Sections

Treatment

Approach Considerations

Early diagnosis and treatment of the underlying cause and/or the institution of secondary preventive measures are imperative in patients with chronic kidney disease (CKD). These steps may delay, or possibly halt, progression of the disease. Early referral to a nephrologist is of extreme importance.

The medical care of patients with CKD should focus on the following:

Delaying or halting the progression of CKD
Diagnosing and treating the pathologic manifestations of CKD
Timely planning for long-term renal replacement therapy

In 2014, the Canadian Society of Nephrology released new guidelines that recommend delaying dialysis in CKD patients without symptoms until their estimated glomerular filtration rate (eGFR) drops to 6 mL/min/1.73 m² or until the first onset of a clinical indication (which includes uremia, fluid overload, and refractory hyperkalemia or acidemia).^{[56, 57]}To ensure prompt recognition of that threshold, close monitoring should begin when eGFR reaches 15 mL/min/1.73 m². Additional factors that may affect dialysis initiation include patient education and modality selection, the severity of existing uremic symptoms, and the rate of renal function decline.^{[56, 57]}

Patients with CKD acutely presenting with indications for dialytic therapy should be transferred to a hospital center where acute dialysis can be performed.

The National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative (KDOQI) has issued several clinical practice guidelines for managing all stages of CKD and related complications in adults. The American Diabetes Association has published clinical practice recommendations on CKD and risk management in patients with diabetes mellitus.^[58]

Delaying or Halting Progression of Chronic Kidney Disease

Measures indicated to delay or halt the progression of chronic kidney disease (CKD) are as follows:

Treatment of the underlying condition if possible
Aggressive blood pressure control to target values per current guidelines
Treatment of hyperlipidemia to target levels per current guidelines
Aggressive glycemic control per the American Diabetes Association (ADA) recommendations (target hemoglobin A1c [HbA1C] < 7%)
Avoidance of nephrotoxins, including intravenous (IV) radiocontrast media, nonsteroidal anti-inflammatory drugs (NSAIDs), and aminoglycosides
Use of renin-angiotensin system (RAS) blockers in patients with diabetic kidney disease (DKD) and proteinuria
Use of sodium–glucose cotransporter 2 (SGLT2) inhibitors
Use of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin-receptor blockers (ARBs) in patients with proteinuria
Use of nonsteroidal mineralocorticoid receptor (MR) antagonists

A prospective cohort study indicated that in patients with advanced CKD and stable hypertension, antihypertensive treatment with ACEIs or ARBs reduces the likelihood of long-term dialysis and lowers the mortality risk as well.^{[59, 60]}

The study involved 28,497 predialysis patients with advanced CKD, hypertension, and anemia. Based on a median follow-up period of 7 months, the investigators found that in those patients who were treated with ACEIs or ARBs, the need for long-term dialysis was 6% lower than in patients who were not treated with these drugs, with the composite outcome of long-term dialysis or death also being 6% lower. The rate of hyperkalemia-associated hospitalization was higher in the ACEI/ARB patients, but no significant increase was found in hyperkalemia-related predialysis mortality.^{[59, 60]}

A retrospective simulation study found that in older patients with CKD, ACEIs and ARBs provided only marginal benefit in preventing progression to end-stage renal disease (ESRD). Among over 370,000 CKD patients aged 70 years and older, the number needed to treat (NNT) to prevent 1 case of ESRD was more than 100 for most patients (even with an exposure time of > 10 y). In younger patients, the the NNT ranged from 9-25. The investigators suggested that the reduced benefits in older patients may reflect differences in baseline risk and life expectancy between older and younger patients.^[61]

Treatment with SGLT2 inhibitors may improve kidney outcomes, especially in patients with DKD. The CREDENCE trial—a double-blind, randomized study of the addition of canagliflozin to RAS blockade in 4401 patients with type 2 diabetes mellitus (T2DM) and CKD—was stopped early when an interim analysis showed a significantly lower risk of kidney failure and cardiovascular events in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years. The relative risk of end-stage kidney disease (ESKD), a doubling of the creatinine level, or death from renal causes was 34% lower (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P < 0.001).^[62] Canagliflozin is indicated to reduce the risk of ESKD, doubling of serum creatinine, cardiovascular (CV) death, and hospitalization for heart failure (HF) in adults with T2DM and diabetic nephropathy with albuminuria ˃300 mg/day.

Another SGLT2 inhibitor, dapagliflozin, was approved to reduce risk of sustained eGFR decline, ESKD, CV death, and hospitalization for HF in adults with CKD who are at risk of progression. This indication is approved for patients with or without T2DM.^{[63, 64, 65]} In the DAPA-CKD trial (n = 4,304) measured outcome of a composite of a sustained decline in the eGFR of at least 50%, ESKD, or death from renal or CV causes. Over a median of 2.4 years, a primary outcome event occurred in 197 of 2152 participants (9.2%) in the dapagliflozin group and 312 of 2152 participants (14.5%) in the placebo group (HR, 0.61; CI, 0.51 to 0.72; P < 0.001).^[64]

Treatment with the SGLT2 inhibitor empagliflozin has been shown to reduce the risk of progression of CKD in patients both with and without diabetes. In the EMPA-KIDNEY trial, progression of kidney disease or death from CV causes occurred in 432 of 3304 patients (13.1%) who received empagliflozin, compared with 558 of 3305 patients (16.9%) who received placebo (hazard ratio, 0.72; 95% confidence interval [CI], 0.64\-0.82; P < 0.001). Results were consistent among patients with or without diabetes and across eGFR ranges.^[66]

In the FIDELIO-DKD trial of finerenone (Kerendia), a first-in-class selective, nonsteroidal mineralocorticoid receptor (MR) antagonist, significant reductions in adverse renal and CV outcomes were seen in patients with T2DM and CKD. After a median follow-up of 2.6 years, finerenone was associated with a 3.4% absolute reduction in the rate of kidney failure, renal death, and a drop in eGFR of at least 40% from baseline.^[67] Those results suggest the possibility of triple therapy with a RAS inhibitor, an SGLT2 inhibitor, and finerenone for DKD.^[68]

Blood pressure control

Aggressive blood pressure control can help to delay the decline in kidney function in patients with CKD. The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII) and American College of Cardiology (ACC) and American Heart Association guidelines suggest a target blood pressure of less than 130/80 mm Hg.^[69]The 2021 Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guideline for blood pressure management for adults with CKD who are not receiving dialysis advises treating to a target systolic blood pressure of less than 120 mm Hg, while stressing the importance of standardized protocols for patient preparation and blood pressure measurement.^[70]

Systolic blood pressure (SBP) control is considered more important than diastolic blood pressure control. However, SBP is also considered difficult to control in elderly patients with CKD.

In a diverse, community-based study by Peralta et al, high SBP appeared to account for most of the risk of progression to ESRD.^[71]The risk began at an SBP of 140 mm Hg, as opposed to the current recommended goal of less than 130 mm Hg. The highest risk was found among patients with an SBP of at least 150 mm Hg. These researchers concluded that to improve blood pressure control in CKD, treatment approaches that lower SBP may be required.^[71]

Use ACEIs or ARBs as tolerated, with close monitoring for renal deterioration and for hyperkalemia. With every dose change, serum creatinine levels need to be monitored. If serum creatinine levels increase more than 30% from baseline after adding RAS blockers, RAS blockers should be stopped. Avoid these agents in patients with advanced renal failure, bilateral renal artery stenosis, or renal artery stenosis in a solitary kidney.

The time of day at which patients take antihypertensive medications can affect circadian patterns of blood pressure, and this may translate into an effect on clinical outcome. Hermida et al reported, after a median follow-up of 5.4 years, that hypertensive patients with CKD who took at least 1 of their antihypertensive medications at bedtime had an adjusted risk for total cardiovascular events that was approximately one third that of patients who took all of their medications upon awakening.^[72]

Management of protein

Data support the use of ACEIs or ARBs in diabetic kidney disease with or without proteinuria. However, in nondiabetic kidney disease, these agents are effective in retarding the progression of disease among patients with proteinuria of more than 500 mg/day.

In the Modification of Diet in Renal Disease (MDRD) Study, dietary protein restriction (0.58 g/kg/day, versus a usual-protein diet of 1.3 g/kg/day) did not significantly affect the mean change in glomerular filtration rate (GFR) over 3 years. Secondary analyses, however, suggested that a low-protein diet may slow the GFR decline in patients with the most rapidly declining GFR and reduce proteinuria.^[73]A meta-analysis by Kasiske et al suggested that dietary protein restriction retards the rate of renal function decline, but the magnitude of the effect is relatively weak.^[74]

National Kidney Foundation (NKF) guidelines advise that if a patient is started on protein restriction, the physician needs to closely monitor the patient's nutritional status.^[51]Predialysis low serum albumin is associated with a poor outcome among dialysis patients. Protein restriction is not recommended in pediatric patients with CKD.

Vitamin D supplementation

Paricalcitol (Zemplar), a synthetic vitamin D analogue, is approved by the US Food and Drug Administration (FDA) for the prevention and treatment of secondary hyperparathyroidism associated with CKD stage 5. However, a meta-analysis has found that paricalcitol also can safely reduce protein excretion in patients with CKD stages 2-5. Whether paricalcitol can slow the development of ESRD or reduce mortality is not yet known.^[75]

In a prospective, controlled study, daily vitamin D supplementation decreased albuminuria in patients with stage 3-4 CKD who had low vitamin D levels and high parathyroid hormone (PTH) levels. The study population was composed of 50 CKD patients with hyperparathyroidism who were given 666 IU of oral cholecalciferol daily and 51 CKD patients without hyperparathyroidism who acted as controls.^{[76, 77]}

At 6 months, cholecalciferol supplementation led to a mean increase in vitamin D (25(OH)D) levels of 53%. Urinary albumin-to-creatinine ratio decreased, from 284 to 167 mg/g, without alterations in other factors that could affect proteinuria. Control patients showed no change.

Changes in 25(OH)D levels were significantly and inversely associated with those in the urinary albumin-to-creatinine ratio , supporting a possible antiproteinuric effect of vitamin D receptor activation. Treated patients also had a mean drop of 13.8% in PTH, with a mild rise in phosphate and calcium-phosphate product. No change was seen in control patients.^{[76, 77]}

Nephrotoxins

A study by Plantinga et al found that a great number of individuals with CKD may be unaware of their disease and thus may be at risk for further kidney injury through use of NSAIDs.^[78]Persons who knew that they had CKD were less likely to use NSAIDs, suggesting that primary care physicians should be involved in communication regarding the risks of NSAIDs.^[78]

However, despite the availability of guidelines and recommendations that include lists of medications that are relatively contraindicated and those that require renal dose adjustment, noncompliance with dosing guidelines and use of relatively contraindicated medications are common in patients with CKD. A cross-sectional study that included 373 adult patients with stage III/IV CKD found that 46.6% of them were prescribed at least one relatively contraindicated drug (acarbose, chlorpropamide, glyburide, nitrofurantoin, or any NSAID) during the 2-year study period; 34.0% were prescribed NSAIDs.^[79]

Encourage smoking cessation, as smokers tend to reach ESRD earlier than nonsmokers. A large-population Norwegian study found that smoking cessation decreased the risk for future onset of kidney failure—especially in men, who tended to be heavier smokers than women in this cross-section.^[80]

Subclinical hypothyroidism

In a study of 113 patients with CKD stages 2-4 and subclinical hypothyroidism, thyroid hormone replacement therapy (THRT) with L-thyroxine delayed the rate of decline in kidney function to ESRD.^{[81, 82]}On average, before patients were treated with THRT, their estimated GFR declined by 4.31 ± 0.51 mL/min per 1.73 m² each year; following treatment, the estimated GFR decline slowed to 1.08 ± 0.36 mL/min per 1.73 m² each year.^{[81, 82]}

Based on the slope of the decline in estimated GFR prior to THRT, linear regression analysis predicted that 53 of the 113 patients (46.9%) would reach stage 5 CKD—where they would require dialysis or a kidney transplant—within 10 years. However, using the altered slope of the decline of estimated GFR after patients received therapy, it was estimated that only 10 patients (8.8%) would reach this outcome in 10 years. Thus, THRT delayed reaching stage 5 CKD in 43 of the predicted 53 patients (81%).^{[81, 82]}

Treating Pathologic Manifestations of Chronic Kidney Disease

Treat these pathologic manifestations of chronic kidney disease (CKD) as follows:

Anemia: When the hemoglobin level is below 10 g/dL, treat with an erythropoiesis-stimulating agent (ESA) such as epoetin alfa or darbepoetin alfa; caution should be exercised in patients with malignancy; alternatively, consider daprodustat, which stabilizes hypoxia-inducible factor (HIF) by inhibiting prolyl hydroxylase (PH) enzymes
Hyperphosphatemia: Treat with dietary phosphate binders and dietary phosphate restriction
Hypocalcemia: Treat with calcium supplements with or without calcitriol
Hyperparathyroidism: Treat with calcitriol, vitamin D analogues, or calcimimetics
Volume overload: Treat with loop diuretics or ultrafiltration
Metabolic acidosis: Treat with oral alkali supplementation
Uremic manifestations: Treat with long-term renal replacement therapy (hemodialysis, peritoneal dialysis, or kidney transplantation)
Cardiovascular complications: Treat as appropriate
Growth failure in children: Treat with growth hormone

Anemia treatment

With erythropoietin treatment, the goal is a hemoglobin level of 10-12 g/dL, as normalization of hemoglobin in patients with CKD stages 4-5 has been associated with an increased risk of adverse outcomes. Before starting erythropoietin, patients should have their iron stores checked. The aim is to keep iron saturation at 30-50% and ferritin at 200-500 ng/mL.

A study by Shurraw et al showed that in people with non–hemodialysis-dependent CKD, a hemoglobin A1c (HbA1c) level higher than 9% is associated with worse clinical outcomes. Lower levels of HbA1c also seemed to be associated with excess mortality. Appropriate and timely control of the HbA1c level in people with diabetes mellitus and CKD may be more important than previously realized, but findings also suggest that intensive glycemic control may lead to increased mortality.^[83]

An alternative to the administration of exogenous ESAs is the use of agents that stimulate endogenous erythropoietin production in the kidney and nonrenal tissues. One such class of agents works to stabilize hypoxia-inducible factor (HIF) by inhibiting prolyl hydroxylase (PH) enzymes.^[84] HIF is a key regulator of erythropoietic gene expression, iron absorption, energy metabolism, pH, and angiogenesis; as its name indicates, HIF is induced by hypoxia.

Daprodustat (Jesduvroq) is the first HIF-PH inhibitor to be approved by the FDA. It is indicated for treatment of anemia due to CKD in adults who have been on dialysis for at least 4 months.^[85]Approval was based on the phase 3 ASCEND clinical trials. The ASCEND-D trial (in patients on dialysis), found daprodustat noninferior to ESAs.^[86]The ASCEND-ND (patients not on dialysis) showed noninferiority of daprodustat compared with darbepoetin alfa with respect to change in hemoglobin level from baseline and first occurrence of a major adverse cardiovascular event.^[87]

Management of mineral and bone disorder

Treatment of abnormal mineral homeostasis in patients with CKD includes the following^[88]:

Lowering high serum phosphorus levels
Maintaining serum calcium levels
Lowering serum parathyroid hormone levels
Providing osteoporosis prophylaxis

The Kidney Disease: Improving Global Outcomes (KDIGO) Implementation Task Force updated its guidelines on the management of CKD–mineral and bone disorder in 2017.^[88] The guidelines, which were issued after weighing the quality and the depth of evidence, when available, propose a common-sense approach to the evaluation and treatment of mineral and bone disorder in different stages of CKD.

The National Kidney Foundation convened a work group to provide a US perspective on the KDOQI CKD-MBD guidelines. While agreeing with most of the KDIGO recommendations, the work group had some concerns about the suggestions related to hypocalcemia and hypercalcemia, phosphate-binder choice, and treatment of abnormal parathyroid hormone concentrations.^[89]

Management of hyperphosphatemia

Definitive evidence on the benefit of lowering phosphate levels in CKD is lacking, and guideline recommendations vary. KDIGO guidelines suggest lowering elevated phosphate levels toward the normal range in stages 3a-5d CKD.^[88]United Kingdom National Institute for Health and Clinical Excellence (NICE) guidelines provide recommendations only for stages 4, 5, and 5d.^[90]

Restricting dietary phosphate is one strategy for correcting hyperphosphatemia. However, because of its complexity and challenges, diet control by itself is insufficient and unreliable for keeping phosphate concentrations within the recommended range. Consequently, the use of phosphate binders (eg, calcium acetate, sevelamer carbonate, lanthanum carbonate) has been proposed as a means of reducing elevated phosphorus levels in patients with CKD.^[91]Unfortunately, calculation of the cost-effectiveness of the various agents is complicated.^[92]

KDIGO guidelines suggest that the choice of phosphate-binding agent for the treatment of hyperphosphatemia take into account CKD stage, presence of other components of CKD mineral and bone disorder, concomitant therapies, and side-effect profile.^[88]For adult patients, NICE guidelines recommend calcium acetate as the first-line phosphate binder to control serum phosphate, in addition to dietary management.^[90]For full discussion of management, see Hyperphosphatemia.

Block et al reported that in patients with CKD who have normal or near-normal serum phosphorus levels, these agents significantly reduce serum and urinary phosphorus and discourage secondary hyperparathyroidism progression. The investigators also reported, however, that phosphate binders encourage vascular calcification.^[93]

These results are in contrast to those reported in previous experimental findings in animals with CKD and in human clinical trials, in which the use of phosphate binders did not reduce elevated phosphorus levels or decrease the progression to secondary hyperparathyroidism. Moreover, the effect of calcification is different among patients taking calcium-containing phosphate binders relative to those taking non–calcium-containing phosphate binders.

Furthermore, no randomized, controlled trials have shown improved mortality in dialysis patients who were treated with phosphate binders, activated vitamin D, or cinacalcet to manage moderate to severe hyperparathyroidism.

Management of metabolic acidosis

Limited but growing evidence suggests that correction of metabolic acidosis in patients with CKD may have beneficial effects on protein and bone metabolism. Experts recommend alkali therapy to maintain the serum bicarbonate concentration above 22 mEq/L.

De Brito-Ashurst et al found that patients with CKD who receive bicarbonate supplementation show a slower decline in renal function.^[94]In this study, 134 adult patients with CKD (ie, creatinine clearance [CrCl], 15-30 mL/min/1.73 m²; serum bicarbonate, 16-20 mmol/L) were randomly assigned to receive oral sodium bicarbonate supplementation or standard care for 2 years. A slower decline in CrCl was observed in the bicarbonate group (1.88 mL/min/1.73 m²) than in the control group (5.93 mL/min/1.73 m²).^[94]

Patients in the bicarbonate group were also less likely to experience rapid disease progression (9%) than were members of the control group (45%), and fewer patients who received bicarbonate supplementation developed ESRD than did controls (6.5% vs 33%, respectively).^[94]In addition, nutritional parameters improved with bicarbonate supplementation.

Correction of acidosis with sodium bicarbonate was associated with significantly slower progression of CKD in the randomized, unblinded Use of Bicarbonate in Chronic Renal Insufficiency (UBI) trial. All 740 patients in UBI, most of whom had stage 3b or 4 CKD, received standard care; the 376 patients in the treatment group also received sodium bicarbonate. Achieving target serum bicarbonate levels (24-28 mmol/L) required an average of about 6 g/day of sodium bicarbonate—an admittedly significant pill burden of four to seven pills twice daily.^[95]

At a mean follow-up of 32.9 months, serum creatinine had doubled in 25 patients in the treatment group and 62 patients in the control group (hazard ratio [HR], 0.36; P < 0.001). Dialysis had been initiated in 26 treatment group versus 45 control patients (HR, 0.5; P = 0.005), and death from any cause had occurred in 25 vs 12 patients, respectively (HR, 0.43; P = 0.01). Patients in the treatment group also showed a trend toward fewer hospitalizations. Fluid overload, uncontrolled blood pressure, and other unwanted effects were not seen in the treatment group.^[95]

Management of cardiovascular risks

Guidelines issued in December 2013 by the Kidney Disease: Improving Global Outcomes (KDIGO) workgroup recommend wider statin use among patients with CKD. Specific recommendations include the following^{[96, 97]}:

Adults aged 50 years or above with an estimated glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m² who are not being treated with long-term dialysis or kidney transplantation should be treated with a statin or a statin plus ezetimibe
Treatment with statins or statin/ezetimibe should not be initiated in adults with dialysis-dependent CKD
Patients already being treated with a statin at the time of dialysis should continue
Adult kidney transplant patients should be treated with a statin because of an increased risk for coronary events
Adults aged 18-49 years with an estimated GFR of less than 60 mL/min/1.73 m² who are not being treated with dialysis or kidney transplantation should be treated with statins if they have coronary disease, diabetes, prior ischemic stroke, or an estimated 10-year risk of coronary death or nonfatal myocardial infarction exceeding 10%
Low-density lipoprotein cholesterol is an insufficient test for cardiovascular risk in individuals with CKD, and adults with newly diagnosed CKD should undergo lipid profile testing
Adults aged 50 years or older with CKD and an estimated GFR of 60 mL/min/1.73 m2 or higher should be treated with a statin

Patients with CKD may require anticoagulation for a variety of indications, such as atrial fibrillation, venous thromboembolism, or prevention of dialysis access thrombosis. A systematic review and meta-analysis of oral anticoagulation in adult patients with CKD concluded that in early-stage CKD, the benefit-risk profile of non–vitamin K oral anticoagulants (NOACs; ie, dabigatran, rivaroxaban, apixaban, edoxaban) was superior to that of vitamin K antagonists (eg, warfarin).^[98]

In the study, which included 45 randomized trials of oral anticoagulation strategies in 34,082 patients with either chronic or dialysis-dependent kidney disease, NOACs provided better prevention of stroke and systemic embolism in CKD patients with atrial fibrillation and early-stage disease. In CKD patients with advanced or end-stage disease, however, the authors found insufficient evidence to recommend wide use of either class of anticoagulants to improve outcomes. Low-certainty evidence suggested lower risk of major bleeding with NOACs versus vitamin K antagonists.^[98]

Renal Replacement Therapy

Indications for renal replacement therapy in patients with chronic kidney disease (CKD) include the following:

Severe metabolic acidosis
Hyperkalemia
Pericarditis
Encephalopathy
Intractable volume overload
Failure to thrive and malnutrition
Peripheral neuropathy
Intractable gastrointestinal symptoms
In asymptomatic adult patients, a glomerular filtration rate (GFR) of 5-9 mL/min/1.73 m², ^[7]irrespective of the cause of the CKD or the presence of absence of other comorbidities

Timely planning for long-term renal replacement therapy

Consider the following:

Early patient education regarding natural disease progression, different dialytic modalities, renal transplantation, and the option to refuse or discontinue chronic dialysis
Timely placement of permanent vascular access (arrange for surgical creation of primary arteriovenous fistula, if possible, and preferably at least 6 mo in advance of the anticipated date of dialysis for patients in whom transplantation is not imminent)
Timely elective peritoneal dialysis catheter insertion
Timely referral for renal transplantation

Protein restriction

Protein restriction early in chronic kidney disease (CKD) as a means to delay a decline in the glomerular filtration rate (GFR) is controversial; however, as the patient approaches CKD stage 5, this strategy is recommended in adults (but not in children) to delay the onset of uremic symptoms.

Piccoli and colleagues observe that the choice of low-protein diets is extremely wide, and that moderate protein restriction may be feasible in the context of several traditional diets, such as the Mediterranean diet, which also address other therapeutic goals in CKD. However, these authors note that diet is deeply rooted in personal preferences and social habits, so the best compliance is probably obtained by personalization and comprehensive counseling.^[99]

Patients with CKD who already are predisposed to becoming malnourished are at higher risk for malnutrition with overly aggressive protein restriction. Malnutrition is a well-established predictor of increased morbidity and mortality in the population with end-stage renal disease (ESRD) and must be avoided if possible.

Salt restriction

Reduction in salt intake may slow the progression of diabetic CKD, at least in part by lowering blood pressure. A meta-analysis found that dietary salt reduction significantly reduced blood pressure in type 1 and type 2 diabetes, with results comparable to those of single-drug therapy.^[100]This finding is consistent with other evidence relating salt intake to blood pressure and albuminuria in hypertensive and normotensive patients. The dietary sodium recommendation for the general population in public health guidelines is less than 5-6 g daily.

Children and adults with tubulointerstitial diseases may experience salt wasting, and salt restriction would not usually be required in that situation.

A randomized, controlled trial by Slagman et al found that moderate dietary sodium reduction (approximately 2500 mg/day of Na⁺ or 6 g/day of NaCl) added to angiotensin-converting enzyme (ACE) inhibition compared with dual blockade (ACE inhibitor [ACEI] and angiotensin receptor blocker [ARB]) was more effective in reducing proteinuria and blood pressure in nondiabetic patients with modest CKD. Furthermore, a low-sodium diet added to dual blockade therapy yielded additional reductions in blood pressure and proteinuria . ^[101]

Vegter et al found that among patients with CKD but without diabetes, a high dietary salt intake (> 14 g/day) interfered with the antiproteinuric effect of ACEI therapy and increased the risk for ESRD.^[102]The risk was independent of blood pressure control.

Other dietary restrictions

The following dietary restrictions may also be indicated:

Phosphate restriction, starting early in CKD
Potassium restriction
Sodium and water restriction as needed to avoid volume overload

Fruits and vegetables

A review of the potential health benefits of plant-based diets in patients with CKD found growing evidence, mostly observational, that in individuals with estimated GFR of 30–59 ml/min per 1.73 m², plant-based diets (eg, Dietary Approaches to Stop Hypertension [DASH] diet, Mediterranean diet) may delay progression to ESRD and dialysis and may potentially improve survival.^{[103, 104]}

A study by Goraya et al showed that increasing the amount of alkali-inducing fruits and vegetables in the diet may help to reduce kidney injury.^[105]In this report, 30 days of a diet that included fruits and vegetables, in amounts calculated to reduce dietary acid by half, resulted in decreased urinary albumin, N-acetyl β-D-glucosaminidase, and transforming growth factor β in patients with moderately reduced estimated GFR as a result of hypertensive nephropathy.^[105]

Nutritional guidelines

The National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative (KDOQI) issued a clinical practice guideline for Nutrition in Chronic Renal Failure, as well as a 2008 revision of recommendations for Nutrition in Children with CKD. For adult patients on maintenance dialysis, the KDOQI guidelines recommend routine assessment of the following nutritional parameters:

Predialysis or stabilized serum albumin: Monthly
Percentage of usual postdialysis (hemodialysis) or postdrain (peritoneal dialysis) body weight: Monthly
Percentage of standard (National Health and Examination Survey II [NHANES II]) body weight: Every 4 months
Subjective global assessment: Every 6 months
Dietary interview and/or diet diary: Every 6 months
Protein Equivalent of Total Nitrogen Appearance normalized to body weight (nPNA): Monthly with hemodialysis; every 3-4 months with peritoneal dialysis

Activity

The KDIGO (Kidney Disease: Improving Global Outcomes) clinical practice guideline recommends that patients with CKD undertake regular exercise, as compatible with cardiovascular health, ideally for at least 30 minutes 5 times per week.^[5] However, studies have found that patients with CKD participate in physical activity only about 9 days per month, and 45% of patients with end-stage kidney disease (ESKD) reported not exercising at all.^[106]

As regards the type of physical exercise, for patients on dialysis the strongest evidence is for aerobic exercise, which can improve physical fitness, muscular strength and quality of life in this cohort. Resistance training has shown benefit for patients with earlier stages of CKD.^[107]Given the limited data available, however, a reasonable approach would be to refer CKD patients to an exercise professional who is qualified to prescribe and supervise an exercise program tailored to the patient's individual situation.

Consultations and Long-Term Monitoring

Consultations for the management of patients with chronic kidney disease (CKD) may include the following:

Early nephrology referral (decreases morbidity and mortality)
Renal dietitian
Surgery for permanent vascular access or for peritoneal catheter placement
Referral to renal transplant center

Patients with CKD should be referred to a nephrologist early in the course of their disease and have continued nephrologic follow-up until initiation of chronic renal replacement therapy, during dialysis, and after kidney transplantation. Moreover, a multidisciplinary approach to care, including involvement of the nephrologist, primary care physician, renal dietitian, nurse, and social worker, should be initiated early in the course of CKD, with close patient follow-up.

Patients should be monitored for obstructive sleep apnea (OSA), which occurs with increased frequency in patients receiving dialysis. Sakaguchi et al also found a high incidence (65%) of OSA in Japanese patients with nondialysis CKD, with the OSA being moderate or severe in about one third of the patients who had it.^[108]The study also found that a decreased glomerular filtration rate (GFR) was associated with an increased risk of OSA.^[108]

Guidelines

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