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Q) I have a patient with stage 3a chronic kidney disease (glomerular filtration rate, 45-60 mL/min/1.73 m2). I have her on a statin and an ACE inhibitor. Is there anything else I can do to slow the progression of kidney disease?
For patients with stage 3a chronic kidney disease (CKD), ongoing evaluation of risk factors and management can impact the rate of disease progression. The cornerstones of CKD care include identification and treatment of the cause; management of hypertension, albuminuria, and diabetes (if applicable); reduction of cardiovascular (CV) risk; and correction of metabolic abnormalities.5
When considering factors that can contribute to kidney injury, clinicians should consider possible pre-, intra-, and post-renal processes that could potentially cause injury.
Prerenal: Approximately 20% of cardiac output is directed to the kidneys. Reduced left ventricular function, diastolic dysfunction, and pulmonary hypertension can all contribute to a reduction in renal blood flow and subsequent kidney injury.6
Intrarenal: Exploration of possible intra-renal processes begins with a thorough history of any familial disease, hematuria, stones, proteinuria, and exposure to nephrotoxins. The nephrotoxicity profile of all medications should be examined, and patients should be educated about products, particularly OTC medications (eg, NSAIDs, common cold preparations, and herbal or weight-loss products), that can be harmful to the kidneys. Patients should also be made aware of the risk for contrast-induced renal injury, especially when considering imaging or cardiac testing. Since diabetes is a leading cause of kidney disease, good diabetic control can reduce nephropathy and slow disease progression.
Postrenal: Benign prostatic hypertrophy, kidney stones, and neurogenic bladder can all cause injury. These warrant further evaluation and treatment.
CKD often worsens existing hypertension, which is an independent risk factor for kidney failure.7 Goal blood pressure (BP) for all patients without significant albuminuria should be < 140/90 mm Hg; for those with urinary albumin ≥ 30 mg/24 h, the goal is < 130/80 mm Hg.8 Choice of antihypertensive agents can be tailored to other comorbidities, but an ACE inhibitor or angiotensin receptor blocker should be considered firstline treatment. Nocturnal hypertension is common in patients with CKD and an independent marker of CV risk. By dosing antihypertensive medications at bedtime, the clinician supports CV risk reduction.9
CKD is an independent risk factor for CV disease, thus risk factor modification should be aggressively pursued. Regardless of the cause of CKD, cigarette smoking has been associated with a more rapid decline in renal function. Patients should be counseled on the risks and offered interventions to assist in smoking cessation.10 There is also emerging evidence that exercise likely benefits the vascular health of the kidneys and appears to slow the rate of kidney decline.11,12 Overall, lifestyle interventions that help mitigate CV risk may directly benefit preservation of kidney function as well.
Metabolic abnormalities increase with CKD progression. Maintaining proper bone health through control of phosphate/acidosis and calcium equilibrium reduces morbidity as it relates to vascular and soft-tissue calcification. This can often be effectively managed through dietary modifications in early to moderate CKD. As the number of functioning nephrons decrease in CKD, so does the ability of the kidney to maintain proper acid/base balance. Persistent metabolic acidosis is related to CKD progression. Acid buffering with oral bicarbonate may be needed to achieve a goal CO2 of 22 to 32 mEq/L.8
Through adoption of a comprehensive approach—one that is inclusive of the patient—optimal outcomes can be achieved for this rapidly growing and often underrecognized population. —CJ, AH-B, IS, BB
Crystal Johnson, PA-C
Angela Harker-Bacchus, FNP-BC
Irina Sadovskaya, PA-C
Beverly Benmoussa, FNP-BC
Transplant Nephrology Extra-Renal CKD Clinic, University of Michigan
References
5. Murphree DD, Thelen SM. Chronic kidney disease in primary care. J Am Board Fam Med. 2010;23(4):542-550.
6. Coppolino G, Presta P, Saturno L, Fuiano G. Acute kidney injury in patients undergoing cardiac surgery. J Nephrol. 2013;26(1):32-40.
7. Ravera M, Re M, Defarri L, et al. Importance of blood pressure control in chronic kidney disease. J Am Soc Nephrol. 2006;17(4 suppl 2):S98-S103.
8. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2013;3(suppl):1-150.
9. Hermida RC, Ayala DE, Mojón A, Fernández JR. Bedtime dosing of antihypertensive medications reduces cardiovascular risk in CKD. J Am Soc Nephrol. 2011;22(12):2313-2321.
10. Ricardo AC, Anderson CA, Yang W, et al. Healthy lifestyle and risk of kidney disease progression, atherosclerotic events, and death in CKD: findings from the Chronic Renal Insufficiency Cohort (CRIC) study. Am J Kidney Dis. 2015;65(3):412-424.
11. Gould DW, Graham-Brown MPM, Watson EL, et al. Physiological benefits of exercise in pre-dialysis chronic kidney disease. Nephrology (Carlton). 2014;19(9):519-527.
12. Robinson-Cohen C, Littman AJ, Duncan GE, et al. Physical activity and change in estimated GFR among persons with CKD. J Am Soc Nephrol. 2014;25(2):399-406.
| Clinician Reviews in partnership with |
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Renal Consult is edited by Jane S. Davis, CRNP, DNP, a member of the Clinician Reviews editorial board, who is a nurse practitioner in the Division of Nephrology at the University of Alabama at Birmingham and is the communications chairperson for the National Kidney Foundation’s Council of Advanced Practitioners (NKF-CAP); and Kim Zuber, PA-C, MSPS, DFAAPA, a retired PA who works with the American Academy of Nephrology PAs and is also past chair of the NKF-CAP. This month’s responses were authored by Cindy Smith, DNP, APRN, CNN-NP, FNP-BC, who practices with Renal Consultants, PLLC, in South Charleston, West Virgina, and Crystal Johnson, PA-C, Angela Harker-Bacchus, FNP-BC, Irina Sadovskaya, PA-C, and Beverly Benmoussa, FNP-BC, who practice in the Transplant Nephrology Extra-Renal CKD Clinic at the University of Michigan.
| Clinician Reviews in partnership with |
|
Renal Consult is edited by Jane S. Davis, CRNP, DNP, a member of the Clinician Reviews editorial board, who is a nurse practitioner in the Division of Nephrology at the University of Alabama at Birmingham and is the communications chairperson for the National Kidney Foundation’s Council of Advanced Practitioners (NKF-CAP); and Kim Zuber, PA-C, MSPS, DFAAPA, a retired PA who works with the American Academy of Nephrology PAs and is also past chair of the NKF-CAP. This month’s responses were authored by Cindy Smith, DNP, APRN, CNN-NP, FNP-BC, who practices with Renal Consultants, PLLC, in South Charleston, West Virgina, and Crystal Johnson, PA-C, Angela Harker-Bacchus, FNP-BC, Irina Sadovskaya, PA-C, and Beverly Benmoussa, FNP-BC, who practice in the Transplant Nephrology Extra-Renal CKD Clinic at the University of Michigan.
| Clinician Reviews in partnership with |
|
Renal Consult is edited by Jane S. Davis, CRNP, DNP, a member of the Clinician Reviews editorial board, who is a nurse practitioner in the Division of Nephrology at the University of Alabama at Birmingham and is the communications chairperson for the National Kidney Foundation’s Council of Advanced Practitioners (NKF-CAP); and Kim Zuber, PA-C, MSPS, DFAAPA, a retired PA who works with the American Academy of Nephrology PAs and is also past chair of the NKF-CAP. This month’s responses were authored by Cindy Smith, DNP, APRN, CNN-NP, FNP-BC, who practices with Renal Consultants, PLLC, in South Charleston, West Virgina, and Crystal Johnson, PA-C, Angela Harker-Bacchus, FNP-BC, Irina Sadovskaya, PA-C, and Beverly Benmoussa, FNP-BC, who practice in the Transplant Nephrology Extra-Renal CKD Clinic at the University of Michigan.
Q) I have a patient with stage 3a chronic kidney disease (glomerular filtration rate, 45-60 mL/min/1.73 m2). I have her on a statin and an ACE inhibitor. Is there anything else I can do to slow the progression of kidney disease?
For patients with stage 3a chronic kidney disease (CKD), ongoing evaluation of risk factors and management can impact the rate of disease progression. The cornerstones of CKD care include identification and treatment of the cause; management of hypertension, albuminuria, and diabetes (if applicable); reduction of cardiovascular (CV) risk; and correction of metabolic abnormalities.5
When considering factors that can contribute to kidney injury, clinicians should consider possible pre-, intra-, and post-renal processes that could potentially cause injury.
Prerenal: Approximately 20% of cardiac output is directed to the kidneys. Reduced left ventricular function, diastolic dysfunction, and pulmonary hypertension can all contribute to a reduction in renal blood flow and subsequent kidney injury.6
Intrarenal: Exploration of possible intra-renal processes begins with a thorough history of any familial disease, hematuria, stones, proteinuria, and exposure to nephrotoxins. The nephrotoxicity profile of all medications should be examined, and patients should be educated about products, particularly OTC medications (eg, NSAIDs, common cold preparations, and herbal or weight-loss products), that can be harmful to the kidneys. Patients should also be made aware of the risk for contrast-induced renal injury, especially when considering imaging or cardiac testing. Since diabetes is a leading cause of kidney disease, good diabetic control can reduce nephropathy and slow disease progression.
Postrenal: Benign prostatic hypertrophy, kidney stones, and neurogenic bladder can all cause injury. These warrant further evaluation and treatment.
CKD often worsens existing hypertension, which is an independent risk factor for kidney failure.7 Goal blood pressure (BP) for all patients without significant albuminuria should be < 140/90 mm Hg; for those with urinary albumin ≥ 30 mg/24 h, the goal is < 130/80 mm Hg.8 Choice of antihypertensive agents can be tailored to other comorbidities, but an ACE inhibitor or angiotensin receptor blocker should be considered firstline treatment. Nocturnal hypertension is common in patients with CKD and an independent marker of CV risk. By dosing antihypertensive medications at bedtime, the clinician supports CV risk reduction.9
CKD is an independent risk factor for CV disease, thus risk factor modification should be aggressively pursued. Regardless of the cause of CKD, cigarette smoking has been associated with a more rapid decline in renal function. Patients should be counseled on the risks and offered interventions to assist in smoking cessation.10 There is also emerging evidence that exercise likely benefits the vascular health of the kidneys and appears to slow the rate of kidney decline.11,12 Overall, lifestyle interventions that help mitigate CV risk may directly benefit preservation of kidney function as well.
Metabolic abnormalities increase with CKD progression. Maintaining proper bone health through control of phosphate/acidosis and calcium equilibrium reduces morbidity as it relates to vascular and soft-tissue calcification. This can often be effectively managed through dietary modifications in early to moderate CKD. As the number of functioning nephrons decrease in CKD, so does the ability of the kidney to maintain proper acid/base balance. Persistent metabolic acidosis is related to CKD progression. Acid buffering with oral bicarbonate may be needed to achieve a goal CO2 of 22 to 32 mEq/L.8
Through adoption of a comprehensive approach—one that is inclusive of the patient—optimal outcomes can be achieved for this rapidly growing and often underrecognized population. —CJ, AH-B, IS, BB
Crystal Johnson, PA-C
Angela Harker-Bacchus, FNP-BC
Irina Sadovskaya, PA-C
Beverly Benmoussa, FNP-BC
Transplant Nephrology Extra-Renal CKD Clinic, University of Michigan
References
5. Murphree DD, Thelen SM. Chronic kidney disease in primary care. J Am Board Fam Med. 2010;23(4):542-550.
6. Coppolino G, Presta P, Saturno L, Fuiano G. Acute kidney injury in patients undergoing cardiac surgery. J Nephrol. 2013;26(1):32-40.
7. Ravera M, Re M, Defarri L, et al. Importance of blood pressure control in chronic kidney disease. J Am Soc Nephrol. 2006;17(4 suppl 2):S98-S103.
8. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2013;3(suppl):1-150.
9. Hermida RC, Ayala DE, Mojón A, Fernández JR. Bedtime dosing of antihypertensive medications reduces cardiovascular risk in CKD. J Am Soc Nephrol. 2011;22(12):2313-2321.
10. Ricardo AC, Anderson CA, Yang W, et al. Healthy lifestyle and risk of kidney disease progression, atherosclerotic events, and death in CKD: findings from the Chronic Renal Insufficiency Cohort (CRIC) study. Am J Kidney Dis. 2015;65(3):412-424.
11. Gould DW, Graham-Brown MPM, Watson EL, et al. Physiological benefits of exercise in pre-dialysis chronic kidney disease. Nephrology (Carlton). 2014;19(9):519-527.
12. Robinson-Cohen C, Littman AJ, Duncan GE, et al. Physical activity and change in estimated GFR among persons with CKD. J Am Soc Nephrol. 2014;25(2):399-406.
Q) I have a patient with stage 3a chronic kidney disease (glomerular filtration rate, 45-60 mL/min/1.73 m2). I have her on a statin and an ACE inhibitor. Is there anything else I can do to slow the progression of kidney disease?
For patients with stage 3a chronic kidney disease (CKD), ongoing evaluation of risk factors and management can impact the rate of disease progression. The cornerstones of CKD care include identification and treatment of the cause; management of hypertension, albuminuria, and diabetes (if applicable); reduction of cardiovascular (CV) risk; and correction of metabolic abnormalities.5
When considering factors that can contribute to kidney injury, clinicians should consider possible pre-, intra-, and post-renal processes that could potentially cause injury.
Prerenal: Approximately 20% of cardiac output is directed to the kidneys. Reduced left ventricular function, diastolic dysfunction, and pulmonary hypertension can all contribute to a reduction in renal blood flow and subsequent kidney injury.6
Intrarenal: Exploration of possible intra-renal processes begins with a thorough history of any familial disease, hematuria, stones, proteinuria, and exposure to nephrotoxins. The nephrotoxicity profile of all medications should be examined, and patients should be educated about products, particularly OTC medications (eg, NSAIDs, common cold preparations, and herbal or weight-loss products), that can be harmful to the kidneys. Patients should also be made aware of the risk for contrast-induced renal injury, especially when considering imaging or cardiac testing. Since diabetes is a leading cause of kidney disease, good diabetic control can reduce nephropathy and slow disease progression.
Postrenal: Benign prostatic hypertrophy, kidney stones, and neurogenic bladder can all cause injury. These warrant further evaluation and treatment.
CKD often worsens existing hypertension, which is an independent risk factor for kidney failure.7 Goal blood pressure (BP) for all patients without significant albuminuria should be < 140/90 mm Hg; for those with urinary albumin ≥ 30 mg/24 h, the goal is < 130/80 mm Hg.8 Choice of antihypertensive agents can be tailored to other comorbidities, but an ACE inhibitor or angiotensin receptor blocker should be considered firstline treatment. Nocturnal hypertension is common in patients with CKD and an independent marker of CV risk. By dosing antihypertensive medications at bedtime, the clinician supports CV risk reduction.9
CKD is an independent risk factor for CV disease, thus risk factor modification should be aggressively pursued. Regardless of the cause of CKD, cigarette smoking has been associated with a more rapid decline in renal function. Patients should be counseled on the risks and offered interventions to assist in smoking cessation.10 There is also emerging evidence that exercise likely benefits the vascular health of the kidneys and appears to slow the rate of kidney decline.11,12 Overall, lifestyle interventions that help mitigate CV risk may directly benefit preservation of kidney function as well.
Metabolic abnormalities increase with CKD progression. Maintaining proper bone health through control of phosphate/acidosis and calcium equilibrium reduces morbidity as it relates to vascular and soft-tissue calcification. This can often be effectively managed through dietary modifications in early to moderate CKD. As the number of functioning nephrons decrease in CKD, so does the ability of the kidney to maintain proper acid/base balance. Persistent metabolic acidosis is related to CKD progression. Acid buffering with oral bicarbonate may be needed to achieve a goal CO2 of 22 to 32 mEq/L.8
Through adoption of a comprehensive approach—one that is inclusive of the patient—optimal outcomes can be achieved for this rapidly growing and often underrecognized population. —CJ, AH-B, IS, BB
Crystal Johnson, PA-C
Angela Harker-Bacchus, FNP-BC
Irina Sadovskaya, PA-C
Beverly Benmoussa, FNP-BC
Transplant Nephrology Extra-Renal CKD Clinic, University of Michigan
References
5. Murphree DD, Thelen SM. Chronic kidney disease in primary care. J Am Board Fam Med. 2010;23(4):542-550.
6. Coppolino G, Presta P, Saturno L, Fuiano G. Acute kidney injury in patients undergoing cardiac surgery. J Nephrol. 2013;26(1):32-40.
7. Ravera M, Re M, Defarri L, et al. Importance of blood pressure control in chronic kidney disease. J Am Soc Nephrol. 2006;17(4 suppl 2):S98-S103.
8. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2013;3(suppl):1-150.
9. Hermida RC, Ayala DE, Mojón A, Fernández JR. Bedtime dosing of antihypertensive medications reduces cardiovascular risk in CKD. J Am Soc Nephrol. 2011;22(12):2313-2321.
10. Ricardo AC, Anderson CA, Yang W, et al. Healthy lifestyle and risk of kidney disease progression, atherosclerotic events, and death in CKD: findings from the Chronic Renal Insufficiency Cohort (CRIC) study. Am J Kidney Dis. 2015;65(3):412-424.
11. Gould DW, Graham-Brown MPM, Watson EL, et al. Physiological benefits of exercise in pre-dialysis chronic kidney disease. Nephrology (Carlton). 2014;19(9):519-527.
12. Robinson-Cohen C, Littman AJ, Duncan GE, et al. Physical activity and change in estimated GFR among persons with CKD. J Am Soc Nephrol. 2014;25(2):399-406.