex ratio was of 1.08. The ADPKD frequency among Moroccans who undergo dialysis was 6.5%. Pain was the most frequent symptom which revealed the disease (21%); while renal failure at different stages was found in 17% of the patients and high blood pressure (HBP) in 11%. The clinic diagnosis was confirmed by echography in 95% of cases. The association with a hepatic cysts was found in 17.8% of the cases. In addition, to HBR and urinary tract infection, the complications were largely dominated by renal chronic failure and the difficulties in taking care of it because of economic problems. Through this the authors discuss and report the profile and the prognostics of this infection in our society, with a special focus on the evolution of the renal function, the delay in the diagnosis and the management.
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PMID:[Autosomal dominant polycystic kidney disease (ADPKD). in Morocco. Multicenter study about 308 families]. 1201 54

Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary renal disorder in humans. Hypertension is one of the major complications, and its control might affect the renal survival and disease mortality. Suitable antihypertensive agents have been discussed based on clinical and animal studies, but no definitive conclusion has been reached. Generally, therefore, all antihypertensives are indiscriminately treated as if providing the same level of blood pressure control. In this study, the blood pressure control of two antihypertensives was investigated using a rat model of ADPKD in humans. Twenty-four male Hannover-Sprague Dawley (Han:SPRD) rats were divided into three groups: a group receiving amlodipine (6 mg/day), a group receiving benazepril (6 mg/day) and an untreated control group. Blood pressure, body weight, and urinary protein excretion were regularly measured up to week 52. Amlodipine and benazepril significantly decreased blood pressure and urinary protein excretion to the same degree. Moreover, a remarkably prolonged survival rate was observed in both groups (at week 52, the survival rate was 25% in controls, 50% in the amlodipine group, and 50% in the benazepril group). Examination at autopsy revealed that enlarged cysts were prevalent in the renal tissue of both experimental all three groups, suggesting that the cystic disease had reached the end-stage in all the animals. In conclusion, both amlodipine and benazepril significantly improved blood pressure control, urinary protein excretion, and survival rate, possibly due to their enhancement of renal survival.
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PMID:The effects of antihypertensive agents on the survival rate of polycystic kidney disease in Han:SPRD rats. 1248 19

Autosomal dominant polycystic kidney disease (ADPKD) is a dominantly inherited systemic disorder equally inherited in men and women characterized by renal cyst development and expansion ultimately leading to renal failure. ADPKD women have a slower rate of progression to renal failure, with a later age of entry into end-stage renal disease (ESRD) as compared with men. Renal cyst growth and renal expansion are the hallmarks of ADPKD, and women will develop renal insufficiency with smaller renal volume than their male counterparts. As well, women have different rates of occurrence of renal and extrarenal complications in ADPKD. Renal complications related to ADPKD, including hypertension and gross hematuria, occur more frequently in men than in women, whereas liver cystic disease occurs earlier and more frequently in women than in men. The presence of polycystic liver disease is related to pregnancy number and oral contraceptive pill use in ADPKD women. Importantly, massive polycystic liver disease requiring surgical intervention occurs primarily in ADPKD women. ADKPD women have a highly successful reproductive course. The chance of a successful pregnancy is excellent in ADPKD women and comparable to healthy unaffected women as long as prepregnancy blood pressure and renal function are normal. Fetal complication rates are no greater than in the general population; however, maternal complication rates in ADPKD women are high with an increased frequency of new or worsening hypertension as well as an increased occurrence of preeclampsia and preterm deliveries. Finally, increasing pregnancy number has minimal or no effect on renal outcome in ADPKD women.
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PMID:Cystic disease in women: clinical characteristics and medical management. 1261 60

Autosomal dominant polycystic kidney disease (ADPKD), a common genetic disease, is characterized by the development of hypertension and end stage renal disease. An increase in the activity of the renin-angiotensin system, due to a renal ischemia caused by cyst expansion, contributes to the development of hypertension and renal failure in ADPKD. Recently, the angiotensinogen (AGT) gene, M235T, and angiotensin II type 1 receptor (ATR) gene, A1166C, polymorphisms have been associated with the susceptibility to develop hypertension and renal disease. We hypothesized that the AGT M235T and ATR A1166C polymorphisms could account for some of the variability in the progression of ADPKD. Genotyping was performed in 108 adult patients with ADPKD, and 105 normotensive healthy controls, using PCR and restriction digestion. We analyzed the effects of the AGT M235T and ATR A1166C polymorphisms on hypertension and age at the end stage renal disease (ESRD). Of the 108 patients with ADPKD, 64 (59%) had hypertension and 24 (22%) reached the ESRD. The prevalence of hypertension were; [MM+MT], [TT] genotypes, 60%, 59% (p=1.00); [AA], [AC+CC] genotypes, 60%, 50% respectively (p=0.54). The ages at the onset of ESRD were; [MM+MT], [TT] genotypes, 50 +/- 9 years, 56 +/- 8 years (p=0.07); [AA], [AC+CC] genotypes, 54 +/- 8 years, 52 +/- 14 years, respectively (p=0.07). There were no differences in the prevalence of hypertension and the ages at the ESRD in relation to the AGT M235T and ATR A1166C polymorphisms. We suggest that the AGT and ATR gene polymorphisms would not have an effect on hypertension or the ESRD in ADPKD.
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PMID:Angiotensinogen and angiotensin II type 1 receptor gene polymorphism in patients with autosomal dominant polycystic kidney disease: effect on hypertension and ESRD. 1295 Jan 20

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by exuberant inflammation and fibrosis, a process believed to contribute to progressive loss of normal renal function. Despite early-onset hypertension and intrarenal renin/angiotensin II (AngII) activation, angiotensin-converting enzyme (ACE) inhibition does not consistently confer renal protection in ADPKD. The hypothesis was that mast cells within the inflammatory interstitium release chymase, an enzyme capable of efficient conversion of AngI to AngII, providing an ACE-independent route of AngII generation. End-stage ADPKD renal tissue extracts and cyst fluids were assayed for time-dependent, chymostatin-inhibitable conversion of (125)I-AngI to (125)I-AngII under conditions of ACE and aminopeptidase inhibition by means of HPLC. Thirteen of 14 ADPKD kidney extracts exhibited chymase-like AngII-generating capacity; calculated initial reaction rates averaged 3.9 +/- 2.9 fmol AngII/min/ micro g protein with a mean maximal conversion of 55% +/- 30% of added substrate. AngII-generating activity was both protein and substrate dependent. All five cyst fluid samples were negative. Chymase-like activity was detectable in only three of six non-ADPKD kidney extracts. Immunoreactive chymase protein was present in/around mast cells within the fibrotic renal interstitium in all samples. Findings demonstrate for the first time the presence of mast cells, mast cell-associated immunoreactive chymase protein, and chymase-like AngII generating capacity in ADPKD cystic kidneys. Results support the potential for ACE-independent AngII generation and for mast cell-initiated inflammatory processes in ADPKD, each with therapeutic implications for ADPKD renal progression.
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PMID:Chymase-like angiotensin II-generating activity in end-stage human autosomal dominant polycystic kidney disease. 1474 98

Among the fatal vascular complications associated with autosomal dominant polycystic disease (ADPKD), ruptured intracerebral aneurysm and ruptured abdominal aortic aneurysm are widely known. However, there are few reports on the dissecting thoracic aortic aneurysm as a fatal complication of ADPKD. We report a case of a 58-year-old man with a history of ADPKD who presented to the emergency department with out-of-hospital cardiac arrest. Immediate cardiopulmonary resuscitation restored a spontaneous circulation successfully and subsequent image study revealed a type I dissecting thoracic aortic aneurysm. Emergency aortic grafting was performed--but he died from postoperative haemorrhage. The surgical specimen of the aorta showed cystic medial necrosis. This rare case emphasizes the need to consider such a diagnosis in a patient with ADPKD who presents to the emergency department with sudden cardiac arrest. In addition, the histological finding indicates the aetiological role of a collagen defect in addition to chronic hypertension in the pathogenesis of aortic dissection in ADPKD patients.
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PMID:Sudden death caused by dissecting thoracic aortic aneurysm in a patient with autosomal dominant polycystic kidney disease. 1545 91

Autosomal dominant polycystic kidney disease (ADPKD) is a common genetic disorder characterized by the formation of fluid-filled cysts in the kidney and progressive renal failure. Other manifestations of ADPKD include the formation of cysts in other organs (liver, pancreas, and spleen), hypertension, cardiac defects, and cerebral aneurysms. The loss of function of the polycystin -1 and -2 results in the formation of epithelium-lined cysts, a process that depends on initial epithelial proliferation. cDNA microarrays powerfully monitor gene expression and have led to the discoveries of pathways regulating complex biological processes. We undertook to profile the gene expression patterns of epithelial cells derived from the cysts of ADPKD patients using the cDNA microarray technique. Candidate genes that were differently expressed in cyst tissues were identified. 19 genes were up-regulated, and 6 down-regulated. Semi-quantitative RT-PCR results were consistent with the microarray findings. To distinguish between normal and epithelial cells, we used the hierarchical method. The results obtained may provide a molecular basis for understanding the biological meaning of cytogenesis.
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PMID:The gene expression profile of cyst epithelial cells in autosomal dominant polycystic kidney disease patients. 1547 26

Autosomal dominant polycystic kidney disease(ADPKD) is rarely observed in the neonatal period. We report 2 cases of ADPKD who showed bilateral enlarged, hyperechoic kidneys and severe hypertension. It is difficult to differentiate ADPKD from autosomal recessive polycystic kidney disease (ARPKD) based on the initial clinical presentations in this period. In both cases, bilateral enlarged kidneys and severe hypertension were detected without oligohydramnion and respiratory distress. The mother of case 1 has polycystic kidneys. The father of case 2 was diagnosed as ADPKD. Case 2 had heart failure due to hypertension. Angiotensin converting enzyme inhibitor (ACE-I) was administered to both patients and resulted in good control of blood pressure. ADPKD in the neonatal and very early infantile period has diverse clinical courses. In general, although severe cases are rare, some cases have renal failure and/or hypertension as we reported. We emphasize that both the prompt diagnosis of ADPKD and the start of medication are of great importance in the neonatal and very early infantile period. We recommend that neonates and infants with a family history of ADPKD undergo screening including physical examinations, blood pressure measurements and urinalysis.
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PMID:[Two cases of autosomal dominant polycystic kidney diseases who presented bilateral enlarged kidneys and severe hypertension in the neonatal period]. 1557 Sep 1

Autosomal dominant polycystic kidney disease (ADPKD) is a generalized disease known to be associated with intracranial aneurysms. Non-aneurysmal intracerebral hemorrhage (ICH) has also been reported in ADPKD. We report a familial clustering of ICH and symptomatic ADPKD. This pedigree had at least six affected family members who suffered from ADPKD, hypertension and non-aneurysmal ICH. The proband demonstrated ADPKD, hypertension and cerebral hemorrhage. To our knowledge, this is the first report of familial ICH in ADPKD, which may have underlying genetic and environmental etiologies.
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PMID:Familial hypertensive intracerebral hemorrhage and autosomal dominant polycystic kidney disease. 1592 88


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