Abstract:Arterial pressure was measured in 94 adult patients with polycystic kidney disease (PKD) and the data obtained were compared with those of two groups of patients with other chronic renal diseases. Patients with PKD having a glomerular filtration rate within normal limits were more frequently hypertensive than those with other renal diseases. This relationship was reversed when patients with severe renal insufficiency were considered.
“…Blood CSA levels in the present study were in the low therapeutic range (table 4) and are thus unlikely to be the causative factor in the etiopathogenesis of the observed hypertension. Furthermore, post transplant hypertension was also observed in the AZA cohort suggesting that the underlying renal disease with its known propensity to hypertension [27], even when renal function is relatively normal, may be playing a role.…”
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 μmol/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.
“…Blood CSA levels in the present study were in the low therapeutic range (table 4) and are thus unlikely to be the causative factor in the etiopathogenesis of the observed hypertension. Furthermore, post transplant hypertension was also observed in the AZA cohort suggesting that the underlying renal disease with its known propensity to hypertension [27], even when renal function is relatively normal, may be playing a role.…”
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 μmol/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.
“…Hypertension is the most frequent initial presentation of ADPKD, occurring in 50% to 75% of cases and usually preceding the onset of renal failure. 2,22 Hypertension is more common in male ADPKD patients, begins early in the course of the disease, and is diagnosed around the fourth decade of life. 21 In a study in 2007, de Almeida et al 23 used 24-hour ambulatory blood pressure monitoring early in the course of ADPKD and found significantly higher systolic, diastolic, and mean 24-hour blood pressures in ADPKD patients who had normal in-office blood pressure than in normotensive controls.…”
Section: ■ Hypertension In Adpkdmentioning
confidence: 99%
“…31 Moreover, another study found that the prevalence of hypertension is higher in ADPKD patients than in those with other nephropathies with preserved renal function, but this association reverses with significant decline in kidney function. 22 Hypertension occurs in 50%-75% of patients with ADPKD Early diagnosis of hypertension and effective control of it, even before ADPKD is diagnosed, is crucial to reduce cardiovascular mortality. Aggressive blood pressure control in the prehypertensive phase of ADPKD will also help reduce the incidence of left ventricular hypertrophy and mitral regurgitation and slow the progression of renal failure (Figure 2).…”
Autosomal dominant polycystic kidney disease (ADPKD) has numerous systemic manifestations and complications. This article gives an overview of hypertension, cardiac complications, and intracranial aneurysms in ADPKD, their pathophysiology, and recent developments in their management.
“…Once on dialysis nearly all affected individuals are hypertensive. [9][10][11][12][13] Hypertension used to be thought to be a significant factor in the progression of renal failure in ADPKD, 14 and it is the major risk factor for the premature cardiovascular disease that occurs, particularly in younger patients, and which in turn is the most frequent cause of mortality in ADPKD patients. 15 It is well recognised that deterioration of renal excretory function in ADPKD follows a unique time course in that glomerular filtration rate remains constant for many years and only declines relatively late in the course of the disease, when mechanical compression of normal renal tissue by cysts occurs.…”
Raised blood pressure (BP) is extremely common in individuals with autosomal dominant polycystic kidney disease (ADPKD) and is almost invariably raised once they develop renal failure. The underlying mechanisms for the rise in BP in individuals with ADPKD are unclear. The progressive number and enlargement of renal cysts, causing structural damage to the kidneys and, thereby, affecting tubular function as well as causing distortion of the glomeruli and renal ischaemia, is likely to be of primary importance.There is some evidence from animal models that there may be over-activity of the intra-renal renin-angiotensin system (RAS) that could account for the rise in BP. Studies in man have shown conflicting results, but a recent more carefully controlled study using both measurements of activity and pharmacological blockade of the RAS clearly demonstrated no evidence of over-activity of the circulating RAS in ADPKD compared to matched individuals with essential hypertension.A more likely explanation for the rise in BP that occurs in ADPKD is retention of sodium and water due to tubular damage. Disappointingly, in spite of good evidence that RAS blocking drugs slow the progression of other renal, particularly glomerular, diseases, there is little evidence to suggest this is true for patients with ADPKD. Nevertheless, there is no doubt that lowering BP in ADPKD is just as important, if not more important, as in essential hypertension to prevent cardiovascular disease and strokes, with a recommended BP target of < 120/80 mmHg.
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