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      Impact of Birth Weight on Familial Aggregation of End-Stage Renal Disease

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          Background: Birth weight (BW) and family history (FH) of end-stage renal disease (ESRD) have been shown to have an independent association with development of subsequent ESRD. This study was undertaken to determine the effects of BW (low BW suggesting a congenital reduction in functional nephron number) on the observed familial aggregation of ESRD. Methods: Cases were identified from the ESRD Network 6 ‘Family History of ESRD’ Study and BW was determined from birth certificate records maintained at the Office of Vital Records, South Carolina Department of Health and Environmental Control. BW and FH of ESRD data were available in 387 patients who initiated dialysis therapy between 1993 and 1997. Multiple logistic regression analysis was performed to assess the risk of low BW (<2,500 g) and high BW (≧4,000 g) on FH of ESRD. Results: A FH of ESRD in first or second-degree relatives was present in 24% of cases. No significant differences were observed in the frequency of a positive FH of ESRD in those with low BW compared to those with normal BW. There was a significant reduction in the prevalence of a FH of ESRD in those with high BW, compared to those with a normal BW (risk ratio 0.32, CI 0.11–0.94). Conclusion: The clustering of either high BW or low BW within multiply affected ESRD families does not account for the observed familial aggregation of ESRD. In addition, high BW was associated with a reduced familial aggregation of ESRD.

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          Genetic susceptibility to end-stage renal disease.

          New methods have been developed to uncover the genotypes that result in complex diseases. End-stage renal disease is a complex disease, without a simple correspondence between genotype and phenotype. Both population-based and family-based epidemiological studies and analysis of model organisms suggest that the pathogenesis of end-stage renal disease may have a genetic component. A number of studies have analyzed candidate nephropathy genes with little success, but recently several well-designed studies of multiplex families with diabetic nephropathy have identified candidate nephropathy susceptibility loci. To date, kidney disease-oriented research has focused on effector mechanisms responsible for the initiation and progression of chronic renal disease. However, because end-stage renal disease is a complex disease, interruption of a single effector pathway is unlikely to result in significant therapeutic benefit. Further understanding of the pathogenesis of kidney disease and the development of new kidney disease therapies will require continued application of genetic and genomic tools to kidney disease research.
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            A Low-Calorie Unrestricted Protein Diet Attenuates Kidney Damage in Uninephrectomized Spontaneously Hypertensive Rats

            Background/Aims: Uninephrectomized, spontaneously hypertensive rats (UNX-SHR) develop glomerular hyperfiltration, hyperfusion, and interstitial infiltrate of the remnant kidney. Consequently, UNX-SHR is a useful animal model to investigate mechanisms involved in the progression of hypertensive renal disease. Methods: Body weight; tail systolic blood pressure (SBP); urine excretion of protein, urea, and electrolytes; and serum biochemistry were determined in UNX-SHR at 2 months of age prior to uninephrectomy (week 0), prior to treatment (week 8) with a low-calorie (LC) or control diet, and one month after diet treatment (week 12). The LC diet was modified to allow equal intake of protein, sodium phosphorus, and other nutrients in both groups. Results: UNX-SHR treated with the LC diet had significantly lower body weights and SBP at the end of the experiment than did the controls (p < 0.0001). Changes in serum biochemistry and 24-hour urinary excretion of protein, sodium, potassium, and urea nitrogen in both groups were not statistically significant. The final glomerular filtration rate and renal plasma flow were similar in both groups, but the LC diet significantly reduced the glomerular damage index (0.0007), mesangial expansion index (p < 0.002), volume of interstitium per cortex (p < 0.0003), tubular interstitium volume fraction (p < 0.0008), glomerular volume (p < 0.02), and remnant kidney weight (p < 0.01). Conclusion: We demonstrated that in UNX-SHR, the prevention of renal damage by LC diet may involve diminished glomerular growth and interstitial infiltrate without changes in renal hemodynamics. Consequently, LC diet, regardless of protein ingestion, may be an important tool in the prevention of renal damage in hypertension. Additional studies of obese-hypertensive rats may confirm the beneficial effect of a LC diet and weight reduction on the renal damage of obesity-hypertension.

              Author and article information

              Am J Nephrol
              American Journal of Nephrology
              S. Karger AG
              April 2003
              17 January 2003
              : 23
              : 2
              : 117-120
              aDepartment of Biometry and Epidemiology, Medical University of South Carolina, Charleston, S.C.; bSoutheastern Kidney Council, Inc./ESRD Network 6, Raleigh, N.C., and cDepartment of Internal Medicine/Section on Nephrology, Wake Forest University School of Medicine, Winston-Salem, N.C., USA
              68037 Am J Nephrol 2003;23:117–120
              © 2003 S. Karger AG, Basel

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              Page count
              Tables: 2, References: 29, Pages: 4
              Self URI (application/pdf):
              Original Article: Bench to Bedside

              Cardiovascular Medicine, Nephrology

              Birth weight, Familial aggregation, End-stage renal disease


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