Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a study to determine the proportion of unrecognised cases and the prevalence of treatable complications of autosomal dominant polycystic kidney disease (ADPKD), 46 probands were identified through genetics and renal clinics in Melbourne, Australia. 321 offspring of the probands who were older than 15 years and had not been previously diagnosed as having ADPKD were identified. 68 (21%) had ultrasound evidence of polycystic kidney disease. Of this previously undiagnosed group, 25 (37%) had one or more treatable complications at the time of diagnosis. The complications included 20 cases of hypertension (diastolic blood pressure 95 mm Hg or above), 7 cases of impaired renal function (serum creatinine 0.12 mmol/l or above), and 4 cases of bacterial urinary tract infection. 8 people had several complications. ADPKD has an important treatable component which is not being treated in a substantial proportion of affected individuals, because the disease is not being diagnosed despite the presence of a positive family history.
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PMID:Treatable complications in undiagnosed cases of autosomal dominant polycystic kidney disease. 167 Jul 85

A total of 316 patients (167 men and 149 women) with autosomal dominant polycystic kidney disease was studied retrospectively by a multi-institute group. With advancing patient age renal function decreased, and blood pressure, prevalence of liver cysts and probability of end stage renal failure increased. The probability of end stage renal failure was 39% in the patients in their sixties. Regression analysis indicated that polycystic kidney disease patients could expect to lose 1.1 ml. per minute of creatinine clearance per year, reaching a level of 10 ml. per minute, a point of end stage renal failure, by the age of 72.7 years. The better prognosis in our study than that reported previously in white patients might be due to the inclusion of more asymptomatic persons and/or milder genotypic expression of polycystic kidney disease in Japan. There was no sex difference in the prevalence of liver cysts (54.6%), pancreatic cysts (7.1%), intracranial aneurysms (8.0%) and hypertension (63.6%). The occurrence of pancreatic cysts was significantly associated with liver cysts. Our study clarifies several clinical characteristics of polycystic kidney disease in Japan.
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PMID:Clinical aspects of polycystic kidney disease. 173 86

There is an excess incidence of ESRD treatment among non-White North Americans that is not completely explained by the racial prevalences of the underlying diseases, including hypertension, which can potentially cause renal disease. The racial difference is particularly striking for presumed nephrosclerosis from hypertension and for nephropathy from Type II diabetes, but is not yet substantiated for ESRD attributed to polycystic kidney disease or Type I diabetes. The existing data are insufficient to support the notion that poorer blood pressure control alone is responsible for the racial differences in incident ESRD. Black race (and possibly Mexican or Native American heritage) may be a specific risk factor for ESRD, independent of hypertension and its treatment.
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PMID:Racial differences in the incidence and progression of renal diseases. 176 85

In order to evaluate the impact of ciclosporin in patients with adult onset polycystic kidney disease (ADPKD) following renal transplantation, we performed a single-center study of all (n = 65) patients with this disorder since 1978, 43 of whom received CSA (PC-CSA) with the remaining 22 treated with azathioprine (PC-AZA). An additional group of 45 age- and time-matched group of non-polycystic CSA-treated patients (nonPC-CSA) were used as a separate control group. Patient and graft survivals at 1 and 5 years were similar in PC-CSA when compared to nonPC-CSA. The commonest causes of death in both groups were cardiovascular related. The incidence of posttransplant hypertension and acute rejection were also similar. Urinary tract infections (UTIs) were, however, more frequent among PC-CSA (11 and 33% pre- and posttransplant respectively) when compared to the nonPC-CSA (2 and 17% pre- and posttransplant respectively). The PC-CSA cohort showed improved 1-year patient and graft survivals when compared to PC-AZA (94 and 70% vs. 72 and 34%) with less rejection episodes (42 vs. 88%) during the first year posttransplant but a higher mean serum creatinine at the end of the first year (2.0 vs. 1.6 mg/dl, 176.6 vs. 141.3 mumol/l). Posttransplant hypertension (67 vs. 70%) and UTIs (33 vs. 33%) were, however, similar in both groups. In summary, renal transplantation in ADPKD in the CSA era is associated with equal patient and graft survivals when compared with nonpolycystic patients of comparable age, but superior results when compared with the earlier azathioprine era.
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PMID:The impact of ciclosporin in patients with adult polycystic kidney disease following transplantation. 176 92

We compared the tubular transport of sodium and the erythrocyte sodium-lithium countertransport activity in hypertensive patients with autosomal dominant polycystic kidney disease (ADPKD) and in normotensive control subjects. In addition, we assessed the effects of inhibition of converting enzyme on renal hemodynamics and sodium excretion in hypertensive patients with ADPKD to provide information on mechanisms responsible for the increased renal vascular resistance and filtration fraction and the adjustment of the pressure-natriuresis relationship during saline expansion, observed in patients with ADPKD, hypertension, and preserved renal function. In comparison with normotensive control subjects, the hypertensive patients with ADPKD had lower renal plasma flows, higher renal vascular resistances and filtration fractions, and similar proximal and distal fractional reabsorptions of sodium. The administration of enalapril resulted in significant increases in the renal plasma flow and significant reductions in mean arterial pressure, renal vascular resistance, and filtration fraction, but the glomerular filtration rate remained unchanged. Despite the significant reduction in mean arterial pressure during inhibition of converting enzyme, the distal fractional reabsorption of sodium decreased while the total fractional excretion of sodium remained unchanged or increased slightly. No significant differences were detected between the normotensive control subjects and the hypertensive patients with ADPKD in erythrocyte sodium-lithium countertransport activity, plasma renin activity, plasma aldosterone concentration, or atrial natriuretic factor. These results suggest that the renal renin-angiotensin system plays a central role in the alterations in renal hemodynamics and sodium management associated with the development of hypertension in ADPKD.
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PMID:Effect of inhibition of converting enzyme on renal hemodynamics and sodium management in polycystic kidney disease. 192 83

The renin-angiotensin-aldosterone system appears to play an important initiating role in the pathogenesis of hypertension in patients with autosomal-dominant polycystic kidney disease (ADPKD). Therefore, angiotensin-converting enzyme (ACE) inhibitors would appear to be appropriate therapy for hypertension in such patients. However, because ADPKD is a bilateral disorder, ACE-inhibitor therapy may worsen renal function, as occurs in patients with bilateral renal artery stenosis. We describe eight episodes of reversible acute renal deterioration in five patients with ADPKD, massive renal involvement, and chronic renal insufficiency. In all cases, ACE-inhibitor therapy either predisposed the patient to or precipitated the acute event. Two of the patients who had acute renal failure while receiving ACE-inhibitor therapy experienced a recurrence when rechallenged with such therapy. Furthermore, patients receiving combined therapy with an ACE inhibitor and a diuretic and patients who experience a cyst hemorrhage while receiving ACE inhibitor therapy are also at risk for reversible renal dysfunction. Caution is therefore recommended in using ACE inhibitors to treat hypertension in patients with ADPKD who are at high risk because of compromised renal function and massive cystic involvement.
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PMID:Reversible renal failure associated with angiotensin-converting enzyme inhibitors in polycystic kidney disease. 159 54

We report on a 6 months old infant with suddenly developed severe arterial hypertension caused by polycystic kidneys. Examinations of the relatives revealed similar changes of the kidneys in 4 adults and 5 children. They were all diagnosed to have autosomal dominant polycystic kidney disease. Excretory kidney function of all patients is normal; however, blood pressure was raised in the adults. We would like to stress the importance of family screening in this disease, in particular with regard to possible early diagnosis and treatment of arterial hypertension. The long-term prognosis of the early manifestation of the dominantly inherited cystic kidney disease is uncertain.
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PMID:[Autosomal dominant polycystic kidney disease in infancy]. 194 47

Several reports in animals, and sporadic case reports in humans, have suggested that kidneys with decreased nephron mass may be more susceptible to the development of focal-segmental glomerosclerosis. This prompted a reexamination of our previously reported group of pediatric donor-adult recipient renal transplant combinations. Data were analyzed from 31 adult recipients who had received renal transplants from cadaver pediatric donors (less than 6 years) with graft function for greater than 6 months and no evidence of chronic rejection. These were compared with a control group transplanted during the same period with adult donor kidneys. Immunosuppression consisted of azathioprine/prednisone or quadruple therapy in 16 and 15 patients respectively. End-stage renal disease (ESRD) was secondary to chronic glomerulonephritis (n = 9), diabetes mellitus (n = 6), polycystic kidney disease (n = 5), and miscellaneous causes (n = 11). Twenty patients had radiographic documentation of renal hypertrophy posttransplant. All patients had serial 24-hr urinalysis for protein and creatinine after transplantation during periods of stable renal function. Ten patients had renal biopsies performed at a mean time from transplant to biopsy of 10.4 +/- 1.6 months. Seven recipients had biopsies that revealed glomerulosclerosis at 13 +/- 6 months posttransplant. Protein excretion and serum creatinine in these patients were significantly higher than in control patients (1.6 +/- 0.37 vs. 0.49 +/- 0.15 g/24 hr and 1.96 +/- 0.11 vs. 1.64 +/- 0.09 mg%; P less than 0.03 and P less than 0.01, respectively). Only 3 of 25 control adult donor recipients developed proteinuria greater than 0.8 g/24 hr within 2 years of transplantation vs. 15/31 pediatric donor recipients. No correlations with the etiology of ESRD, age (greater than or less than 40 years), weight, sex, diabetes, hypertension, or the number of acute rejection episodes could be found. Our data suggest that adult recipients of pediatric donor renal transplants may be at greater risk for the development of glomerulosclerosis than those recipients receiving adult donor kidneys.
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PMID:The development of proteinuria and focal-segmental glomerulosclerosis in recipients of pediatric donor kidneys. 194 66

Hypertension has been reported to occur in 50 to 75 percent of subjects with autosomal dominant polycystic kidney disease (ADPKD) prior to the onset of marked renal insufficiency but concurrent with cystic deformation of the renal parenchyma. The present study was undertaken to examine whether the renal structural abnormalities are greater in hypertensive (HBP) versus normotensive (NBP) male and female patients with ADPKD who were matched within gender groups for age, body surface area, serum creatinine concentration (males HBP 1.2 +/- 0.02 vs. NBP 1.1 +/- 0.03 mg/dl. NS: females HBP 0.9 +/- 0.03 vs. NBP 0.9 +/- 0.02 mg/dl, NS) and creatinine clearance (males HBP 100 +/- 3 vs. NBP 108 +/- 3 ml/min/1.73 m2, NS: females HBP 97 +/- 3 vs. NBP 96 +/- 2 ml/min/1.73 m2, NS). Renal volume was significantly greater in the HBP compared to the NBP group (males HBP 624 +/- 47 vs. NBP 390 +/- 43 cm3, P less than 0.0005; females HBP 446 +/- 32 vs. NBP 338 +/- 24 cm3, P less than 0.002). Since increased renal volume is due to increased cysts, the results indicate that the early high incidence of hypertension in ADPKD correlates with the renal structural abnormalities in this disorder.
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PMID:Renal structure and hypertension in autosomal dominant polycystic kidney disease. 207 59

To appraise the prognosis of adult polycystic kidney disease (APKD), 107 patients (58 male and 49 female) were studied retrospectively. The mean age at the time of diagnosis was 45.9 years (ages ranging from 18 to 83 years). Ninety-eight patients had symptomatic APKD. At diagnosis, 30 of these patients had normal renal function, and 68 presented with chronic renal failure (serum creatinine higher than 1.5 mg/dl). Nine of the 107 patients were asymptomatic. Hypertension was the most common feature in symptomatic APKD, present in 51% of these patients as initial manifestation, and was observed in 46% of the patients with normal renal function. Forty of the 107 patients (37%) went into end-stage renal disease (ESRD) at a mean age of 52.7 years. The probability of being alive and not having ESRD, estimated using a time-to-event analysis, was 74% by the age of 50, 51% by the age of 58 and 37% by the age of 70 years. Thus, the prognosis for patients with APKD is better than some reports suggested some years ago.
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PMID:Clinical features and prognosis of adult polycystic kidney disease. 207 5


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