Shape of the Relationship between Hypertension and the Rate of Progression of Renal Failure in Autosomal Dominant Polycystic Kidney Disease

Nephron ◽  
1992 ◽  
Vol 62 (1) ◽  
pp. 52-57 ◽  
Author(s):  
Ana Gonzalo ◽  
Araceli Gallego ◽  
Maite Rivera ◽  
Luis Orte ◽  
Joaquín Ortuño
Keyword(s):  
Renal Failure ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Polycystic Kidney ◽  
Rate Of Progression ◽  
Progression Of Renal Failure ◽  
Autosomal Dominant Polycystic Kidney ◽  
The Relationship

scholarly journals Factors influencing progression of renal failure in autosomal dominant polycystic kidney disease.

1995 ◽  
Vol 6 (6) ◽  
pp. 1634-1642
Author(s):  
G Choukroun ◽  
Y Itakura ◽  
G Albouze ◽  
J L Christophe ◽  
N K Man ◽  
...  
Keyword(s):  
Renal Failure ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Protein Intake ◽  
Pressure Control ◽  
Polycystic Kidney ◽  
Rate Of Progression ◽  
Progression Of Renal Failure ◽  
Autosomal Dominant Polycystic Kidney

Autosomal dominant polycystic kidney disease (ADPKD) frequently leads to end-stage renal failure (ESRF) in the sixth decade of life, but considerable heterogeneity exists in the rate of progression of renal failure. The respective contribution of genetic factors and of potentially amendable factors, such as blood pressure control or protein intake limitation, on the rate of progression in ADPKD patients is still debated. To evaluate the role of factors influencing the rate of progression of renal failure in ADPKD, we retrospectively analyzed the annual rate of decline of creatinine clearance (Ccr) in 109 ADPKD patients followed from the time a Ccr value of 30 to 50 mL per min/1.73 m2 was measured until ESRD and need for hemodialysis (Study A), and in 48 undialyzed ADPKD patients followed for at least 4 yr from the time a Ccr value of 50 to 60 mL per min/1.73 m2 was measured (Study B). In Study A, the decline in Ccr (delta Ccr) (mean +/- SE) was 5.8 +/- 0.2 mL per min/1.73 m2 per year in the whole series, and was lower in females than in males (5.0 +/- 0.2 versus 6.4 +/- 0.2, P < 0.001). Accordingly, ESRF was reached at a later age in female patients (55.1 +/- 1.2 versus 50.6 +/- 1.2 yr, P < 0.01). The age at ESRF in male patients was lower when the disease was transmitted by mother than by father (46.3 +/- 1.9 versus 54.1 +/- 1.8 yr, P < 0.01), whereas no significant effect of the gender of the affected parent was apparent in female patients. By regression analysis, there was a positive but weak relationship between delta Ccr and mean arterial pressure (average value during follow-up, 107 +/- 1 mm Hg, r = 0.224, P < 0.05) but not with dietary protein intake (mean value in follow-up, 0.87 +/- 0.03 g/kg per day, r = 0.10, P = 0.33) nor with proteinuria at baseline, which was lower than 0.3 g/day in 104 cases (r = 0.10, P = 0.28). There was a negative relationship between age at ESRF and delta Ccr (r = 0.245, P < 0.05), with a later and slower progression in older subjects. In Study B, the mean decline in renal function during follow-up was 5.3 +/- 0.4 mL/min/1.73 m2 per year, a value close to that observed in Study A. By multiple regression analysis of the overall population (studies A and B combined), only MAP, age and gender were independent predictive factors of delta Ccr but all studied parameters taken together accounted for at best 20% of delta Ccr variation. We conclude that the rate of progression of renal failure in ADPKD patients is mainly determined by gene expression, with female gender and older age associated with a slower progression, whereas blood pressure control, but not protein intake, exerts a limited beneficial influence on the rate of progression in patients with advanced polycystic kidney disease who already have significant renal insufficiency.

scholarly journals Influence of ACE I/D gene polymorphism in the progression of renal failure in autosomal dominant polycystic kidney disease: a meta-analysis

2006 ◽  
Vol 21 (11) ◽  
pp. 3155-3163 ◽  
Author(s):  
Tiago Veiga Pereira ◽  
Ane Cláudia Fernandes Nunes ◽  
Martina Rudnicki ◽  
Ricardo Magistroni ◽  
Alberto Albertazzi ◽  
...  
Keyword(s):  
Renal Failure ◽  
Kidney Disease ◽  
Gene Polymorphism ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Meta Analysis ◽  
Polycystic Kidney ◽  
Progression Of Renal Failure ◽  
Autosomal Dominant Polycystic Kidney

scholarly journals Recent advances in the clinical management of autosomal dominant polycystic kidney disease

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 116 ◽  
Author(s):  
Roser Torra
Keyword(s):  
Renal Failure ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Polycystic Kidney ◽  
Hepatic Cysts ◽  
Live Births ◽  
Recent Advances ◽  
Systemic Disorder ◽  
Autosomal Dominant Polycystic Kidney

Autosomal dominant polycystic kidney disease (ADPKD) is a genetic systemic disorder causing the development of renal and hepatic cysts and decline in renal function. It affects around 1 in 1,000 live births. Early hypertension and progressive renal failure due to massive enlargement of cysts and fibrosis are hallmarks of the disease. This article reviews recent advances in ADPKD and focuses mainly on diagnosis, management, and prediction of the course of the disease.

scholarly journals The effect of uninephrectomy on progression of renal failure in autosomal dominant polycystic kidney disease.

1992 ◽  
Vol 3 (5) ◽  
pp. 1119-1123
Author(s):  
M Zeier ◽  
S Geberth ◽  
A Gonzalo ◽  
D Chauveau ◽  
J P Grünfeld ◽  
...  
Keyword(s):  
Renal Failure ◽  
Kidney Disease ◽  
Serum Creatinine ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Polycystic Kidney ◽  
End Stage Renal Failure ◽  
Significant Difference ◽  
Autosomal Dominant Polycystic Kidney ◽  
End Stage

The evolution of renal failure was compared in 47 patients (21 male, 26 female) with autosomal dominant polycystic kidney disease (ADPKD) in Germany, France, Spain, and Portugal who had undergone uninephrectomy (UNX) (median age at uninephrectomy, 41 yr; range, 22 to 54) and 47 non-UNX matched controls. UNX was usually performed because of uncontrolled urinary tract infection (N = 30), stones (N = 8), trauma (N = 2), or hemorrhage (N = 7). Median serum creatinine at UNX was 2.1 mg/dL (0.9 to 4.3). Twenty-eight of the 47 uninephrectomized patients progressed to end-stage renal failure. When the age at renal death was evaluated by survival analysis, only minor and nonsignificant acceleration was seen in the uninephrectomized patients (median, 50 yr; p25 = 43.6 yr; p75 = 58.3 yr, where p is the percentile) compared with non-UNX patients matched for age, sex, and serum creatinine at the time of UNX in the propositus (51.2 yr; p25 = 48.6 yr; p75 = 56.1 yr). In addition, the median interval for serum creatinine to rise from 4 to 8 mg/dL was similar in UNX (21.3 months) versus nonuninephrectomized ADPKD patients (21.9 months). Renal survival differed in the two genders. In females, no significant difference of age at renal death was found between UNX (median age, 51.6 yr) and non-UNX ADPKD patients (53.7 yr). In male UNX patients, age at renal death was slightly (but not significantly) less than in non-UNX patients (median age, 47.3 versus 52.7 yr). All male patients reaching end-stage renal failure before age 44 were severely hypertensive.

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