Screening for Subclinical Nephropathy in Relatives of Dialysis Patients

Despite the availability of improved medical therapy to slow the progression of nephropathy, a worldwide epidemic of end‐stage renal disease (ESRD) exists. Many patients are not diagnosed until the late stages of disease, as early kidney disease may be asymptomatic. Ideally all adults would be routinely screened for evidence of early kidney disease and associated risk factors such as hypertension and diabetes mellitus. Unfortunately this would be a massive and expensive undertaking. A more practical, cost‐effective solution might be to direct screening at those individuals who are known to be at high risk for the development of nephropathy. The familial clustering of ESRD has been reported for many types of renal disease. We propose that the routine screening of first‐ and second‐degree relatives of ESRD patients for nephropathy might be an efficient way to detect subclinical renal disease. Early detection and intensive treatment of renal disease may help to curb the current epidemic of ESRD.

[1]  R. Lifton,et al.  IgA nephropathy, the most common cause of glomerulonephritis, is linked to 6q22–23 , 2000, Nature Genetics.

[2]  J. Kaplan,et al.  Mutations in ACTN4, encoding α-actinin-4, cause familial focal segmental glomerulosclerosis , 2000, Nature Genetics.

[3]  D. Bowden,et al.  Analysis of the HNF4α gene in Caucasian Type II diabetic nephropathic patients , 2000, Diabetologia.

[4]  B. Freedman,et al.  Familial clustering of end-stage renal disease in blacks with HIV-associated nephropathy. , 1999, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[5]  M. Pericak-Vance,et al.  Linkage of a gene causing familial focal segmental glomerulosclerosis to chromosome 11 and further evidence of genetic heterogeneity. , 1999, Genomics.

[6]  R. Holman,et al.  Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. , 1998 .

[7]  Uk-Prospective-Diabetes-Study-Group Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33) , 1998, The Lancet.

[8]  P. Whelton,et al.  Familial aggregation of renal disease in a population-based case-control study. , 1998, Journal of the American Society of Nephrology : JASN.

[9]  J. Seidman,et al.  A locus for inherited focal segmental glomerulosclerosis maps to chromosome 19q13. , 1998, Kidney international.

[10]  B. Freedman,et al.  Family history of end-stage renal disease among incident dialysis patients. , 1997, Journal of the American Society of Nephrology : JASN.

[11]  G. Kaysen,et al.  Effect of lipid-lowering therapy on the progression of renal disease in nondiabetic nephrotic patients. , 1997, Contributions to nephrology.

[12]  B. Freedman,et al.  Familial clustering of end-stage renal disease in blacks with lupus nephritis. , 1997, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[13]  I. Lauder,et al.  Treatment of hyperlipidaemia in patients with non-insulin-dependent diabetes mellitus with progressive nephropathy. , 1997, Contributions to nephrology.

[14]  D. Warnock,et al.  Kidney disease in the first-degree relatives of African-Americans with hypertensive end-stage renal disease. , 1996, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[15]  M. Lishner,et al.  Long-term renoprotective effect of angiotensin-converting enzyme inhibition in non-insulin-dependent diabetes mellitus. A 7-year follow-up study. , 1996, Archives of internal medicine.

[16]  B. Freedman,et al.  Familial predisposition to nephropathy in African-Americans with non-insulin-dependent diabetes mellitus. , 1995, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[17]  G. Beck,et al.  The Effects of Dietary Protein Restriction and Blood-Pressure Control on the Progression of Chronic Renal Disease , 1994 .

[18]  A. Krolewski,et al.  Hypercholesterolemia--a determinant of renal function loss and deaths in IDDM patients with nephropathy. , 1994, Kidney international. Supplement.

[19]  A Fournier,et al.  The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy. , 1994, The New England journal of medicine.

[20]  R. Bain,et al.  The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy. , 1993 .

[21]  R. Bain,et al.  The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy. The Collaborative Study Group. , 1993, The New England journal of medicine.

[22]  R. Neuwirth,et al.  Renal function change in hypertensive members of the Multiple Risk Factor Intervention Trial. Racial and treatment effects. The MRFIT Research Group. , 1992, JAMA.

[23]  R. Luke,et al.  Changing patterns of end-stage renal disease due to hypertension. , 1991, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[24]  E. Seaquist,et al.  Familial clustering of diabetic kidney disease. Evidence for genetic susceptibility to diabetic nephropathy. , 1989, The New England journal of medicine.

[25]  M. Blaufox,et al.  Prognostic value of serum creatinine and effect of treatment of hypertension on renal function. Results from the hypertension detection and follow-up program. The Hypertension Detection and Follow-up Program Cooperative Group. , 1989, Hypertension.

[26]  L. Wolff,et al.  Relationship between lactate dehydrogenase and myeloperoxidase levels in human gingival crevicular fluid and clinical and microbial measurements. , 1988, Journal of clinical periodontology.

[27]  S. Colagiuri,et al.  The Diabetes Control and Complications Trial , 1983, Henry Ford Hospital medical journal.