Kim Zuber, PA-C, MSPS, DFAAPA

We buried George today. He died of the usual consequences of old age: heart disease, hypertension, kidney disease, Alzheimer’s. However, I cannot think of George without a smile on my face and a thank you in my heart. You see, because of George, I am a better practitioner … and a much better storyteller!

George first came to my clinic for patients with chronic kidney disease many years ago. He had failing kidneys as a result of his hypertension and needed closer monitoring than we were presently able to do during office visits alone. He arrived with his daughter at his side and a scowl on his face. As he took off his coat to have his blood pressure checked, I noticed that one elbow was red and swollen. I asked him what had happened. He said (and I quote): “The General cheats!” His daughter rolled her eyes.

The story, as told by George and supplemented by his daughter, is that George and “The General” (in seven years, I never did learn his actual name) had a standing racquetball date on Friday mornings at Andrews Air Force Base; then they would go to lunch. You see, before the indignities of aging caught up with him, George was a feared and respected Navy Admiral and a good friend of The General. Both George and The General were in the mild to moderate stages of Alzheimer’s and argued frequently over scoring during their racquetball game. In practical terms, the score was a fluid idea that was always wrong, and neither George nor The General ever had any idea what the real score was. However, as aging warriors are wont to do, they insisted on arguing every point, even if they could not remember what the point was! In fact, during these Friday morning racquetball games, there was an MP posted near the door to help The Admiral and The General negotiate. 

In the Washington, DC, area, we are defined by what we do. The first question anyone asks is “And what do you do?” This can be a put-down, but more often than not, it is a stepping-stone for fascinating discussions. When I meet you in my office, though, you are older and retired, and society tends to consider you not as vital. I have a social history in your chart, but that’s not the same as asking you about what you do. I have the older gentleman who always arrives alone and whose chart says he’s retired from working at National Geographic. That is not the same as knowing he was the videographer for 40 years of National Geographic specials about climbing K2, swimming with sharks, hiking the desert, or canoeing the Amazon.

Knowing this explains his neuropathy: hours of standing in rivers. His amputations: frostbite at the tips of his fingers and toes. His single status: As he explained to me, “I never really had much time for a wife or kids.… I was always traveling so much.” If I had not asked him more during the social history, I would have missed out on many a great story.

I have met retired Secret Service agents, the public relations man for the US Postal Service who was the driving force behind the “Donate Life” stamp, a 15th-generation relative of George Washington, a survivor from D-Day. I have gotten tips from a mom on how to put up with a 15-year-old without killing her, stories of what it was like to be the first black man with a degree telling Southern whites what to do, what it was like to volunteer at the White House, and what it was like to build a bridge. I have learned about history and geography—as well as patience and wonder—from the stories I have heard.

There is a Jewish retirement home in Rockville, Maryland, near my office. The gerontologist who runs the home specializes in Alzheimer’s, and many of the residents there are in different stages of the disease. However, Rockville is near the NIH, the National Cancer Institute, the Genome Project, the FDA, the National Institute of Standards and Technology, the US Navy Research Lab, and the Goddard Space Center (NASA). There are more Nobel Prize winners in this 10-square-mile area than in any other place in the United States. As the gerontologist has told me, “These patients are the most brilliant minds of two generations. They could lose 75% of their brain function and still be smarter than I am.” As you can imagine, any mini-mental test or standardized Alzheimer’s protocol is totally ineffective for these residents. A detailed social history is more important than a “one-size-fits-all” mental screening test.

I used to feel that patients should be told what to do. After 27 years of practice, I no longer believe that. I cannot cure your kidney disease; you will eventually die on me. All my patients do, just as George did. But I want my wake to be like George’s—with stories, and friends, and laughter. If we are to pass this way only once, let us enjoy the time we have together.

We buried George today. He died of the usual consequences of old age: heart disease, hypertension, kidney disease, Alzheimer’s. However, I cannot think of George without a smile on my face and a thank you in my heart. You see, because of George, I am a better practitioner … and a much better storyteller!

George first came to my clinic for patients with chronic kidney disease many years ago. He had failing kidneys as a result of his hypertension and needed closer monitoring than we were presently able to do during office visits alone. He arrived with his daughter at his side and a scowl on his face. As he took off his coat to have his blood pressure checked, I noticed that one elbow was red and swollen. I asked him what had happened. He said (and I quote): “The General cheats!” His daughter rolled her eyes.

The story, as told by George and supplemented by his daughter, is that George and “The General” (in seven years, I never did learn his actual name) had a standing racquetball date on Friday mornings at Andrews Air Force Base; then they would go to lunch. You see, before the indignities of aging caught up with him, George was a feared and respected Navy Admiral and a good friend of The General. Both George and The General were in the mild to moderate stages of Alzheimer’s and argued frequently over scoring during their racquetball game. In practical terms, the score was a fluid idea that was always wrong, and neither George nor The General ever had any idea what the real score was. However, as aging warriors are wont to do, they insisted on arguing every point, even if they could not remember what the point was! In fact, during these Friday morning racquetball games, there was an MP posted near the door to help The Admiral and The General negotiate. 

In the Washington, DC, area, we are defined by what we do. The first question anyone asks is “And what do you do?” This can be a put-down, but more often than not, it is a stepping-stone for fascinating discussions. When I meet you in my office, though, you are older and retired, and society tends to consider you not as vital. I have a social history in your chart, but that’s not the same as asking you about what you do. I have the older gentleman who always arrives alone and whose chart says he’s retired from working at National Geographic. That is not the same as knowing he was the videographer for 40 years of National Geographic specials about climbing K2, swimming with sharks, hiking the desert, or canoeing the Amazon.

Knowing this explains his neuropathy: hours of standing in rivers. His amputations: frostbite at the tips of his fingers and toes. His single status: As he explained to me, “I never really had much time for a wife or kids.… I was always traveling so much.” If I had not asked him more during the social history, I would have missed out on many a great story.

I have met retired Secret Service agents, the public relations man for the US Postal Service who was the driving force behind the “Donate Life” stamp, a 15th-generation relative of George Washington, a survivor from D-Day. I have gotten tips from a mom on how to put up with a 15-year-old without killing her, stories of what it was like to be the first black man with a degree telling Southern whites what to do, what it was like to volunteer at the White House, and what it was like to build a bridge. I have learned about history and geography—as well as patience and wonder—from the stories I have heard.

There is a Jewish retirement home in Rockville, Maryland, near my office. The gerontologist who runs the home specializes in Alzheimer’s, and many of the residents there are in different stages of the disease. However, Rockville is near the NIH, the National Cancer Institute, the Genome Project, the FDA, the National Institute of Standards and Technology, the US Navy Research Lab, and the Goddard Space Center (NASA). There are more Nobel Prize winners in this 10-square-mile area than in any other place in the United States. As the gerontologist has told me, “These patients are the most brilliant minds of two generations. They could lose 75% of their brain function and still be smarter than I am.” As you can imagine, any mini-mental test or standardized Alzheimer’s protocol is totally ineffective for these residents. A detailed social history is more important than a “one-size-fits-all” mental screening test.

I used to feel that patients should be told what to do. After 27 years of practice, I no longer believe that. I cannot cure your kidney disease; you will eventually die on me. All my patients do, just as George did. But I want my wake to be like George’s—with stories, and friends, and laughter. If we are to pass this way only once, let us enjoy the time we have together.

We buried George today. He died of the usual consequences of old age: heart disease, hypertension, kidney disease, Alzheimer’s. However, I cannot think of George without a smile on my face and a thank you in my heart. You see, because of George, I am a better practitioner … and a much better storyteller!

George first came to my clinic for patients with chronic kidney disease many years ago. He had failing kidneys as a result of his hypertension and needed closer monitoring than we were presently able to do during office visits alone. He arrived with his daughter at his side and a scowl on his face. As he took off his coat to have his blood pressure checked, I noticed that one elbow was red and swollen. I asked him what had happened. He said (and I quote): “The General cheats!” His daughter rolled her eyes.

The story, as told by George and supplemented by his daughter, is that George and “The General” (in seven years, I never did learn his actual name) had a standing racquetball date on Friday mornings at Andrews Air Force Base; then they would go to lunch. You see, before the indignities of aging caught up with him, George was a feared and respected Navy Admiral and a good friend of The General. Both George and The General were in the mild to moderate stages of Alzheimer’s and argued frequently over scoring during their racquetball game. In practical terms, the score was a fluid idea that was always wrong, and neither George nor The General ever had any idea what the real score was. However, as aging warriors are wont to do, they insisted on arguing every point, even if they could not remember what the point was! In fact, during these Friday morning racquetball games, there was an MP posted near the door to help The Admiral and The General negotiate. 

In the Washington, DC, area, we are defined by what we do. The first question anyone asks is “And what do you do?” This can be a put-down, but more often than not, it is a stepping-stone for fascinating discussions. When I meet you in my office, though, you are older and retired, and society tends to consider you not as vital. I have a social history in your chart, but that’s not the same as asking you about what you do. I have the older gentleman who always arrives alone and whose chart says he’s retired from working at National Geographic. That is not the same as knowing he was the videographer for 40 years of National Geographic specials about climbing K2, swimming with sharks, hiking the desert, or canoeing the Amazon.

Knowing this explains his neuropathy: hours of standing in rivers. His amputations: frostbite at the tips of his fingers and toes. His single status: As he explained to me, “I never really had much time for a wife or kids.… I was always traveling so much.” If I had not asked him more during the social history, I would have missed out on many a great story.

I have met retired Secret Service agents, the public relations man for the US Postal Service who was the driving force behind the “Donate Life” stamp, a 15th-generation relative of George Washington, a survivor from D-Day. I have gotten tips from a mom on how to put up with a 15-year-old without killing her, stories of what it was like to be the first black man with a degree telling Southern whites what to do, what it was like to volunteer at the White House, and what it was like to build a bridge. I have learned about history and geography—as well as patience and wonder—from the stories I have heard.

There is a Jewish retirement home in Rockville, Maryland, near my office. The gerontologist who runs the home specializes in Alzheimer’s, and many of the residents there are in different stages of the disease. However, Rockville is near the NIH, the National Cancer Institute, the Genome Project, the FDA, the National Institute of Standards and Technology, the US Navy Research Lab, and the Goddard Space Center (NASA). There are more Nobel Prize winners in this 10-square-mile area than in any other place in the United States. As the gerontologist has told me, “These patients are the most brilliant minds of two generations. They could lose 75% of their brain function and still be smarter than I am.” As you can imagine, any mini-mental test or standardized Alzheimer’s protocol is totally ineffective for these residents. A detailed social history is more important than a “one-size-fits-all” mental screening test.

I used to feel that patients should be told what to do. After 27 years of practice, I no longer believe that. I cannot cure your kidney disease; you will eventually die on me. All my patients do, just as George did. But I want my wake to be like George’s—with stories, and friends, and laughter. If we are to pass this way only once, let us enjoy the time we have together.

For many years, the medical community speculated about the possibility of organ transplantation. The first successful transplant of any kind involving humans was a corneal transplant in 1905.¹

It wasn’t until 1954 that the first successful organ transplant, a kidney transplant between identical twins, occurred.² Several new concepts emerged: organ rejection plays a major role in the failure or success of a transplant; and donors and recipients must be matched based on blood group.

Today, about 169,000 people in the US live with a donated kidney. Each year, some 10,500 cadaveric organs are transplanted, and 6,400 donors are living donors.³ The National Kidney Foundation’s recent 10-year initiative, End the Wait!,⁴ seeks to close the gap between the more than 50,000 people on the transplant waiting list³ and the number of available donor organs.

Since many patients live for years with their transplanted organs, the primary care clinician is likely to see transplant recipients in a family practice or internal medicine setting. While each patient has unique needs, there are commonalities among them.

Renal Consult welcomes any additional comments or questions regarding care of the renal patient. Please address them to [email protected].
Jane S. Davis, CRNP, DNP

Q: I have a 70-year-old male patient who is losing kidney function. He asked me about transplantation, but I really don’t know whether he is eligible to get on the list. Who is eligible? Is there an age limit? Are patients with chronic illnesses (hepatitis B, hepatitis C, HIV) eligible? How long is the list? Where can I find these answers?

There are no specific guidelines regarding eligibility or age restrictions for kidney transplantation in the United States. Most transplant centers look at patients older than 65 a little more carefully than younger patients—they have to be in good health apart from their renal disease. Some centers will not transplant patients older than 70, while others transplant patients who are 80 or older.¹⁵ The best thing to do is to refer the patient to the local center or call and find out. Again, the Organ Procurement and Transplantation Network,⁷ which lists transplant centers and contact information, can be accessed at optn.transplant.hrsa.gov/mem bers/search.asp

Chronic illnesses are not automatic rule-outs for the most part. Very few centers transplant HIV-positive patients, but this does occur, especially in major cities with a large population of persons with HIV (eg, Washington, DC; San Francisco, New York City, Cincinnati). An infectious disease specialist must follow these patients after transplantation and adjust their HAART (highly active antiretroviral therapy) medications to compensate for both the decreased renal function and anti-rejection medications.  Hepatitis B and C patients are often accepted as long as liver biopsy shows no cirrhosis and the viral load is low or manageable. If the patient is found to have cirrhosis or decompensation, a combined liver-kidney transplant can be planned, although the success rate of this procedure is low.^16,17

Patients with certain types of hepatitis C may be eligible to receive a kidney from a donor with hepatitis C¹⁸ in order to shorten the wait time and make use of a kidney that cannot be transplanted into a person not infected with hepatitis C.

Transplant waiting lists vary by region across the country. There is a centralized electronic list managed by UNOS, on which eligible recipients are placed once they have been approved by the transplant center, following the medical work-up and acceptance by the transplant committee at each center. This is referred to as “being listed” or “on the list.” Patients begin to accrue waiting time as soon as they are added, and this list is precise to the second! There is a list for each blood type, with its own set of waiting times in each region.²⁰ Average waiting times, by blood type (ie, ABO), can be searched at www.ustransplant.org/Calcula tors/KidneyWaitTime.aspx

When a donor organ becomes available and has been evaluated by the procurement team, the donor’s information is entered into the system and the computer generates a list of eligible candidates, based on a variety of factors. This is called a “match-run.”

Waiting time is the most important factor, but consideration is given to patients younger than 18, those who have previously donated an organ, and those with high antibody levels (ie, panel-reactive antibodies, or PRAs). Patients in the latter group may find it more difficult to locate a compatible donor, as these patients have been sensitized as a result of prior transplantation, pregnancy, or blood transfusions. It is very rare for a patient to be a perfect match (0 mismatch), but should the right organ become available, the matched patient receives priority consideration.

Besides the ABO match, human leukocyte antigen (HLA) matching of six main HLA antibodies is done.  Within each of these six antibodies (HLA-A, B, C, DP, DR, DQ), subgroup matching is also done because some HLA subgroups are more highly correlated with rejection than others.^21,22 A more complete explanation of organ matching and allocation can be found on the “Transplant Living” Web site: www.transplantliving.org/beforethetransplant/allocation/matchingorgans.aspx.

Patients should be encouraged to access “Transplant Living” (www.transplantliving.org) and UNOS for information and links. Additional information about transplantation, eligibility, performance statistics, policies, procedures, and other questions and answers, for both clinicians and patients, can be found on the Organ Procurement and Transplantation Network Web site (optn.transplant.hrsa.gov).
Annette Needham, MSN, ARNP, NP-C, CNN-NP, CCTC, Florida Hospital Transplant Center, Orlando

References
1. Armitage WJ, Tullo AB, Larkin DFP. The first successful full-thickness corneal transplant: a commentary on Eduard Zirm’s landmark paper of 1906. Br J Ophthalmol. 2006;90(10):1222-1223.

2. Kidney transplantation: past, present, and future. www.stanford.edu/dept/HPS/transplant/html/history.html. Accessed September 16, 2011.

3. United States Renal Data System. Atlas. www .usrds.org/atlas.htm. Accessed September 16, 2011.

4. National Kidney Foundation. End the wait! www.kidney.org/news/end_the_wait/index.cfm. Accessed September 16, 2011.

5. National Kidney Foundation. Kidney transplant (2011). www.kidney.org/atoz/content/kidneytransnewlease.cfm. Accessed September 16, 2011.

6. United States Renal Data Systems. Presentations and posters (2000-2011). www.usrds.org/presentations.htm. Accessed September 16, 2011.

7. Organ Procurement and Transplantation Network. Members: member directory. optn.transplant.hrsa.gov/members/search.asp. Accessed September 16, 2011.

8. Jensen P, Møller B, Hansen S. Skin cancer in kidney and heart transplant recipients and different long-term immunosuppressive therapy regimens. J Am Acad Dermatol. 2000;42(2 pt 1):307.

9. Wong G, Chapman JR, Craig JC. Cancer screening in renal transplant recipients: what is the evidence? Clin J Am Soc Nephrol. 2008;3 suppl 2:S87-S100.

10. Parker A, Bowles K, Bradley JA, et al; Haemato-oncology subgroup of the British Committee for Standards in Haematology and the British Transplantation Society. Diagnosis of post-transplant lymphoproliferative disorder in solid organ transplant patients. Br J Haematol. 2010;149(5):675-692.

11. Transplant Living. After the transplant (2011). www.transplantliving.org/afterthetransplant/default.aspx. Accessed September 16, 2011.

12. United Network for Organ Sharing. www.unos.org. Accessed September 16, 2011.

13. Kidney Disease Improving Global Outcomes. Managing your adult patients who have a kidney transplant (2010). www.kidney.org/professionals/tools/pdf/02-50-4079_ABB_ManagingTransRecip Bk_PC.pdf. Accessed September 16, 2011.

14. Abbud-Filho M, Adams P, Alberu J, et al. A report of the Lisbon Conference on the care of the kidney transplant recipient. Transplantation. 2007; (Suppl 8):83:1-22.

15. Heldal K, Hartmann A, Leivestad T, et al. Risk variables associated with the outcome of kidney recipients >70 years of age in the new millennium. Nephrol Dial Transplant. 2011;26(8):2706-2711.

16. Chava SP, Singh B, Stangou A, et al. Simultaneous combined liver and kidney transplantation: a single center experience. Clin Transplant. 2010; 24(3):E62-E68.

17. Ruiz R, Kunitake H, Wilkinson AH, et al. Long-term analysis of combined liver and kidney transplantation at a single center. Arch Surg. 2006;141 (8):735-741.

18. Veroux P, Veroux M, Puliatti C, et al. Kidney transplantation from hepatitis C virus-positive donors into hepatitis C virus-positive recipients: a safe way to expand the donor pool? Transplant Proc. 2005;37(6):2571-2573.

19. United States Renal Data Systems, Annual Data Reports. National Kidney and Urologic Disease Information Clearinghouse. Figure 6ii. Transplant (kidney only) wait list and wait times. www.usrds.org/2010/pdf/v2_07.pdf. Accessed September 16, 2011.

20. Arbor Research Collaborative for Health. Kidney waiting time calculator. www.ustransplant.org/Calculators/KidneyWaitTime.aspx. Accessed September 16, 2011.

21. Karakayali FY, Ozdemir H, Kivrakdal S, et al. Recurrent glomerular diseases after renal transplantation. Transplant Proc. 2006;38(2):470-472.

22. Nojima M, Ichikawa Y, Ihara H, et al. Significant effect of HLA-DRB1 matching on acute rejection of kidney transplants within 3 months. Transplant Proc. 2001;33(1-2):1182-1184.

For many years, the medical community speculated about the possibility of organ transplantation. The first successful transplant of any kind involving humans was a corneal transplant in 1905.¹

It wasn’t until 1954 that the first successful organ transplant, a kidney transplant between identical twins, occurred.² Several new concepts emerged: organ rejection plays a major role in the failure or success of a transplant; and donors and recipients must be matched based on blood group.

Today, about 169,000 people in the US live with a donated kidney. Each year, some 10,500 cadaveric organs are transplanted, and 6,400 donors are living donors.³ The National Kidney Foundation’s recent 10-year initiative, End the Wait!,⁴ seeks to close the gap between the more than 50,000 people on the transplant waiting list³ and the number of available donor organs.

Since many patients live for years with their transplanted organs, the primary care clinician is likely to see transplant recipients in a family practice or internal medicine setting. While each patient has unique needs, there are commonalities among them.

Renal Consult welcomes any additional comments or questions regarding care of the renal patient. Please address them to [email protected].
Jane S. Davis, CRNP, DNP

Q: I have a 70-year-old male patient who is losing kidney function. He asked me about transplantation, but I really don’t know whether he is eligible to get on the list. Who is eligible? Is there an age limit? Are patients with chronic illnesses (hepatitis B, hepatitis C, HIV) eligible? How long is the list? Where can I find these answers?

There are no specific guidelines regarding eligibility or age restrictions for kidney transplantation in the United States. Most transplant centers look at patients older than 65 a little more carefully than younger patients—they have to be in good health apart from their renal disease. Some centers will not transplant patients older than 70, while others transplant patients who are 80 or older.¹⁵ The best thing to do is to refer the patient to the local center or call and find out. Again, the Organ Procurement and Transplantation Network,⁷ which lists transplant centers and contact information, can be accessed at optn.transplant.hrsa.gov/mem bers/search.asp

Chronic illnesses are not automatic rule-outs for the most part. Very few centers transplant HIV-positive patients, but this does occur, especially in major cities with a large population of persons with HIV (eg, Washington, DC; San Francisco, New York City, Cincinnati). An infectious disease specialist must follow these patients after transplantation and adjust their HAART (highly active antiretroviral therapy) medications to compensate for both the decreased renal function and anti-rejection medications.  Hepatitis B and C patients are often accepted as long as liver biopsy shows no cirrhosis and the viral load is low or manageable. If the patient is found to have cirrhosis or decompensation, a combined liver-kidney transplant can be planned, although the success rate of this procedure is low.^16,17

Patients with certain types of hepatitis C may be eligible to receive a kidney from a donor with hepatitis C¹⁸ in order to shorten the wait time and make use of a kidney that cannot be transplanted into a person not infected with hepatitis C.

Transplant waiting lists vary by region across the country. There is a centralized electronic list managed by UNOS, on which eligible recipients are placed once they have been approved by the transplant center, following the medical work-up and acceptance by the transplant committee at each center. This is referred to as “being listed” or “on the list.” Patients begin to accrue waiting time as soon as they are added, and this list is precise to the second! There is a list for each blood type, with its own set of waiting times in each region.²⁰ Average waiting times, by blood type (ie, ABO), can be searched at www.ustransplant.org/Calcula tors/KidneyWaitTime.aspx

When a donor organ becomes available and has been evaluated by the procurement team, the donor’s information is entered into the system and the computer generates a list of eligible candidates, based on a variety of factors. This is called a “match-run.”

Waiting time is the most important factor, but consideration is given to patients younger than 18, those who have previously donated an organ, and those with high antibody levels (ie, panel-reactive antibodies, or PRAs). Patients in the latter group may find it more difficult to locate a compatible donor, as these patients have been sensitized as a result of prior transplantation, pregnancy, or blood transfusions. It is very rare for a patient to be a perfect match (0 mismatch), but should the right organ become available, the matched patient receives priority consideration.

Besides the ABO match, human leukocyte antigen (HLA) matching of six main HLA antibodies is done.  Within each of these six antibodies (HLA-A, B, C, DP, DR, DQ), subgroup matching is also done because some HLA subgroups are more highly correlated with rejection than others.^21,22 A more complete explanation of organ matching and allocation can be found on the “Transplant Living” Web site: www.transplantliving.org/beforethetransplant/allocation/matchingorgans.aspx.

Patients should be encouraged to access “Transplant Living” (www.transplantliving.org) and UNOS for information and links. Additional information about transplantation, eligibility, performance statistics, policies, procedures, and other questions and answers, for both clinicians and patients, can be found on the Organ Procurement and Transplantation Network Web site (optn.transplant.hrsa.gov).
Annette Needham, MSN, ARNP, NP-C, CNN-NP, CCTC, Florida Hospital Transplant Center, Orlando

References
1. Armitage WJ, Tullo AB, Larkin DFP. The first successful full-thickness corneal transplant: a commentary on Eduard Zirm’s landmark paper of 1906. Br J Ophthalmol. 2006;90(10):1222-1223.

2. Kidney transplantation: past, present, and future. www.stanford.edu/dept/HPS/transplant/html/history.html. Accessed September 16, 2011.

3. United States Renal Data System. Atlas. www .usrds.org/atlas.htm. Accessed September 16, 2011.

4. National Kidney Foundation. End the wait! www.kidney.org/news/end_the_wait/index.cfm. Accessed September 16, 2011.

5. National Kidney Foundation. Kidney transplant (2011). www.kidney.org/atoz/content/kidneytransnewlease.cfm. Accessed September 16, 2011.

6. United States Renal Data Systems. Presentations and posters (2000-2011). www.usrds.org/presentations.htm. Accessed September 16, 2011.

7. Organ Procurement and Transplantation Network. Members: member directory. optn.transplant.hrsa.gov/members/search.asp. Accessed September 16, 2011.

8. Jensen P, Møller B, Hansen S. Skin cancer in kidney and heart transplant recipients and different long-term immunosuppressive therapy regimens. J Am Acad Dermatol. 2000;42(2 pt 1):307.

9. Wong G, Chapman JR, Craig JC. Cancer screening in renal transplant recipients: what is the evidence? Clin J Am Soc Nephrol. 2008;3 suppl 2:S87-S100.

10. Parker A, Bowles K, Bradley JA, et al; Haemato-oncology subgroup of the British Committee for Standards in Haematology and the British Transplantation Society. Diagnosis of post-transplant lymphoproliferative disorder in solid organ transplant patients. Br J Haematol. 2010;149(5):675-692.

11. Transplant Living. After the transplant (2011). www.transplantliving.org/afterthetransplant/default.aspx. Accessed September 16, 2011.

12. United Network for Organ Sharing. www.unos.org. Accessed September 16, 2011.

13. Kidney Disease Improving Global Outcomes. Managing your adult patients who have a kidney transplant (2010). www.kidney.org/professionals/tools/pdf/02-50-4079_ABB_ManagingTransRecip Bk_PC.pdf. Accessed September 16, 2011.

14. Abbud-Filho M, Adams P, Alberu J, et al. A report of the Lisbon Conference on the care of the kidney transplant recipient. Transplantation. 2007; (Suppl 8):83:1-22.

15. Heldal K, Hartmann A, Leivestad T, et al. Risk variables associated with the outcome of kidney recipients >70 years of age in the new millennium. Nephrol Dial Transplant. 2011;26(8):2706-2711.

16. Chava SP, Singh B, Stangou A, et al. Simultaneous combined liver and kidney transplantation: a single center experience. Clin Transplant. 2010; 24(3):E62-E68.

17. Ruiz R, Kunitake H, Wilkinson AH, et al. Long-term analysis of combined liver and kidney transplantation at a single center. Arch Surg. 2006;141 (8):735-741.

18. Veroux P, Veroux M, Puliatti C, et al. Kidney transplantation from hepatitis C virus-positive donors into hepatitis C virus-positive recipients: a safe way to expand the donor pool? Transplant Proc. 2005;37(6):2571-2573.

19. United States Renal Data Systems, Annual Data Reports. National Kidney and Urologic Disease Information Clearinghouse. Figure 6ii. Transplant (kidney only) wait list and wait times. www.usrds.org/2010/pdf/v2_07.pdf. Accessed September 16, 2011.

20. Arbor Research Collaborative for Health. Kidney waiting time calculator. www.ustransplant.org/Calculators/KidneyWaitTime.aspx. Accessed September 16, 2011.

21. Karakayali FY, Ozdemir H, Kivrakdal S, et al. Recurrent glomerular diseases after renal transplantation. Transplant Proc. 2006;38(2):470-472.

22. Nojima M, Ichikawa Y, Ihara H, et al. Significant effect of HLA-DRB1 matching on acute rejection of kidney transplants within 3 months. Transplant Proc. 2001;33(1-2):1182-1184.

For many years, the medical community speculated about the possibility of organ transplantation. The first successful transplant of any kind involving humans was a corneal transplant in 1905.¹

It wasn’t until 1954 that the first successful organ transplant, a kidney transplant between identical twins, occurred.² Several new concepts emerged: organ rejection plays a major role in the failure or success of a transplant; and donors and recipients must be matched based on blood group.

Today, about 169,000 people in the US live with a donated kidney. Each year, some 10,500 cadaveric organs are transplanted, and 6,400 donors are living donors.³ The National Kidney Foundation’s recent 10-year initiative, End the Wait!,⁴ seeks to close the gap between the more than 50,000 people on the transplant waiting list³ and the number of available donor organs.

Since many patients live for years with their transplanted organs, the primary care clinician is likely to see transplant recipients in a family practice or internal medicine setting. While each patient has unique needs, there are commonalities among them.

Renal Consult welcomes any additional comments or questions regarding care of the renal patient. Please address them to [email protected].
Jane S. Davis, CRNP, DNP

Q: I have a 70-year-old male patient who is losing kidney function. He asked me about transplantation, but I really don’t know whether he is eligible to get on the list. Who is eligible? Is there an age limit? Are patients with chronic illnesses (hepatitis B, hepatitis C, HIV) eligible? How long is the list? Where can I find these answers?

There are no specific guidelines regarding eligibility or age restrictions for kidney transplantation in the United States. Most transplant centers look at patients older than 65 a little more carefully than younger patients—they have to be in good health apart from their renal disease. Some centers will not transplant patients older than 70, while others transplant patients who are 80 or older.¹⁵ The best thing to do is to refer the patient to the local center or call and find out. Again, the Organ Procurement and Transplantation Network,⁷ which lists transplant centers and contact information, can be accessed at optn.transplant.hrsa.gov/mem bers/search.asp

Chronic illnesses are not automatic rule-outs for the most part. Very few centers transplant HIV-positive patients, but this does occur, especially in major cities with a large population of persons with HIV (eg, Washington, DC; San Francisco, New York City, Cincinnati). An infectious disease specialist must follow these patients after transplantation and adjust their HAART (highly active antiretroviral therapy) medications to compensate for both the decreased renal function and anti-rejection medications.  Hepatitis B and C patients are often accepted as long as liver biopsy shows no cirrhosis and the viral load is low or manageable. If the patient is found to have cirrhosis or decompensation, a combined liver-kidney transplant can be planned, although the success rate of this procedure is low.^16,17

Patients with certain types of hepatitis C may be eligible to receive a kidney from a donor with hepatitis C¹⁸ in order to shorten the wait time and make use of a kidney that cannot be transplanted into a person not infected with hepatitis C.

Transplant waiting lists vary by region across the country. There is a centralized electronic list managed by UNOS, on which eligible recipients are placed once they have been approved by the transplant center, following the medical work-up and acceptance by the transplant committee at each center. This is referred to as “being listed” or “on the list.” Patients begin to accrue waiting time as soon as they are added, and this list is precise to the second! There is a list for each blood type, with its own set of waiting times in each region.²⁰ Average waiting times, by blood type (ie, ABO), can be searched at www.ustransplant.org/Calcula tors/KidneyWaitTime.aspx

When a donor organ becomes available and has been evaluated by the procurement team, the donor’s information is entered into the system and the computer generates a list of eligible candidates, based on a variety of factors. This is called a “match-run.”

Waiting time is the most important factor, but consideration is given to patients younger than 18, those who have previously donated an organ, and those with high antibody levels (ie, panel-reactive antibodies, or PRAs). Patients in the latter group may find it more difficult to locate a compatible donor, as these patients have been sensitized as a result of prior transplantation, pregnancy, or blood transfusions. It is very rare for a patient to be a perfect match (0 mismatch), but should the right organ become available, the matched patient receives priority consideration.

Besides the ABO match, human leukocyte antigen (HLA) matching of six main HLA antibodies is done.  Within each of these six antibodies (HLA-A, B, C, DP, DR, DQ), subgroup matching is also done because some HLA subgroups are more highly correlated with rejection than others.^21,22 A more complete explanation of organ matching and allocation can be found on the “Transplant Living” Web site: www.transplantliving.org/beforethetransplant/allocation/matchingorgans.aspx.

Patients should be encouraged to access “Transplant Living” (www.transplantliving.org) and UNOS for information and links. Additional information about transplantation, eligibility, performance statistics, policies, procedures, and other questions and answers, for both clinicians and patients, can be found on the Organ Procurement and Transplantation Network Web site (optn.transplant.hrsa.gov).
Annette Needham, MSN, ARNP, NP-C, CNN-NP, CCTC, Florida Hospital Transplant Center, Orlando

References
1. Armitage WJ, Tullo AB, Larkin DFP. The first successful full-thickness corneal transplant: a commentary on Eduard Zirm’s landmark paper of 1906. Br J Ophthalmol. 2006;90(10):1222-1223.

2. Kidney transplantation: past, present, and future. www.stanford.edu/dept/HPS/transplant/html/history.html. Accessed September 16, 2011.

3. United States Renal Data System. Atlas. www .usrds.org/atlas.htm. Accessed September 16, 2011.

4. National Kidney Foundation. End the wait! www.kidney.org/news/end_the_wait/index.cfm. Accessed September 16, 2011.

5. National Kidney Foundation. Kidney transplant (2011). www.kidney.org/atoz/content/kidneytransnewlease.cfm. Accessed September 16, 2011.

6. United States Renal Data Systems. Presentations and posters (2000-2011). www.usrds.org/presentations.htm. Accessed September 16, 2011.

7. Organ Procurement and Transplantation Network. Members: member directory. optn.transplant.hrsa.gov/members/search.asp. Accessed September 16, 2011.

8. Jensen P, Møller B, Hansen S. Skin cancer in kidney and heart transplant recipients and different long-term immunosuppressive therapy regimens. J Am Acad Dermatol. 2000;42(2 pt 1):307.

9. Wong G, Chapman JR, Craig JC. Cancer screening in renal transplant recipients: what is the evidence? Clin J Am Soc Nephrol. 2008;3 suppl 2:S87-S100.

10. Parker A, Bowles K, Bradley JA, et al; Haemato-oncology subgroup of the British Committee for Standards in Haematology and the British Transplantation Society. Diagnosis of post-transplant lymphoproliferative disorder in solid organ transplant patients. Br J Haematol. 2010;149(5):675-692.

11. Transplant Living. After the transplant (2011). www.transplantliving.org/afterthetransplant/default.aspx. Accessed September 16, 2011.

12. United Network for Organ Sharing. www.unos.org. Accessed September 16, 2011.

13. Kidney Disease Improving Global Outcomes. Managing your adult patients who have a kidney transplant (2010). www.kidney.org/professionals/tools/pdf/02-50-4079_ABB_ManagingTransRecip Bk_PC.pdf. Accessed September 16, 2011.

14. Abbud-Filho M, Adams P, Alberu J, et al. A report of the Lisbon Conference on the care of the kidney transplant recipient. Transplantation. 2007; (Suppl 8):83:1-22.

15. Heldal K, Hartmann A, Leivestad T, et al. Risk variables associated with the outcome of kidney recipients >70 years of age in the new millennium. Nephrol Dial Transplant. 2011;26(8):2706-2711.

16. Chava SP, Singh B, Stangou A, et al. Simultaneous combined liver and kidney transplantation: a single center experience. Clin Transplant. 2010; 24(3):E62-E68.

17. Ruiz R, Kunitake H, Wilkinson AH, et al. Long-term analysis of combined liver and kidney transplantation at a single center. Arch Surg. 2006;141 (8):735-741.

18. Veroux P, Veroux M, Puliatti C, et al. Kidney transplantation from hepatitis C virus-positive donors into hepatitis C virus-positive recipients: a safe way to expand the donor pool? Transplant Proc. 2005;37(6):2571-2573.

19. United States Renal Data Systems, Annual Data Reports. National Kidney and Urologic Disease Information Clearinghouse. Figure 6ii. Transplant (kidney only) wait list and wait times. www.usrds.org/2010/pdf/v2_07.pdf. Accessed September 16, 2011.

20. Arbor Research Collaborative for Health. Kidney waiting time calculator. www.ustransplant.org/Calculators/KidneyWaitTime.aspx. Accessed September 16, 2011.

21. Karakayali FY, Ozdemir H, Kivrakdal S, et al. Recurrent glomerular diseases after renal transplantation. Transplant Proc. 2006;38(2):470-472.

22. Nojima M, Ichikawa Y, Ihara H, et al. Significant effect of HLA-DRB1 matching on acute rejection of kidney transplants within 3 months. Transplant Proc. 2001;33(1-2):1182-1184.

For many years, the medical community speculated about the possibility of organ transplantation. The first successful transplant of any kind involving humans was a corneal transplant in 1905.¹

It wasn’t until 1954 that the first successful organ transplant, a kidney transplant between identical twins, occurred.² Several new concepts emerged: organ rejection plays a major role in the failure or success of a transplant; and donors and recipients must be matched based on blood group.

Today, about 169,000 people in the US live with a donated kidney. Each year, some 10,500 cadaveric organs are transplanted, and 6,400 donors are living donors.³ The National Kidney Foundation’s recent 10-year initiative, End the Wait!,⁴ seeks to close the gap between the more than 50,000 people on the transplant waiting list³ and the number of available donor organs.

Since many patients live for years with their transplanted organs, the primary care clinician is likely to see transplant recipients in a family practice or internal medicine setting. While each patient has unique needs, there are commonalities among them.

Renal Consult welcomes any additional comments or questions regarding care of the renal patient. Please address them to [email protected].
Jane S. Davis, CRNP, DNP

Q: I am in primary care and have a kidney transplant patient that I see annually for her Pap test and pelvic exam. Is there anything in particular that I am supposed to look for? I feel out of my comfort zone.

As with most people, preventive care is vital and posttransplant patients are no different. However, there are a few “special circumstances” to keep in mind.

Besides ascertaining that posttransplant patients are taking their medications every day, determine whether they have recently had a generic substituted for their regular anti-rejection meds. Many transplant medications have generic equivalents now; while we want changes made only with the approval of a transplant center, it is legal for a pharmacy to substitute a generic without notifying the transplant nephrologist. We have seen rejection, toxicities, or changes in creatinine levels due to substitution of generics—or even substitution from one generic equivalent to another. These medications have a small effective window and have to be closely monitored whenever different manufacturers are used.

In addition, some patients will stop taking their immunosuppressive drug, either because they “feel better” and don’t believe they need it anymore, or because they can no longer afford it. Medicare will only pay for 36 months of these medications, and patients often halve the dose or stop taking the medication altogether when the cost becomes too high.⁵

There is a very useful Web site on transplant medications from the United States Renal Data System.⁶ The site, which also offers a wealth of information on chronic kidney disease (CKD), is www.usrds.org/presentations.htm

Dosing for any medication is based on the patient’s glomerular filtration rate (GFR). Your transplant patients have been taught their baseline creatinine level, but some do forget. Even after transplant (whether of a kidney, a pancreas, a liver, lungs, or a heart), the immunosuppressive medications will affect the GFR, and the patient is a CKD patient.

If a patient’s creatinine level is 1.9 mg/dL (normal range, 0.6 to 1.2), but it has varied between 1.8 and 2.0 ever since the transplant and they are not having any other issues, this is “normal” for them and no cause for alarm. On the other hand, if the creatinine level is 1.9 mg/dL and the patient reports that it is always 1.2, they need immediate referral. If the patient is new to the area, you can find a local transplant center on the Organ Procurement and Transplantation Network directory⁷:  optn.transplant.hrsa.gov/mem bers/search.asp

Screening for infections and malignancies is another important aspect of posttransplant care. I advise all patients to see a dermatologist at least once annually, as the risk for skin cancer is increased sevenfold in a transplant patient, compared with the general population.⁸ Annual Pap test, pelvic exam, and mammogram are important for female posttransplant patients, as is annual prostate-specific antigen testing for male posttransplant patients older than 45 with a life expectancy of at least 10 years.⁹

During the physical exam, the clinician should always check for lymphadenopathy or any other “lumps and bumps,” as posttransplant lymphoproliferative disorder is also a risk associated with long-term immunosuppression.¹⁰ A wonderful online resource for patients and providers, “Transplant Living,”¹¹ has an excellent section on posttransplant care: www.transplantliving.org/af terthetransplant/default.aspx. This Web site is managed by the United Network of Organ Sharing¹² (UNOS; www.unos.org), the organization that manages organ transplantation and donation under contract with the federal government.

Routine vaccinations are recommended—especially pneumococcal vaccine and an annual flu shot. Diphtheria-pertussis-tetanus, hepatitis A, hepatitis B, inactivated polio, and typhoid are also acceptable vaccines for a transplant patient. Vaccines that are contraindicated after transplantation include varicella, bacillus Calmette-Guérin, smallpox, intranasal influenza, live oral typhoid, measles, mumps, rubella, oral polio, live Japanese B encephalitis, and yellow fever.^13,14

References
1. Armitage WJ, Tullo AB, Larkin DFP. The first successful full-thickness corneal transplant: a commentary on Eduard Zirm’s landmark paper of 1906. Br J Ophthalmol. 2006;90(10):1222-1223.

2. Kidney transplantation: past, present, and future. www.stanford.edu/dept/HPS/transplant/html/history.html. Accessed September 16, 2011.

3. United States Renal Data System. Atlas. www .usrds.org/atlas.htm. Accessed September 16, 2011.

4. National Kidney Foundation. End the wait! www.kidney.org/news/end_the_wait/index.cfm. Accessed September 16, 2011.

5. National Kidney Foundation. Kidney transplant (2011). www.kidney.org/atoz/content/kidneytransnewlease.cfm. Accessed September 16, 2011.

6. United States Renal Data Systems. Presentations and posters (2000-2011). www.usrds.org/presentations.htm. Accessed September 16, 2011.

7. Organ Procurement and Transplantation Network. Members: member directory. optn.transplant.hrsa.gov/members/search.asp. Accessed September 16, 2011.

8. Jensen P, Møller B, Hansen S. Skin cancer in kidney and heart transplant recipients and different long-term immunosuppressive therapy regimens. J Am Acad Dermatol. 2000;42(2 pt 1):307.

9. Wong G, Chapman JR, Craig JC. Cancer screening in renal transplant recipients: what is the evidence? Clin J Am Soc Nephrol. 2008;3 suppl 2:S87-S100.

10. Parker A, Bowles K, Bradley JA, et al; Haemato-oncology subgroup of the British Committee for Standards in Haematology and the British Transplantation Society. Diagnosis of post-transplant lymphoproliferative disorder in solid organ transplant patients. Br J Haematol. 2010;149(5):675-692.

11. Transplant Living. After the transplant (2011). www.transplantliving.org/afterthetransplant/default.aspx. Accessed September 16, 2011.

12. United Network for Organ Sharing. www.unos.org. Accessed September 16, 2011.

13. Kidney Disease Improving Global Outcomes. Managing your adult patients who have a kidney transplant (2010). www.kidney.org/professionals/tools/pdf/02-50-4079_ABB_ManagingTransRecip Bk_PC.pdf. Accessed September 16, 2011.

14. Abbud-Filho M, Adams P, Alberu J, et al. A report of the Lisbon Conference on the care of the kidney transplant recipient. Transplantation. 2007; (Suppl 8):83:1-22.

15. Heldal K, Hartmann A, Leivestad T, et al. Risk variables associated with the outcome of kidney recipients >70 years of age in the new millennium. Nephrol Dial Transplant. 2011;26(8):2706-2711.

16. Chava SP, Singh B, Stangou A, et al. Simultaneous combined liver and kidney transplantation: a single center experience. Clin Transplant. 2010; 24(3):E62-E68.

17. Ruiz R, Kunitake H, Wilkinson AH, et al. Long-term analysis of combined liver and kidney transplantation at a single center. Arch Surg. 2006;141 (8):735-741.

18. Veroux P, Veroux M, Puliatti C, et al. Kidney transplantation from hepatitis C virus-positive donors into hepatitis C virus-positive recipients: a safe way to expand the donor pool? Transplant Proc. 2005;37(6):2571-2573.

19. United States Renal Data Systems, Annual Data Reports. National Kidney and Urologic Disease Information Clearinghouse. Figure 6ii. Transplant (kidney only) wait list and wait times. www.usrds.org/2010/pdf/v2_07.pdf. Accessed September 16, 2011.

20. Arbor Research Collaborative for Health. Kidney waiting time calculator. www.ustransplant.org/Calculators/KidneyWaitTime.aspx. Accessed September 16, 2011.

21. Karakayali FY, Ozdemir H, Kivrakdal S, et al. Recurrent glomerular diseases after renal transplantation. Transplant Proc. 2006;38(2):470-472.

22. Nojima M, Ichikawa Y, Ihara H, et al. Significant effect of HLA-DRB1 matching on acute rejection of kidney transplants within 3 months. Transplant Proc. 2001;33(1-2):1182-1184.

For many years, the medical community speculated about the possibility of organ transplantation. The first successful transplant of any kind involving humans was a corneal transplant in 1905.¹

It wasn’t until 1954 that the first successful organ transplant, a kidney transplant between identical twins, occurred.² Several new concepts emerged: organ rejection plays a major role in the failure or success of a transplant; and donors and recipients must be matched based on blood group.

Today, about 169,000 people in the US live with a donated kidney. Each year, some 10,500 cadaveric organs are transplanted, and 6,400 donors are living donors.³ The National Kidney Foundation’s recent 10-year initiative, End the Wait!,⁴ seeks to close the gap between the more than 50,000 people on the transplant waiting list³ and the number of available donor organs.

Since many patients live for years with their transplanted organs, the primary care clinician is likely to see transplant recipients in a family practice or internal medicine setting. While each patient has unique needs, there are commonalities among them.

Renal Consult welcomes any additional comments or questions regarding care of the renal patient. Please address them to [email protected].
Jane S. Davis, CRNP, DNP

Q: I am in primary care and have a kidney transplant patient that I see annually for her Pap test and pelvic exam. Is there anything in particular that I am supposed to look for? I feel out of my comfort zone.

As with most people, preventive care is vital and posttransplant patients are no different. However, there are a few “special circumstances” to keep in mind.

Besides ascertaining that posttransplant patients are taking their medications every day, determine whether they have recently had a generic substituted for their regular anti-rejection meds. Many transplant medications have generic equivalents now; while we want changes made only with the approval of a transplant center, it is legal for a pharmacy to substitute a generic without notifying the transplant nephrologist. We have seen rejection, toxicities, or changes in creatinine levels due to substitution of generics—or even substitution from one generic equivalent to another. These medications have a small effective window and have to be closely monitored whenever different manufacturers are used.

In addition, some patients will stop taking their immunosuppressive drug, either because they “feel better” and don’t believe they need it anymore, or because they can no longer afford it. Medicare will only pay for 36 months of these medications, and patients often halve the dose or stop taking the medication altogether when the cost becomes too high.⁵

There is a very useful Web site on transplant medications from the United States Renal Data System.⁶ The site, which also offers a wealth of information on chronic kidney disease (CKD), is www.usrds.org/presentations.htm

Dosing for any medication is based on the patient’s glomerular filtration rate (GFR). Your transplant patients have been taught their baseline creatinine level, but some do forget. Even after transplant (whether of a kidney, a pancreas, a liver, lungs, or a heart), the immunosuppressive medications will affect the GFR, and the patient is a CKD patient.

If a patient’s creatinine level is 1.9 mg/dL (normal range, 0.6 to 1.2), but it has varied between 1.8 and 2.0 ever since the transplant and they are not having any other issues, this is “normal” for them and no cause for alarm. On the other hand, if the creatinine level is 1.9 mg/dL and the patient reports that it is always 1.2, they need immediate referral. If the patient is new to the area, you can find a local transplant center on the Organ Procurement and Transplantation Network directory⁷:  optn.transplant.hrsa.gov/mem bers/search.asp

Screening for infections and malignancies is another important aspect of posttransplant care. I advise all patients to see a dermatologist at least once annually, as the risk for skin cancer is increased sevenfold in a transplant patient, compared with the general population.⁸ Annual Pap test, pelvic exam, and mammogram are important for female posttransplant patients, as is annual prostate-specific antigen testing for male posttransplant patients older than 45 with a life expectancy of at least 10 years.⁹

During the physical exam, the clinician should always check for lymphadenopathy or any other “lumps and bumps,” as posttransplant lymphoproliferative disorder is also a risk associated with long-term immunosuppression.¹⁰ A wonderful online resource for patients and providers, “Transplant Living,”¹¹ has an excellent section on posttransplant care: www.transplantliving.org/af terthetransplant/default.aspx. This Web site is managed by the United Network of Organ Sharing¹² (UNOS; www.unos.org), the organization that manages organ transplantation and donation under contract with the federal government.

Routine vaccinations are recommended—especially pneumococcal vaccine and an annual flu shot. Diphtheria-pertussis-tetanus, hepatitis A, hepatitis B, inactivated polio, and typhoid are also acceptable vaccines for a transplant patient. Vaccines that are contraindicated after transplantation include varicella, bacillus Calmette-Guérin, smallpox, intranasal influenza, live oral typhoid, measles, mumps, rubella, oral polio, live Japanese B encephalitis, and yellow fever.^13,14

References
1. Armitage WJ, Tullo AB, Larkin DFP. The first successful full-thickness corneal transplant: a commentary on Eduard Zirm’s landmark paper of 1906. Br J Ophthalmol. 2006;90(10):1222-1223.

2. Kidney transplantation: past, present, and future. www.stanford.edu/dept/HPS/transplant/html/history.html. Accessed September 16, 2011.

3. United States Renal Data System. Atlas. www .usrds.org/atlas.htm. Accessed September 16, 2011.

4. National Kidney Foundation. End the wait! www.kidney.org/news/end_the_wait/index.cfm. Accessed September 16, 2011.

5. National Kidney Foundation. Kidney transplant (2011). www.kidney.org/atoz/content/kidneytransnewlease.cfm. Accessed September 16, 2011.

6. United States Renal Data Systems. Presentations and posters (2000-2011). www.usrds.org/presentations.htm. Accessed September 16, 2011.

7. Organ Procurement and Transplantation Network. Members: member directory. optn.transplant.hrsa.gov/members/search.asp. Accessed September 16, 2011.

8. Jensen P, Møller B, Hansen S. Skin cancer in kidney and heart transplant recipients and different long-term immunosuppressive therapy regimens. J Am Acad Dermatol. 2000;42(2 pt 1):307.

9. Wong G, Chapman JR, Craig JC. Cancer screening in renal transplant recipients: what is the evidence? Clin J Am Soc Nephrol. 2008;3 suppl 2:S87-S100.

10. Parker A, Bowles K, Bradley JA, et al; Haemato-oncology subgroup of the British Committee for Standards in Haematology and the British Transplantation Society. Diagnosis of post-transplant lymphoproliferative disorder in solid organ transplant patients. Br J Haematol. 2010;149(5):675-692.

11. Transplant Living. After the transplant (2011). www.transplantliving.org/afterthetransplant/default.aspx. Accessed September 16, 2011.

12. United Network for Organ Sharing. www.unos.org. Accessed September 16, 2011.

13. Kidney Disease Improving Global Outcomes. Managing your adult patients who have a kidney transplant (2010). www.kidney.org/professionals/tools/pdf/02-50-4079_ABB_ManagingTransRecip Bk_PC.pdf. Accessed September 16, 2011.

14. Abbud-Filho M, Adams P, Alberu J, et al. A report of the Lisbon Conference on the care of the kidney transplant recipient. Transplantation. 2007; (Suppl 8):83:1-22.

15. Heldal K, Hartmann A, Leivestad T, et al. Risk variables associated with the outcome of kidney recipients >70 years of age in the new millennium. Nephrol Dial Transplant. 2011;26(8):2706-2711.

16. Chava SP, Singh B, Stangou A, et al. Simultaneous combined liver and kidney transplantation: a single center experience. Clin Transplant. 2010; 24(3):E62-E68.

17. Ruiz R, Kunitake H, Wilkinson AH, et al. Long-term analysis of combined liver and kidney transplantation at a single center. Arch Surg. 2006;141 (8):735-741.

18. Veroux P, Veroux M, Puliatti C, et al. Kidney transplantation from hepatitis C virus-positive donors into hepatitis C virus-positive recipients: a safe way to expand the donor pool? Transplant Proc. 2005;37(6):2571-2573.

19. United States Renal Data Systems, Annual Data Reports. National Kidney and Urologic Disease Information Clearinghouse. Figure 6ii. Transplant (kidney only) wait list and wait times. www.usrds.org/2010/pdf/v2_07.pdf. Accessed September 16, 2011.

20. Arbor Research Collaborative for Health. Kidney waiting time calculator. www.ustransplant.org/Calculators/KidneyWaitTime.aspx. Accessed September 16, 2011.

21. Karakayali FY, Ozdemir H, Kivrakdal S, et al. Recurrent glomerular diseases after renal transplantation. Transplant Proc. 2006;38(2):470-472.

22. Nojima M, Ichikawa Y, Ihara H, et al. Significant effect of HLA-DRB1 matching on acute rejection of kidney transplants within 3 months. Transplant Proc. 2001;33(1-2):1182-1184.

For many years, the medical community speculated about the possibility of organ transplantation. The first successful transplant of any kind involving humans was a corneal transplant in 1905.¹

It wasn’t until 1954 that the first successful organ transplant, a kidney transplant between identical twins, occurred.² Several new concepts emerged: organ rejection plays a major role in the failure or success of a transplant; and donors and recipients must be matched based on blood group.

Today, about 169,000 people in the US live with a donated kidney. Each year, some 10,500 cadaveric organs are transplanted, and 6,400 donors are living donors.³ The National Kidney Foundation’s recent 10-year initiative, End the Wait!,⁴ seeks to close the gap between the more than 50,000 people on the transplant waiting list³ and the number of available donor organs.

Since many patients live for years with their transplanted organs, the primary care clinician is likely to see transplant recipients in a family practice or internal medicine setting. While each patient has unique needs, there are commonalities among them.

Renal Consult welcomes any additional comments or questions regarding care of the renal patient. Please address them to [email protected].
Jane S. Davis, CRNP, DNP

Q: I am in primary care and have a kidney transplant patient that I see annually for her Pap test and pelvic exam. Is there anything in particular that I am supposed to look for? I feel out of my comfort zone.

As with most people, preventive care is vital and posttransplant patients are no different. However, there are a few “special circumstances” to keep in mind.

Besides ascertaining that posttransplant patients are taking their medications every day, determine whether they have recently had a generic substituted for their regular anti-rejection meds. Many transplant medications have generic equivalents now; while we want changes made only with the approval of a transplant center, it is legal for a pharmacy to substitute a generic without notifying the transplant nephrologist. We have seen rejection, toxicities, or changes in creatinine levels due to substitution of generics—or even substitution from one generic equivalent to another. These medications have a small effective window and have to be closely monitored whenever different manufacturers are used.

In addition, some patients will stop taking their immunosuppressive drug, either because they “feel better” and don’t believe they need it anymore, or because they can no longer afford it. Medicare will only pay for 36 months of these medications, and patients often halve the dose or stop taking the medication altogether when the cost becomes too high.⁵

There is a very useful Web site on transplant medications from the United States Renal Data System.⁶ The site, which also offers a wealth of information on chronic kidney disease (CKD), is www.usrds.org/presentations.htm

Dosing for any medication is based on the patient’s glomerular filtration rate (GFR). Your transplant patients have been taught their baseline creatinine level, but some do forget. Even after transplant (whether of a kidney, a pancreas, a liver, lungs, or a heart), the immunosuppressive medications will affect the GFR, and the patient is a CKD patient.

If a patient’s creatinine level is 1.9 mg/dL (normal range, 0.6 to 1.2), but it has varied between 1.8 and 2.0 ever since the transplant and they are not having any other issues, this is “normal” for them and no cause for alarm. On the other hand, if the creatinine level is 1.9 mg/dL and the patient reports that it is always 1.2, they need immediate referral. If the patient is new to the area, you can find a local transplant center on the Organ Procurement and Transplantation Network directory⁷:  optn.transplant.hrsa.gov/mem bers/search.asp

Screening for infections and malignancies is another important aspect of posttransplant care. I advise all patients to see a dermatologist at least once annually, as the risk for skin cancer is increased sevenfold in a transplant patient, compared with the general population.⁸ Annual Pap test, pelvic exam, and mammogram are important for female posttransplant patients, as is annual prostate-specific antigen testing for male posttransplant patients older than 45 with a life expectancy of at least 10 years.⁹

During the physical exam, the clinician should always check for lymphadenopathy or any other “lumps and bumps,” as posttransplant lymphoproliferative disorder is also a risk associated with long-term immunosuppression.¹⁰ A wonderful online resource for patients and providers, “Transplant Living,”¹¹ has an excellent section on posttransplant care: www.transplantliving.org/af terthetransplant/default.aspx. This Web site is managed by the United Network of Organ Sharing¹² (UNOS; www.unos.org), the organization that manages organ transplantation and donation under contract with the federal government.

Routine vaccinations are recommended—especially pneumococcal vaccine and an annual flu shot. Diphtheria-pertussis-tetanus, hepatitis A, hepatitis B, inactivated polio, and typhoid are also acceptable vaccines for a transplant patient. Vaccines that are contraindicated after transplantation include varicella, bacillus Calmette-Guérin, smallpox, intranasal influenza, live oral typhoid, measles, mumps, rubella, oral polio, live Japanese B encephalitis, and yellow fever.^13,14

References
1. Armitage WJ, Tullo AB, Larkin DFP. The first successful full-thickness corneal transplant: a commentary on Eduard Zirm’s landmark paper of 1906. Br J Ophthalmol. 2006;90(10):1222-1223.

2. Kidney transplantation: past, present, and future. www.stanford.edu/dept/HPS/transplant/html/history.html. Accessed September 16, 2011.

3. United States Renal Data System. Atlas. www .usrds.org/atlas.htm. Accessed September 16, 2011.

4. National Kidney Foundation. End the wait! www.kidney.org/news/end_the_wait/index.cfm. Accessed September 16, 2011.

5. National Kidney Foundation. Kidney transplant (2011). www.kidney.org/atoz/content/kidneytransnewlease.cfm. Accessed September 16, 2011.

6. United States Renal Data Systems. Presentations and posters (2000-2011). www.usrds.org/presentations.htm. Accessed September 16, 2011.

7. Organ Procurement and Transplantation Network. Members: member directory. optn.transplant.hrsa.gov/members/search.asp. Accessed September 16, 2011.

8. Jensen P, Møller B, Hansen S. Skin cancer in kidney and heart transplant recipients and different long-term immunosuppressive therapy regimens. J Am Acad Dermatol. 2000;42(2 pt 1):307.

9. Wong G, Chapman JR, Craig JC. Cancer screening in renal transplant recipients: what is the evidence? Clin J Am Soc Nephrol. 2008;3 suppl 2:S87-S100.

10. Parker A, Bowles K, Bradley JA, et al; Haemato-oncology subgroup of the British Committee for Standards in Haematology and the British Transplantation Society. Diagnosis of post-transplant lymphoproliferative disorder in solid organ transplant patients. Br J Haematol. 2010;149(5):675-692.

11. Transplant Living. After the transplant (2011). www.transplantliving.org/afterthetransplant/default.aspx. Accessed September 16, 2011.

12. United Network for Organ Sharing. www.unos.org. Accessed September 16, 2011.

13. Kidney Disease Improving Global Outcomes. Managing your adult patients who have a kidney transplant (2010). www.kidney.org/professionals/tools/pdf/02-50-4079_ABB_ManagingTransRecip Bk_PC.pdf. Accessed September 16, 2011.

14. Abbud-Filho M, Adams P, Alberu J, et al. A report of the Lisbon Conference on the care of the kidney transplant recipient. Transplantation. 2007; (Suppl 8):83:1-22.

15. Heldal K, Hartmann A, Leivestad T, et al. Risk variables associated with the outcome of kidney recipients >70 years of age in the new millennium. Nephrol Dial Transplant. 2011;26(8):2706-2711.

16. Chava SP, Singh B, Stangou A, et al. Simultaneous combined liver and kidney transplantation: a single center experience. Clin Transplant. 2010; 24(3):E62-E68.

17. Ruiz R, Kunitake H, Wilkinson AH, et al. Long-term analysis of combined liver and kidney transplantation at a single center. Arch Surg. 2006;141 (8):735-741.

18. Veroux P, Veroux M, Puliatti C, et al. Kidney transplantation from hepatitis C virus-positive donors into hepatitis C virus-positive recipients: a safe way to expand the donor pool? Transplant Proc. 2005;37(6):2571-2573.

19. United States Renal Data Systems, Annual Data Reports. National Kidney and Urologic Disease Information Clearinghouse. Figure 6ii. Transplant (kidney only) wait list and wait times. www.usrds.org/2010/pdf/v2_07.pdf. Accessed September 16, 2011.

20. Arbor Research Collaborative for Health. Kidney waiting time calculator. www.ustransplant.org/Calculators/KidneyWaitTime.aspx. Accessed September 16, 2011.

21. Karakayali FY, Ozdemir H, Kivrakdal S, et al. Recurrent glomerular diseases after renal transplantation. Transplant Proc. 2006;38(2):470-472.

22. Nojima M, Ichikawa Y, Ihara H, et al. Significant effect of HLA-DRB1 matching on acute rejection of kidney transplants within 3 months. Transplant Proc. 2001;33(1-2):1182-1184.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: I was treating a patient for an uncomplicated urinary tract infection with trimethoprim–sulfamethoxazole (TMP-SMX). The pharmacist called and said the patient could not have any sulfa medications because she was going to donate a kidney to her brother. How do you explain this, and what should be my next step?

There is limited available evidence to support an answer to this question. Instead, I will provide a brief report of the available evidence, followed by the opinions of five experts in kidney transplantation.

TMP-SMX is a combination of two antimicrobial agents that act synergistically against a variety of bacteria.⁹ TMP decreases urinary excretion of potassium, leading to hyperkalemia—especially in persons with kidney disease or in those also taking other drugs that cause hyperkalemia.¹⁰ This scenario is unlikely, because the transplant team would have assessed the potential donor’s kidney function. When dosing the drug, clinicians should consider renal function and adjust the dose in those with a creatinine clearance less than or equal to 30 mL/min. Nephrotoxicity is uncommon in patients who take this drug; however, TMP is known to decrease tubular secretion of creatinine and may interfere with certain creatinine assays, leading to an artificial rise in serum creatinine. This is not reflective of a true reduction in the GFR and often is mild and reversible with discontinuation of the medication.

Querying experienced transplant professionals (two nephrologists, two transplant coordinators, and one doctoral-prepared pharmacist) yielded similar results. They all agreed that the only plausible reason to withhold TMP-SMX from this potential kidney donor was the risk of a transient rise in creatinine due to impaired secretion associated with TMP use. Many transplant teams recommend avoiding any medications that may affect the kidneys. So considering the lack of available evidence, I would recommend that you consult with the transplant team where your patient’s brother is receiving care before you prescribe TMP-SMX.

Debra Hain, PhD, APRN, GNP-BC
Florida Atlantic University, Boca Raton; Cleveland Clinic Florida; Department of Nephrology, Weston

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: I was treating a patient for an uncomplicated urinary tract infection with trimethoprim–sulfamethoxazole (TMP-SMX). The pharmacist called and said the patient could not have any sulfa medications because she was going to donate a kidney to her brother. How do you explain this, and what should be my next step?

There is limited available evidence to support an answer to this question. Instead, I will provide a brief report of the available evidence, followed by the opinions of five experts in kidney transplantation.

TMP-SMX is a combination of two antimicrobial agents that act synergistically against a variety of bacteria.⁹ TMP decreases urinary excretion of potassium, leading to hyperkalemia—especially in persons with kidney disease or in those also taking other drugs that cause hyperkalemia.¹⁰ This scenario is unlikely, because the transplant team would have assessed the potential donor’s kidney function. When dosing the drug, clinicians should consider renal function and adjust the dose in those with a creatinine clearance less than or equal to 30 mL/min. Nephrotoxicity is uncommon in patients who take this drug; however, TMP is known to decrease tubular secretion of creatinine and may interfere with certain creatinine assays, leading to an artificial rise in serum creatinine. This is not reflective of a true reduction in the GFR and often is mild and reversible with discontinuation of the medication.

Querying experienced transplant professionals (two nephrologists, two transplant coordinators, and one doctoral-prepared pharmacist) yielded similar results. They all agreed that the only plausible reason to withhold TMP-SMX from this potential kidney donor was the risk of a transient rise in creatinine due to impaired secretion associated with TMP use. Many transplant teams recommend avoiding any medications that may affect the kidneys. So considering the lack of available evidence, I would recommend that you consult with the transplant team where your patient’s brother is receiving care before you prescribe TMP-SMX.

Debra Hain, PhD, APRN, GNP-BC
Florida Atlantic University, Boca Raton; Cleveland Clinic Florida; Department of Nephrology, Weston

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: I was treating a patient for an uncomplicated urinary tract infection with trimethoprim–sulfamethoxazole (TMP-SMX). The pharmacist called and said the patient could not have any sulfa medications because she was going to donate a kidney to her brother. How do you explain this, and what should be my next step?

There is limited available evidence to support an answer to this question. Instead, I will provide a brief report of the available evidence, followed by the opinions of five experts in kidney transplantation.

TMP-SMX is a combination of two antimicrobial agents that act synergistically against a variety of bacteria.⁹ TMP decreases urinary excretion of potassium, leading to hyperkalemia—especially in persons with kidney disease or in those also taking other drugs that cause hyperkalemia.¹⁰ This scenario is unlikely, because the transplant team would have assessed the potential donor’s kidney function. When dosing the drug, clinicians should consider renal function and adjust the dose in those with a creatinine clearance less than or equal to 30 mL/min. Nephrotoxicity is uncommon in patients who take this drug; however, TMP is known to decrease tubular secretion of creatinine and may interfere with certain creatinine assays, leading to an artificial rise in serum creatinine. This is not reflective of a true reduction in the GFR and often is mild and reversible with discontinuation of the medication.

Querying experienced transplant professionals (two nephrologists, two transplant coordinators, and one doctoral-prepared pharmacist) yielded similar results. They all agreed that the only plausible reason to withhold TMP-SMX from this potential kidney donor was the risk of a transient rise in creatinine due to impaired secretion associated with TMP use. Many transplant teams recommend avoiding any medications that may affect the kidneys. So considering the lack of available evidence, I would recommend that you consult with the transplant team where your patient’s brother is receiving care before you prescribe TMP-SMX.

Debra Hain, PhD, APRN, GNP-BC
Florida Atlantic University, Boca Raton; Cleveland Clinic Florida; Department of Nephrology, Weston

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: I have a patient with CKD stage 4 (GFR, 30 mL/min/1.73m²). My supervising physician said to take him off his hydrochlorothiazide (50 mg qd) and start furosemide. Why do I do this, and at what dose do I start?

Thiazide diuretics work by blocking approximately 40% of sodium chloride reabsorption in the distal convoluting tubule of the nephron. This process increases the fractional excretion of sodium and provides a natriuresis with reduced blood pressure (BP). Thiazides also have a second mode of action in lowering BP by reducing peripheral vascular resistance.⁵

It is generally thought that thiazides are ineffective in patients with more advanced CKD because of more proximal sodium reabsorption in the nephron. This results in less sodium being delivered to the distal tubule and therefore less thiazide diuretic action in the distal tubule.⁵

The National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative (K/DOQI)⁶ recommends that hypertension in CKD be treated with combination therapy: renin-angiotensin system blockade (ACE inhibitor/angiotensin receptor blocker) and thiazide diuretics in patients with CKD stages 1 to 3; and loop diuretics in those with CKD stages 4 and 5. No large study has evaluated thiazide diuretic use in patients with CKD stages 4 and 5. In one small study (n = 7) in which thiazides were compared with loop diuretics, there was similar BP control between the groups, but patients in the thiazide group had superior urinary fractional sodium excretion.⁵

There is new concern that thiazides may partially contribute to the increased risk for metabolic syndrome or diabetes. Reungjui et al⁷ have used animal models to demonstrate that the hypokalemic and hyperuricemic effects of thiazides are the culprits for this risk. They recommend managing the potassium and uric acid levels to manage or prevent this risk.

When a change is made from thiazides to loop diuretics, K/DOQI recommends starting furosemide at 40 mg/d and titrating upward as needed for BP and edema control. In my experience, counseling patients to follow a low-sodium diet (the American Heart Association recommends restricting sodium intake to 1500 mg/d) allows for a lower dose of furosemide (20 mg) to be effective.⁸

Elizabeth Evans, DNP
Renal Medicine Associates, Albuquerque, NM

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: I have a patient with CKD stage 4 (GFR, 30 mL/min/1.73m²). My supervising physician said to take him off his hydrochlorothiazide (50 mg qd) and start furosemide. Why do I do this, and at what dose do I start?

Thiazide diuretics work by blocking approximately 40% of sodium chloride reabsorption in the distal convoluting tubule of the nephron. This process increases the fractional excretion of sodium and provides a natriuresis with reduced blood pressure (BP). Thiazides also have a second mode of action in lowering BP by reducing peripheral vascular resistance.⁵

It is generally thought that thiazides are ineffective in patients with more advanced CKD because of more proximal sodium reabsorption in the nephron. This results in less sodium being delivered to the distal tubule and therefore less thiazide diuretic action in the distal tubule.⁵

The National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative (K/DOQI)⁶ recommends that hypertension in CKD be treated with combination therapy: renin-angiotensin system blockade (ACE inhibitor/angiotensin receptor blocker) and thiazide diuretics in patients with CKD stages 1 to 3; and loop diuretics in those with CKD stages 4 and 5. No large study has evaluated thiazide diuretic use in patients with CKD stages 4 and 5. In one small study (n = 7) in which thiazides were compared with loop diuretics, there was similar BP control between the groups, but patients in the thiazide group had superior urinary fractional sodium excretion.⁵

There is new concern that thiazides may partially contribute to the increased risk for metabolic syndrome or diabetes. Reungjui et al⁷ have used animal models to demonstrate that the hypokalemic and hyperuricemic effects of thiazides are the culprits for this risk. They recommend managing the potassium and uric acid levels to manage or prevent this risk.

When a change is made from thiazides to loop diuretics, K/DOQI recommends starting furosemide at 40 mg/d and titrating upward as needed for BP and edema control. In my experience, counseling patients to follow a low-sodium diet (the American Heart Association recommends restricting sodium intake to 1500 mg/d) allows for a lower dose of furosemide (20 mg) to be effective.⁸

Elizabeth Evans, DNP
Renal Medicine Associates, Albuquerque, NM

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: I have a patient with CKD stage 4 (GFR, 30 mL/min/1.73m²). My supervising physician said to take him off his hydrochlorothiazide (50 mg qd) and start furosemide. Why do I do this, and at what dose do I start?

Thiazide diuretics work by blocking approximately 40% of sodium chloride reabsorption in the distal convoluting tubule of the nephron. This process increases the fractional excretion of sodium and provides a natriuresis with reduced blood pressure (BP). Thiazides also have a second mode of action in lowering BP by reducing peripheral vascular resistance.⁵

It is generally thought that thiazides are ineffective in patients with more advanced CKD because of more proximal sodium reabsorption in the nephron. This results in less sodium being delivered to the distal tubule and therefore less thiazide diuretic action in the distal tubule.⁵

The National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative (K/DOQI)⁶ recommends that hypertension in CKD be treated with combination therapy: renin-angiotensin system blockade (ACE inhibitor/angiotensin receptor blocker) and thiazide diuretics in patients with CKD stages 1 to 3; and loop diuretics in those with CKD stages 4 and 5. No large study has evaluated thiazide diuretic use in patients with CKD stages 4 and 5. In one small study (n = 7) in which thiazides were compared with loop diuretics, there was similar BP control between the groups, but patients in the thiazide group had superior urinary fractional sodium excretion.⁵

There is new concern that thiazides may partially contribute to the increased risk for metabolic syndrome or diabetes. Reungjui et al⁷ have used animal models to demonstrate that the hypokalemic and hyperuricemic effects of thiazides are the culprits for this risk. They recommend managing the potassium and uric acid levels to manage or prevent this risk.

When a change is made from thiazides to loop diuretics, K/DOQI recommends starting furosemide at 40 mg/d and titrating upward as needed for BP and edema control. In my experience, counseling patients to follow a low-sodium diet (the American Heart Association recommends restricting sodium intake to 1500 mg/d) allows for a lower dose of furosemide (20 mg) to be effective.⁸

Elizabeth Evans, DNP
Renal Medicine Associates, Albuquerque, NM

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: In my orthopedic practice, we have a woman we are treating conservatively for low back pain (NSAIDs, muscle relaxants, and physical therapy). Her primary care provider told her that she cannot take the NSAIDs because of her kidney disease (she has chronic kidney disease [CKD] stage 3). Is there a safe dose of NSAIDs that she can use, or do I need to start narcotics? I would rather not do that!

Unfortunately, all NSAIDs increase the risk for acute kidney injury (AKI) and may exacerbate progression to chronic renal failure, particularly when large doses are taken chronically.^3,4 Increased incidence of renal injury with NSAIDs has been seen in patients with existing CKD, hypertension, diabetes, and frequent hospitalizations.³ Most renal damage associated with NSAIDs is related to inhibition of prostaglandin synthesis (discussed below), but NSAIDs can also cause other types of kidney injury, such as interstitial nephritis, analgesic nephropathy, and membranous nephropathy. NSAID use is also associated with hyperkalemia, hyponatremia, and edema (sodium retention).

The primary mechanism of NSAID nephrotoxicity is inhibition of prostaglandin synthesis in the setting of decreased renal perfusion.³ Prostaglandins induce vasodilation of the afferent arterioles to maintain renal perfusion (and consequently GFR). If renal perfusion or effective fluid volume decreases (as in dehydration, diuretic therapy, heart failure, and cirrhosis), renal perfusion is maintained by increasing prostaglandin synthesis. NSAIDs block prostaglandin synthesis, therefore blunting this protective mechanism. Blocking prostaglandin with NSAIDs when renal perfusion is decreased can cause an AKI.

AKI can occur in patients with or without CKD, and it is associated with increased morbidity and mortality. AKI due to NSAID use may progress to end-stage renal disease if the NSAID is not stopped promptly. When NSAIDs are discontinued, renal function most often stabilizes, but residual renal insufficiency is likely to be permanent. In some patients, even after discontinuing the NSAID, the AKI progresses to more advanced kidney disease.

All NSAIDs carry the same risk for acute and chronic kidney disease, with little evidence to suggest that some are safer than others. Higher doses are more likely to cause renal damage, but dosing to prevent renal damage has not been defined. Indomethacin and ketorolac have most frequently been associated with AKI. If appropriate for the patient, acetaminophen 650 mg taken three times daily (scheduled, not “as needed”) can provide pain relief with less risk for kidney injury.

Additionally, narcotic medications are often necessary when treating severe pain in patients with high risk for NSAID-associated kidney injury.

Catherine Wells, DNP, ACNP, CNN-NP
University of Mississippi Health Care, Division of Nephrology, Jackson

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: In my orthopedic practice, we have a woman we are treating conservatively for low back pain (NSAIDs, muscle relaxants, and physical therapy). Her primary care provider told her that she cannot take the NSAIDs because of her kidney disease (she has chronic kidney disease [CKD] stage 3). Is there a safe dose of NSAIDs that she can use, or do I need to start narcotics? I would rather not do that!

Unfortunately, all NSAIDs increase the risk for acute kidney injury (AKI) and may exacerbate progression to chronic renal failure, particularly when large doses are taken chronically.^3,4 Increased incidence of renal injury with NSAIDs has been seen in patients with existing CKD, hypertension, diabetes, and frequent hospitalizations.³ Most renal damage associated with NSAIDs is related to inhibition of prostaglandin synthesis (discussed below), but NSAIDs can also cause other types of kidney injury, such as interstitial nephritis, analgesic nephropathy, and membranous nephropathy. NSAID use is also associated with hyperkalemia, hyponatremia, and edema (sodium retention).

The primary mechanism of NSAID nephrotoxicity is inhibition of prostaglandin synthesis in the setting of decreased renal perfusion.³ Prostaglandins induce vasodilation of the afferent arterioles to maintain renal perfusion (and consequently GFR). If renal perfusion or effective fluid volume decreases (as in dehydration, diuretic therapy, heart failure, and cirrhosis), renal perfusion is maintained by increasing prostaglandin synthesis. NSAIDs block prostaglandin synthesis, therefore blunting this protective mechanism. Blocking prostaglandin with NSAIDs when renal perfusion is decreased can cause an AKI.

AKI can occur in patients with or without CKD, and it is associated with increased morbidity and mortality. AKI due to NSAID use may progress to end-stage renal disease if the NSAID is not stopped promptly. When NSAIDs are discontinued, renal function most often stabilizes, but residual renal insufficiency is likely to be permanent. In some patients, even after discontinuing the NSAID, the AKI progresses to more advanced kidney disease.

All NSAIDs carry the same risk for acute and chronic kidney disease, with little evidence to suggest that some are safer than others. Higher doses are more likely to cause renal damage, but dosing to prevent renal damage has not been defined. Indomethacin and ketorolac have most frequently been associated with AKI. If appropriate for the patient, acetaminophen 650 mg taken three times daily (scheduled, not “as needed”) can provide pain relief with less risk for kidney injury.

Additionally, narcotic medications are often necessary when treating severe pain in patients with high risk for NSAID-associated kidney injury.

Catherine Wells, DNP, ACNP, CNN-NP
University of Mississippi Health Care, Division of Nephrology, Jackson

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: In my orthopedic practice, we have a woman we are treating conservatively for low back pain (NSAIDs, muscle relaxants, and physical therapy). Her primary care provider told her that she cannot take the NSAIDs because of her kidney disease (she has chronic kidney disease [CKD] stage 3). Is there a safe dose of NSAIDs that she can use, or do I need to start narcotics? I would rather not do that!

Unfortunately, all NSAIDs increase the risk for acute kidney injury (AKI) and may exacerbate progression to chronic renal failure, particularly when large doses are taken chronically.^3,4 Increased incidence of renal injury with NSAIDs has been seen in patients with existing CKD, hypertension, diabetes, and frequent hospitalizations.³ Most renal damage associated with NSAIDs is related to inhibition of prostaglandin synthesis (discussed below), but NSAIDs can also cause other types of kidney injury, such as interstitial nephritis, analgesic nephropathy, and membranous nephropathy. NSAID use is also associated with hyperkalemia, hyponatremia, and edema (sodium retention).

The primary mechanism of NSAID nephrotoxicity is inhibition of prostaglandin synthesis in the setting of decreased renal perfusion.³ Prostaglandins induce vasodilation of the afferent arterioles to maintain renal perfusion (and consequently GFR). If renal perfusion or effective fluid volume decreases (as in dehydration, diuretic therapy, heart failure, and cirrhosis), renal perfusion is maintained by increasing prostaglandin synthesis. NSAIDs block prostaglandin synthesis, therefore blunting this protective mechanism. Blocking prostaglandin with NSAIDs when renal perfusion is decreased can cause an AKI.

AKI can occur in patients with or without CKD, and it is associated with increased morbidity and mortality. AKI due to NSAID use may progress to end-stage renal disease if the NSAID is not stopped promptly. When NSAIDs are discontinued, renal function most often stabilizes, but residual renal insufficiency is likely to be permanent. In some patients, even after discontinuing the NSAID, the AKI progresses to more advanced kidney disease.

All NSAIDs carry the same risk for acute and chronic kidney disease, with little evidence to suggest that some are safer than others. Higher doses are more likely to cause renal damage, but dosing to prevent renal damage has not been defined. Indomethacin and ketorolac have most frequently been associated with AKI. If appropriate for the patient, acetaminophen 650 mg taken three times daily (scheduled, not “as needed”) can provide pain relief with less risk for kidney injury.

Additionally, narcotic medications are often necessary when treating severe pain in patients with high risk for NSAID-associated kidney injury.

Catherine Wells, DNP, ACNP, CNN-NP
University of Mississippi Health Care, Division of Nephrology, Jackson

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: I work in a cardiology practice. We received a note from the dialysis center telling us that one of our patients is hypotensive (systole < 100 mm Hg) during his dialysis treatment. His BP is usually 140/86 mm Hg in the office. Why the difference?

When considering BP values within this population, it is important to keep in mind that BP in dialysis patients can vary widely, with lower values in the period immediately following dialysis, then slowly increasing as patients’ fluid levels rise.

There are a few reasons why hypotension typically occurs during treatment. Taking sedating medication just before arriving for dialysis can dramatically lower BP during dialysis and should generally be avoided; advise the patient to take the medication after dialysis or at night instead.¹¹ Many antihypertensive drugs that are removed by dialysis are often prescribed to be taken at night.

Another common reason for hypotension during dialysis is large-volume fluid removal. Patients are advised to limit fluids between treatments to avoid fluid overload, thereby limiting the volume of removal needed. Incorrect dry weight calculations can also cause hypotension during dialysis; if a patient gains weight that is not fluid related and attempts are made to dialyze the patient to the dry weight, hypotension can occur.¹¹ The patient who sees another practitioner right before dialysis may appear volume-overloaded—or immediately after dialysis, may appear volume-depleted; neither impression is correct. Also, a 2- to 4-kg weight gain between dialysis treatments is acceptable.

It has been learned through observational research that hemodialysis patients tend to have higher mortality rates with a predialysis systolic BP (SBP) below 110 mm Hg, a postdialysis SBP greater than 180 mm Hg, or a postdialysis diastolic BP exceeding 110 mm Hg.¹² According to the National Kidney Foundation’s K/DOQI practice guidelines,¹³ a predialysis BP of 140/90 mm Hg and a postdialysis BP of 130/80 mm Hg are reasonable targets. However, as with all guidelines, goals must be individualized to fit the patient’s age, comorbidities, and symptoms.¹⁴ This is a delicate balance, and safe management requires ongoing communication between providers.

Of interest, researchers for the Dialysis Outcomes and Practice Patterns Study suggested that patients with a predialysis SBP of 110 to 130 mm Hg had a higher risk for mortality than those with an SBP of 130 to 140 mm Hg. The same study showed an increased risk for death in patients with predialysis SBP greater than 160 mm Hg.¹⁴

Kristina Unterseher, CNN-NP
Idaho Nephrology Associates, Boise

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: I work in a cardiology practice. We received a note from the dialysis center telling us that one of our patients is hypotensive (systole < 100 mm Hg) during his dialysis treatment. His BP is usually 140/86 mm Hg in the office. Why the difference?

When considering BP values within this population, it is important to keep in mind that BP in dialysis patients can vary widely, with lower values in the period immediately following dialysis, then slowly increasing as patients’ fluid levels rise.

There are a few reasons why hypotension typically occurs during treatment. Taking sedating medication just before arriving for dialysis can dramatically lower BP during dialysis and should generally be avoided; advise the patient to take the medication after dialysis or at night instead.¹¹ Many antihypertensive drugs that are removed by dialysis are often prescribed to be taken at night.

Another common reason for hypotension during dialysis is large-volume fluid removal. Patients are advised to limit fluids between treatments to avoid fluid overload, thereby limiting the volume of removal needed. Incorrect dry weight calculations can also cause hypotension during dialysis; if a patient gains weight that is not fluid related and attempts are made to dialyze the patient to the dry weight, hypotension can occur.¹¹ The patient who sees another practitioner right before dialysis may appear volume-overloaded—or immediately after dialysis, may appear volume-depleted; neither impression is correct. Also, a 2- to 4-kg weight gain between dialysis treatments is acceptable.

It has been learned through observational research that hemodialysis patients tend to have higher mortality rates with a predialysis systolic BP (SBP) below 110 mm Hg, a postdialysis SBP greater than 180 mm Hg, or a postdialysis diastolic BP exceeding 110 mm Hg.¹² According to the National Kidney Foundation’s K/DOQI practice guidelines,¹³ a predialysis BP of 140/90 mm Hg and a postdialysis BP of 130/80 mm Hg are reasonable targets. However, as with all guidelines, goals must be individualized to fit the patient’s age, comorbidities, and symptoms.¹⁴ This is a delicate balance, and safe management requires ongoing communication between providers.

Of interest, researchers for the Dialysis Outcomes and Practice Patterns Study suggested that patients with a predialysis SBP of 110 to 130 mm Hg had a higher risk for mortality than those with an SBP of 130 to 140 mm Hg. The same study showed an increased risk for death in patients with predialysis SBP greater than 160 mm Hg.¹⁴

Kristina Unterseher, CNN-NP
Idaho Nephrology Associates, Boise

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: I work in a cardiology practice. We received a note from the dialysis center telling us that one of our patients is hypotensive (systole < 100 mm Hg) during his dialysis treatment. His BP is usually 140/86 mm Hg in the office. Why the difference?

When considering BP values within this population, it is important to keep in mind that BP in dialysis patients can vary widely, with lower values in the period immediately following dialysis, then slowly increasing as patients’ fluid levels rise.

There are a few reasons why hypotension typically occurs during treatment. Taking sedating medication just before arriving for dialysis can dramatically lower BP during dialysis and should generally be avoided; advise the patient to take the medication after dialysis or at night instead.¹¹ Many antihypertensive drugs that are removed by dialysis are often prescribed to be taken at night.

Another common reason for hypotension during dialysis is large-volume fluid removal. Patients are advised to limit fluids between treatments to avoid fluid overload, thereby limiting the volume of removal needed. Incorrect dry weight calculations can also cause hypotension during dialysis; if a patient gains weight that is not fluid related and attempts are made to dialyze the patient to the dry weight, hypotension can occur.¹¹ The patient who sees another practitioner right before dialysis may appear volume-overloaded—or immediately after dialysis, may appear volume-depleted; neither impression is correct. Also, a 2- to 4-kg weight gain between dialysis treatments is acceptable.

It has been learned through observational research that hemodialysis patients tend to have higher mortality rates with a predialysis systolic BP (SBP) below 110 mm Hg, a postdialysis SBP greater than 180 mm Hg, or a postdialysis diastolic BP exceeding 110 mm Hg.¹² According to the National Kidney Foundation’s K/DOQI practice guidelines,¹³ a predialysis BP of 140/90 mm Hg and a postdialysis BP of 130/80 mm Hg are reasonable targets. However, as with all guidelines, goals must be individualized to fit the patient’s age, comorbidities, and symptoms.¹⁴ This is a delicate balance, and safe management requires ongoing communication between providers.

Of interest, researchers for the Dialysis Outcomes and Practice Patterns Study suggested that patients with a predialysis SBP of 110 to 130 mm Hg had a higher risk for mortality than those with an SBP of 130 to 140 mm Hg. The same study showed an increased risk for death in patients with predialysis SBP greater than 160 mm Hg.¹⁴

Kristina Unterseher, CNN-NP
Idaho Nephrology Associates, Boise

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.