The Rate of Progression of Renal Failure in ADPKD

Author(s):  
Gabriel Choukroun ◽  
Yukihiro Itakura ◽  
N. K. Man ◽  
Jean-Louis Christophe ◽  
Ginette Albouze ◽  
...  
2003 ◽  
Vol 89 (4) ◽  
pp. 491-497 ◽  
Author(s):  
Shu-Tzu Chen ◽  
Sheng-Jeng Peng ◽  
Jiun-Rong Chen

The objective of the present experiment was to examine the effect of substituting different quantities of soyabean protein for casein on renal function and lipid metabolism in rats with chronic renal failure induced by a five-sixths nephrectomy. Experimental animals were subjected to a nephrectomy and fed either casein or soyabean protein (200 or 100 g/kg diet). The diets were isoenergetic with identical fat, Na, K and P contents. Rats ingesting 200 g casein/kg diet showed a significantly (P<0·05) accelerated course of chronic renal failure, while the soyabean-protein groups showed retarded progression of the experimentally induced renal disease and hypercholesterolaemic effects. Rats in the low-soyabean-protein diet (100 g/kg) also demonstrated increased serum albumin and decreased serum triacylglycerol, total cholesterol concentrations and blood urea-N; however, the low-casein diet significantly (P<0·05) increased serum triacylglycerol. Results of the present study show that the replacement of casein by soyabean protein was related to the rate of progression of renal failure and improvement in lipid profiles in serum of five-sixths nephrectomized rats.


1995 ◽  
Vol 6 (6) ◽  
pp. 1634-1642
Author(s):  
G Choukroun ◽  
Y Itakura ◽  
G Albouze ◽  
J L Christophe ◽  
N K Man ◽  
...  

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.


1987 ◽  
Vol 5 (3-4) ◽  
pp. 163-174 ◽  
Author(s):  
Susan P. A. Rigden ◽  
Kathryn M. Start ◽  
Lesley Rees

Normal renal function is an essential prerequisite for normal nutrition. Renal failure results in malnutrition and growth retardation, which are particularly marked when renal failure has its onset early in life. Conversely, the careful application of nutritional therapy can ameliorate the effects of renal failure and allow improved well being and growth and possibly retard the rate of progression of renal failure. Nutritional therapy includes the provision of an adequate energy intake, appropriate intakes of water, electrolytes, vitamins and minerals and regulation of protein and phosphorus intakes. In this paper the theoretical considerations underlying these objectives are reviewed and practical ways of achieving them with least disruption to the child and his family suggested.


Nephron ◽  
1994 ◽  
Vol 68 (1) ◽  
pp. 32-37 ◽  
Author(s):  
Ana Gonzalo ◽  
Araceli Gallego ◽  
Maite Rivera ◽  
Nieves Gallego ◽  
Joaquín Ortuño

Toxins ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 50
Author(s):  
Satoshi Kumakura ◽  
Emiko Sato ◽  
Akiyo Sekimoto ◽  
Yamato Hashizume ◽  
Shu Yamakage ◽  
...  

Nicotinamide adenine dinucleotide (NAD+) supplies energy for deoxidation and anti-inflammatory reactions fostering the production of adenosine triphosphate (ATP). The kidney is an essential regulator of body fluids through the excretion of numerous metabolites. Chronic kidney disease (CKD) leads to the accumulation of uremic toxins, which induces chronic inflammation. In this study, the role of NAD+ in kidney disease was investigated through the supplementation of nicotinamide (Nam), a precursor of NAD+, to an adenine-induced CKD mouse model. Nam supplementation reduced kidney inflammation and fibrosis and, therefore, prevented the progression of kidney disease. Notably, Nam supplementation also attenuated the accumulation of glycolysis and Krebs cycle metabolites that occurs in renal failure. These effects were due to increased NAD+ supply, which accelerated NAD+-consuming metabolic pathways. Our study suggests that Nam administration may be a novel therapeutic approach for CKD prevention.


Nephron ◽  
1990 ◽  
Vol 55 (2) ◽  
pp. 203-209 ◽  
Author(s):  
M.H. De Keijzer ◽  
A.P. Provoost

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