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Previous Volume 350:151-164 January 8, 2004 Number 2 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Polycystic kidney diseases are a leading cause of end-stage renal failure and a common indication for dialysis or renal transplantation. Recent advances have led to insights into mechanisms underlying the cause and prognosis of these diseases and suggest new directions for treatment.

Polycystic kidney disease may arise sporadically as a developmental abnormality or may be acquired in adult life, but most forms are hereditary. Among the acquired forms, simple cysts can develop in kidneys as a consequence of aging; dialysis, drugs, and hormones can cause multicystic disease^1,2; and renal cysts are often secondary manifestations of genetic proliferative syndromes.¹ The . . . [Full Text of this Article]

Autosomal Dominant Polycystic Kidney Disease

Autosomal Recessive Polycystic Kidney Disease

Familial Nephronophthisis

Medullary Cystic Kidney Disease

Cell Biology

Proliferation and Apoptosis

Secretion

Cell–Matrix Interactions

Polarity

Signal Transduction

Cilia

Molecular Biology

PKD Genes and Mutations

Polycystic Kidney Disease Proteins

            Polycystin-1

            Polycystin-2

            Fibrocystin

            Nephrocystin

Functions of Polycystins

Developmental Regulation and Programming

Prospects for Prognosis and Therapy

Source Information

From the Department of Medicine, Division of Nephrology, Mount Sinai School of Medicine, New York.

Address reprint requests to Dr. Wilson at the Department of Medicine, Division of Nephrology, Mount Sinai School of Medicine, 1425 Madison Ave., East Bldg., Rm. 11-23, New York, NY 10029, or at pat.wilson@mssm.edu.

Related Letters:

Polycystic Kidney Disease
Bleyer A. J., Hart T. C., Wilson P. D.
Extract | Full Text | PDF  
N Engl J Med 2004; 350:2622, Jun 17, 2004. Correspondence

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