Master of Science in Nursing (MSN) Student Scholarship

Date Written

Summer 8-3-2017

Document Type

Project

Course Number

NURS 5330

Course Name

Advanced Pathophysiology

Professor’s Name

Dr. Chovan, Dr. Butz, and Dr. Cacchillo

Keywords

kidney disease, polycystic disease, polycystic kidney disease

Subject Categories

Medicine and Health Sciences | Nursing

Abstract

This nurse is currently employed at an outpatient ambulatory hemodialysis (HD) clinic. National statistics revealed more than 660,000 Americans being treated for end stage renal disease (ESRD) and at the state level, Ohio has 16,182 individuals which are on routine HD with the primary causes attributed to diabetes and hypertension (HTN) (National Kidney Foundation [NKF], 2017). This nurse discovered a small patient population ascertained ESRD from an inherited familial disorder, particularly polycystic kidney disease (PKD). PKD is the fourth leading cause kidney failure and approximately 600,000 individuals have been diagnosed with PKD in the United States (U.S.) (NKF, 2017). PKD causes multiple fluid cysts to grow in the kidneys, depending on the size and amount they can damage the kidney, decrease kidney function, and lead to renal failure (NKF, 2017). There are three types of PKD: autosomal dominant polycystic kidney disease (ADPKD), autosomal recessive polycystic kidney disease (ARPKD), and acquired cystic kidney disease (ACKD). ADPKD, which is the most predominant occurring in 300,000 to 600,000 individuals per year (Srivastava & Patel, 2014). ADPKD is the most commonly inherited human renal disease with mutations on two genes, PKD1 and PKD2, mutations from PKD1 account for 85% of ADPKD cases (Sweeney Jr & Avner, 2014). The PKD1 gene is located on chromosome 16 and the PKD2 gene is located on chromosome 4, both genes encode for membrane proteins polycystin-1 and polycystin-2, mutations lead to increased levels of cyclic adenosine monophosphate causing cystogenesis (Srivastava & Patel, 2014). Autosomal dominant diseases affect males and females equally, 50% of the offspring of affected parent will have the disease, and generations are not skipped. Most patients with PKD do not present with clinical manifestations until later in in life due to the slow growth of the cysts which contributes to a loss of nephrons and a decline in the glomerular filtration rate (GFR) (Srivastava & Patel, 2014).

Included in

Nursing Commons

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