3 17 1 Lab 3b Months Again 10 10
JAMA. Author manuscript; available in PMC 2020 Oct 1.
Published in concluding edited course as:
PMCID: PMC7015670
NIHMSID: NIHMS1069237
Chronic Kidney Disease Diagnosis and Direction
A Review
Abstract
IMPORTANCE
Chronic kidney disease (CKD) is the 16th leading crusade of years of life lost worldwide. Appropriate screening, diagnosis, and management by primary intendance clinicians are necessary to prevent adverse CKD-associated outcomes, including cardiovascular disease, finish-stage kidney disease, and decease.
OBSERVATIONS
Divers as a persistent abnormality in kidney construction or role (eg, glomerular filtration charge per unit [GFR] <60 mL/min/1.73 m2 or albuminuria ≥xxx mg per 24 hours) for more than 3 months, CKD affects 8% to 16% of the population worldwide. In adult countries, CKD is virtually usually attributed to diabetes and hypertension. All the same, less than 5% of patients with early CKD report awareness of their disease. Among individuals diagnosed equally having CKD, staging and new risk assessment tools that incorporate GFR and albuminuria can help guide handling, monitoring, and referral strategies. Optimal direction of CKD includes cardiovascular risk reduction (eg, statins and blood pressure level direction), treatment of albuminuria (eg, angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers), avoidance of potential nephrotoxins (eg, nonsteroidal anti-inflammatory drugs), and adjustments to drug dosing (eg, many antibiotics and oral hypoglycemic agents). Patients also require monitoring for complications of CKD, such as hyperkalemia, metabolic acidosis, hyperphosphatemia, vitamin D deficiency, secondary hyperparathyroidism, and anemia. Those at high adventure of CKD progression (eg, estimated GFR <xxx mL/min/i.73 10002, albuminuria ≥300 mg per 24 hours, or rapid decline in estimated GFR) should be promptly referred to a nephrologist.
CONCLUSIONS AND RELEVANCE
Diagnosis, staging, and advisable referral of CKD past primary care clinicians are important in reducing the burden of CKD worldwide.
Chronic kidney illness (CKD) affects between eight% and xvi% of the population worldwide and is often underrecognized past patients and clinicians.ane–4 Defined by a glomerular filtration rate (GFR) of less than 60 mL/min/ane.73 mii, albuminuria of at least 30 mg per 24 hours, or markers of kidney damage (eg, hematuria or structural abnormalities such as polycystic or dysplastic kidneys) persisting for more than than three months,5 CKD is more prevalent in low- and middle-income than in high-income countries.vi Globally, CKD is near commonly attributed to diabetes and/or hypertension, but other causes such every bit glomerulonephritis, infection, and environmental exposures (such as air pollution, herbal remedies, and pesticides) are common in Asia, sub-Saharan Africa, and many developing countries.iv Genetic chance factors may likewise contribute to CKD chance. For example, sickle jail cell trait and the presence of 2 APOL1 run a risk alleles, both common in people of African ancestry simply non European ancestry, may double the gamble of CKD.4,7–10
In the United states, the average rate of GFR turn down is approximately 1 mL/min/1.73 10002 per year in the general population,11,12 and the lifetime run a risk of developing a GFR of less than 60 mL/min/ane.73 mtwo is more than than 50%.13 Early detection and treatment by chief care clinicians is important because progressive CKD is associated with agin clinical outcomes, including end-phase kidney affliction (ESKD), cardiovascular disease, and increased mortality.14–17 Recent professional guidelines suggest a chance-based arroyo to the evaluation and management of CKD.5,18–20 This review includes give-and-take of new calculators for determining hazard of CKD progression that may be useful in clinical practice (eg, https://kidneyfailurerisk.com/) and focuses on the diagnosis, evaluation, and management of CKD for chief care clinicians. Considerations for referral to a nephrologist and dialysis initiation are also covered.
Methods
A literature search to April 2019 was conducted using Medline and PubMed with search terms including CKD, chronic renal failure, chronic renal insufficiency, epidemiology, incidence, prevalence, occurrence, diagnosis, assessment, identification, screening, workup,etiology,causes,management,treatment,intervention,therapy, and prevention. Results were restricted to English-linguistic communication, human studies, and academic journals and guidelines. The initial search resulted in 998 articles, including clinical trials, meta-analyses, practice guidelines, and systematic reviews, and was later on expanded to include review articles and observational studies, including cross-sectional studies, and more contempo publications contained in reference lists of identified manufactures. All clinical trials for treatment or prevention of CKD were included without regard to written report size or age of patient population.
Clinical Presentation
Chronic kidney illness is typically identified through routine screening with serum chemistry contour and urine studies or as an incidental finding. Less unremarkably, patients may present with symptoms such as gross hematuria, "foamy urine" (a sign of albuminuria), nocturia, flank pain, or decreased urine output. If CKD is avant-garde, patients may report fatigue, poor appetite, nausea, vomiting, metal gustation, unintentional weight loss, pruritus, changes in mental status, dyspnea, or peripheral edema.21
In evaluating a patient with known or suspected CKD, clinicians should inquire almost additional symptoms that might suggest a systemic cause (eg, hemoptysis, rash, lymphadenopathy, hearing loss, neuropathy) or urinary obstacle (eg, urinary hesitancy, urgency, or frequency or incomplete bladder elimination).21 Moreover, patients should be assessed for risk factors of kidney affliction, including prior exposure to potential nephrotoxins (eg, nonsteroidal anti-inflammatory drugs [NSAIDs], phosphate-based bowel preparations, herbal remedies such equally those containing aristolochic acid, antibiotic therapies such equally gentamicin, and chemotherapies), history of nephrolithiasis or recurrent urinary tract infections, presence of comorbidities (eg, hypertension, diabetes, autoimmune affliction, chronic infections), family history of kidney disease, and, if bachelor, other known genetic risk factors such every bit sickle cell trait.9,18,21–24
A detailed physical exam may provide additional clues regarding the underlying cause of CKD and should include careful evaluation of a patient's book condition. Signs of book depletion may reflect poor oral intake, vomiting, diarrhea, or overdiuresis, whereas signs of volume overload may be due to decompensated eye failure, liver failure, or nephrotic syndrome. The presence of arterial-venous nicking or retinopathy on retinal examination suggests long-continuing hypertension or diabetes. Patients with carotid or abdominal bruits may have renovascular disease. Flank pain or enlarged kidneys should prompt consideration of obstructive uropathy, nephrolithiasis, pyelonephritis, or polycystic kidney disease. Neuropathy may be due to diabetes or less commonly vasculitis, or amyloidosis. Skin findings may include rash (systemic lupus erythematosus, acute interstitial nephritis), palpable purpura (Henoch-Schonlein purpura, cryoglobulinemia, vasculitis), telangiectasias (scleroderma, Fabry disease), or extensive sclerosis (scleroderma). Patients with advanced CKD may exhibit pallor, peel excoriations, muscle wasting, asterixis, myoclonic jerks, altered mental status, and pericardial rub.21
CKD Definition and Staging
Chronic kidney disease is defined every bit the presence of an aberration in kidney structure or function persisting for more iii months.5,25 This includes one or more of the following: (1) GFR less than 60 mL/min/1.73 mii; (ii) albuminuria (ie, urine albumin ≥30 mg per 24 hours or urine albumin-to-creatinine ratio [ACR] ≥30 mg/chiliad); (3) abnormalities in urine sediment, histology, or imaging suggestive of kidney impairment; (iv) renal tubular disorders; or (5) history of kidney transplantation.five If the duration of kidney disease is unclear, echo assessments should exist performed to distinguish CKD from acute kidney injury (modify in kidney function occurring within 2–vii days) and acute kidney disease (kidney harm or decreased kidney function present for ≤three months).25 Evaluation for the etiology of CKD should exist guided by a patient's clinical history, physical examination, and urinary findings (Figure 1).5,18,21
Considerations for Diagnosis, Staging, and Referral of Patients With Chronic Kidney Disease
a Other imaging modalities or urine studies may also be considered.
b A multifariousness of scores are available, eg, https://kidneyfailurerisk.com/.
Once a diagnosis of CKD has been made, the adjacent footstep is to decide staging, which is based on GFR, albuminuria, and cause of CKD (Effigy 2).v Staging of GFR is classified as G1 (GFR ≥90 mL/min/i.73 m2), G2 (GFR 60–89 mL/min/1.73 m2), G3a (45–59 mL/min/1.73 m2), G3b (30–44 mL/min/1.73 chiliad2), G4 (15–29 mL/min/one.73 m2), and G5 (<15 mL/min/i.73 m2).5 Although GFR can be directly measured by clearance of agents such as iohexol or iothalamate,26–28 the evolution of estimating equations (eg, the Chronic Kidney Illness Epidemiology Collaboration [CKD-EPI] and Modification of Diet in Renal Disease Study [MDRD] equations) has largely replaced the need for direct measurement in clinical practice.29–31 Clinical laboratories now routinely report estimated GFR (eGFR) based on filtration markers. The most common filtration marker used is creatinine, a 113 dalton byproduct of creatine metabolism25 and one for which laboratory assays have been standardized since 2003.32 The preferred estimating equation in the Us and much of the world is the CKD-EPI 2009 creatinine equation, which is more than accurate than the before MDRD equation, particularly for eGFR values greater than 60 mL/min/1.73 m2 (https://www.kidney.org/professionals/kdoqi/gfr_calculator).29,30 In situations requiring boosted accuracy and precision, cystatin C tin be used with creatinine in the CKD-EPI 2012 creatinine-cystatin C equation.31 Adding cystatin C may be particularly useful for individuals with altered creatinine production and/or metabolism (eg, extremely high or low body size or muscle mass, limb amputation, loftier-protein nutrition, employ of creatinine supplements, or use of drugs affecting tubular secretion of creatinine).5,25
Definition and Prognosis of Chronic Kidney Disease past GFR and Albuminuria Categories, KDIGO 2012
GFR indicates glomerular filtration rate; KDIGO, Kidney Affliction Improving Global Outcomes. Categories are grouped by run a risk of progression, which includes chronic kidney disease progression, defined by a pass up in GFR category (accompanied past a ≥25% decrease in estimated GFR from baseline) or sustained reject in estimated GFR greater than v mL/min/1.73 thousand2 per year. Light-green indicates low chance (if no other markers of kidney disease and no CKD); xanthous, moderately increased risk; orange: high gamble; and red, very high risk. Reproduced with permission from Kidney International Supplements.five
Albuminuria should ideally be quantified by a urine ACR. Albuminuria staging is classified as A1 (urine ACR <xxx mg/g), A2 (30–300 mg/g), and A3 (>300 mg/yard).5 Guidelines recommend the use of urine ACR to stage CKD rather than urine protein-to-creatinine ratio because assays for the former are more than likely to be standardized and have better precision at lower values of albuminuria.5,33 The most precise measurements come from a first forenoon sample or 24-hour collection, as there is high biological variability in urine albumin excretion over the course of the day.5,34,35 Random samples, yet, are also acceptable in initial screening.5 Compared with urine protein-to-creatinine ratio, urine ACR is believed to be a more sensitive and specific mark of glomerular pathologyv since some urine proteins such as uromodulin are nowadays (and may even be protective) in normal physiology.36–38 If tubular or overflow proteinuria is suspected, then urine protein electrophoresis or testing for the specific poly peptide tin can be pursued (eg, immunoglobulin heavy and light chains, α1-microglobulin, and βtwo-microglobulin).5 Imaging by kidney ultrasound to assess morphology and to rule out urinary obstruction should be considered in all patients diagnosed every bit having CKD.five
Cause of CKD can be difficult to discern but is generally classified by the presence or absence of systemic disease and the location of anatomic abnormality. Examples of systemic disease include diabetes, autoimmune disorders, chronic infection, malignancy, and genetic disorders in which the kidney is non the only organ affected. Anatomic locations are divided into glomerular, tubulointerstitial, vascular, and cystic/built diseases.v Determining the crusade of CKD may have important implications on prognosis and handling. For example, polycystic kidney affliction may progress to ESKD faster than other causes and often requires evaluation for extrarenal manifestations and consideration of specific therapies such as tolvaptan, a vasopressin V2 receptor antagonist that slows decline in GFR.39,forty Patients with unexplained causes of CKD should exist referred to a nephrologist.
Screening for CKD
Given that most patients with CKD are asymptomatic, screening may be important to early on detection of illness.18 The National Kidney Foundation has developed a kidney profile examination that includes measuring both serum creatinine for estimating GFR and urine ACR.41 A take a chance-based approach to screening is suggested by many clinical do guidelines, with screening recommended in those older than 60 years or with a history of diabetes or hypertension.xviii–20 Screening should also exist considered in those with clinical risk factors, including autoimmune disease, obesity, kidney stones, recurrent urinary tract infections, reduced kidney mass, exposure to certain medications such as NSAIDs or lithium, and prior episodes of astute kidney injury, amid others (Box).9,xviii,42–45 However, no randomized clinical trials take demonstrated that screening asymptomatic patients for CKD improves outcomes.
Other Risk Factors for CKD
In that location are several sociodemographic factors that contribute to increased adventure of CKD, including nonwhite race, depression education, low income, and food insecurity.18,43,46 Compared with whites, African Americans and Pacific Islanders have a substantially greater take a chance of ESKD.47 This is in part due to an increased prevalence of hypertension, diabetes, and obesity.xi Withal, genetic factors probable too contribute. More specifically, risk alleles in the cistron encoding apolipoprotein L1 (APOL1) may increment adventure of kidney illness in a recessive genetic manner7,viii: individuals with two APOL1 risk alleles (present in approximately 13% of African Americans) have a 2-fold risk of CKD progression and up to a 29-fold hazard of specific CKD etiologies (eg, focal-segmental glomerulosclerosis and HIV-associated nephropathy) compared with those with 0 or 1 adventure allele.eleven,44,45,48,49 Sickle prison cell trait (nowadays in approximately 8% of African Americans) has besides been associated with an increased chance of kidney disease. Compared with noncarriers, individuals with sickle cell trait have a i.8-fold odds of incident CKD, i.3-fold odds of eGFR decline greater than 3 mL/min/1.73 m2, and ane.9-fold odds of albuminuria.9
Management of Patients With CKD
Reducing Risk of Cardiovascular Disease
The prevalence of cardiovascular affliction is markedly college among individuals with CKD compared with those without CKD. For example, in a Medicare five% sample, 65% of the 175 840 adults aged 66 years or older with CKD had cardiovascular disease compared with 32% of the 1 086 232 without CKD.47 Moreover, presence of CKD is associated with worse cardiovascular outcomes. For example, in the aforementioned population, the presence of CKD was associated with lower 2-twelvemonth survival in people with coronary artery disease (77% vs 87%), acute myocardial infarction (69% vs 82%), centre failure (65% vs 76%), atrial fibrillation (70% vs 83%), and cerebrovascular blow/transient ischemic attack (73% vs 83%).47
Therefore, a major component of CKD management is reduction of cardiovascular hazard. It is recommended that patients aged 50 years or older with CKD be treated with a low- to moderate-dose statin regardless of low-density lipoprotein cholesterol level.50–52 Smoking cessation should also exist encouraged.five,53 Both the Eighth Articulation National Commission (JNC viii) and Kidney Disease: Improving Global Outcomes (KDIGO) guidelines have recommended goal systolic and diastolic blood pressures of less than 140 mm Hg and less than 90 mm Hg, respectively, among adults with CKD based on expert stance.v,54 The KDIGO guidelines farther recommend that adults with urine ACR of at to the lowest degree 30 mg per 24 hours (or equivalent) have systolic and diastolic claret pressures maintained below 130 mm Hg and 80 mm Hg, respectively.5 More recently, the Systolic Blood Pressure level Intervention Trial (SPRINT) demonstrated that among individuals with increased risk of cardiovascular disease but without diabetes, more intensive blood pressure level command (goal systolic blood pressure <120 mm Hg) was associated with a 25% lower (1.65% vs ii.19% per twelvemonth) chance of a major cardiovascular event and a 27% lower hazard of all-cause mortality compared with standard claret force per unit area control (goal systolic blood pressure <140 mm Hg).55 The intensive handling group had a greater risk of at least a 30% refuse in eGFR to a level below 60 mL/min/1.73 mtwo; however, this may have been due to hemodynamic changes rather than true kidney function loss.55,56 Importantly, the benefits of intensive blood pressure control on cardiovascular events were similar in participants with and without baseline CKD.57
Management of Hypertension
Many guidelines provide algorithms detailing which agents should exist used to treat hypertension in people with CKD.54,58 Presence and severity of albuminuria should be evaluated. Blockade of the renin-angiotensin-aldosterone organization with either an angiotensin-converting enzyme inhibitor (ACE-I) or an angiotensin Two receptor blocker (ARB) is recommended for adults with diabetes and a urine ACR of at to the lowest degree 30 mg per 24 hours or whatsoever adult with a urine ACR of at to the lowest degree 300 mg per 24 hours.five,18,58 Dual therapy with an ACE-I and an ARB is generally avoided, given associated risks of hyperkalemia and acute kidney injury.5,18,59 Aldosterone receptor antagonists may besides be considered in patients with albuminuria, resistant hypertension, or heart failure with reduced ejection fraction.58,60–64
Management of Diabetes Mellitus
Optimal management of diabetes is also important. First, glycemic control may delay progression of CKD, with most guidelines recommending a goal hemoglobin A1c of ~ 7.0%.5,18,19,65–67 Second, dose adjustments in oral hypoglycemic agents may be necessary. In full general, drugs that are largely cleared past the kidneys (eg, glyburide) should be avoided, whereas drugs metabolized by the liver and/or partially excreted past the kidneys (eg, metformin and some dipeptidyl peptidase 4 [DPP-four] and sodium-glucose cotransporter-2 [SGLT-2] inhibitors) may require dose reduction or discontinuation, particularly when eGFR falls beneath 30 mL/min/1.73 ktwo.xviii,xix Tertiary, use of specific medication classes such equally SGLT-ii inhibitors in those with severely increased albuminuria should exist considered. The Canagliflozin and Renal Events in Diabetes with Established Nephropathy Clinical Evaluation (CREDENCE) trial demonstrated that, amid 4401 patients with type 2 diabetes and CKD phase G2-G3/A3 (baseline eGFR 30 to <90 mL/min/1.73 gtwo and urine ACR>300 to 5000 mg/24 hours) taking ACE-I or ARB therapy, those randomized to canagliflozin had a 30% lower risk (43.2 vs 61.2 events per 1000 patient-years) of developing the primary composite renal outcome (doubling of serum creatinine, ESKD, or death from a renal or cardiovascular cause) compared with those randomized to placebo.68 Prior trials have likewise suggested cardiovascular benefit with this class of medications, which may extend to patients with CKD who take lower levels of albuminuria.69,70
Nephrotoxins
All patients with CKD should be counseled to avoid nephrotoxins. Although a complete list is beyond the scope of this review, a few warrant mentioning. Routine administration of NSAIDs in CKD is non recommended, especially amongst individuals who are taking ACE-I or ARB therapy.5,18 Herbal remedies are non regulated by the United states of america Food and Drug Administration, and some (such equally those containing aristolochic acid or anthraquinones) have been reported to crusade a myriad of kidney abnormalities, including astute tubular necrosis, acute or chronic interstitial nephritis, nephrolithiasis, rhabdomyolysis, hypokalemia, and Fanconi syndrome.22 Phosphate-based bowel preparations (both oral and enema formulations) are readily available over the counter and tin lead to acute phosphate nephropathy.23,24 Proton pump inhibitors are widely used and have been associated with acute interstitial nephritis in instance reports and incident CKD in population-based studies.71–73 In the population-based Atherosclerosis Gamble in Communities cohort, the incidence of CKD was 14.2 events in those taking proton pump inhibitors and x.7 per grand events in people who did not take them.71 Uniform discontinuation of proton pump inhibitors in CKD is non necessary. However, indications for use should be addressed at each primary intendance visit.
Drug Dosing
Adjustments in drug dosing are frequently required in patients with CKD. Of annotation, the traditional Cockcroft-Gault equation ofttimes poorly reflects measured GFR, whereas estimation of GFR using the CKD-EPI equation probable correlates amend with drug clearance by the kidneys.74,75 Common medications that require dose reductions include near antibiotics, direct oral anticoagulants, gabapentin and pregabalin, oral hypoglycemic agents, insulin, chemotherapeutic agents, and opiates, among others.v,eighteen In general, use of medications with low likelihood of benefit should be minimized because patients with CKD are at loftier run a risk of adverse drug events.76–79 Gadolinium-based dissimilarity agents are contraindicated in individuals with acute kidney injury, eGFR less than 30 mL/min/i.73 mtwo, or ESKD given the risk of nephrogenic systemic fibrosis, a painful and debilitating disorder characterized past marked fibrosis of the skin and occasionally other organs.5,eighteen,lxxx,81 Newer macrocyclic chelate formulations (eg, gadoteridol, gadobutrol, or gadoterate) are much less likely to cause nephrogenic systemic fibrosis, but the best prevention may all the same be to avoid gadolinium altogether. If administration of gadolinium is deemed essential, the patient must be counseled on the potential risk of nephrogenic systemic fibrosis and a nephrologist may be consulted for consideration of postexposure hemodialysis.five,18,80–82
Dietary Management
Dietary management to prevent CKD progression is controversial since large trials have had equivocal results.83–85 For instance, the MDRD written report evaluated 2 levels of poly peptide restriction in 840 patients, finding that a low-poly peptide diet compared with usual protein intake resulted in slower GFR decline but after the initial 4 months, and that a very depression-protein diet compared with a low-protein diet was not significantly associated with slower GFR decline. Both levels of protein restriction appeared to have benefit in the subgroup with proteinuria greater than 3 one thousand per day, although this grouping was modest.83 Other, smaller trials have suggested a benefit of poly peptide restriction in the prevention of CKD progression or ESKD.86–88 The KDIGO guidelines recommend that protein intake be reduced to less than 0.8 g/kg per day (with proper instruction) in adults with CKD stages G4-G5 and to less than 1.three grand/kg per day in other adult patients with CKD at risk of progression.v The possible benefits of dietary protein restriction must be balanced with the concern of precipitating malnutrition and/or protein wasting syndrome.5,83,84,89 Lower dietary acid loads (eg, more fruits and vegetables and less meats, eggs, and cheeses) may as well help protect confronting kidney injury.ninety,91 Low-sodium diets (generally <two g per twenty-four hours) are recommended for patients with hypertension, proteinuria, or fluid overload.five
Monitoring of Established CKD and Treatment of Complications
In one case CKD is established, the KDIGO guidelines recommend monitoring eGFR and albuminuria at least one time annually. For patients at high risk, these measures should be monitored at least twice per year; patients at very high risk should be monitored at least 3 times per twelvemonth (Effigy 2).five Patients with moderate to severe CKD are at increased take a chance of developing electrolyte abnormalities, mineral and bone disorders, and anemia.92 Screening and frequency of assessment for laboratory abnormalities is dictated by stage of CKD and includes measurement of consummate blood count, bones metabolic panel, serum albumin, phosphate, parathyroid hormone, 25-hydroxyvitamin D, and lipid console (Tabular array).v,50,93,94
Table.
Screening, Monitoring, and Management of the Complications of Chronic Kidney Disease (CKD)
| Complication | Relevant Tests | Frequency of Repeat Testing | Management |
|---|---|---|---|
| Anemia | Hemoglobin | No anemia: CKD stages G1-G2: when clinically indicated CKD stage G3: at least once per year CKD stages G4-G5: at least twice per year With anemia: CKD stages 3–v: at to the lowest degree every 3 months | Rule out other causes of anemia: iron deficiency, vitamin B12 deficiency, folate deficiency, occult bleeding Consider iron supplementation and referral to a nephrologist for erythropoietin-stimulating agent therapy when hemoglobin <10 g/dL |
| Mineral and bone disorder | Serum calcium, phosphate, parathyroid hormone, 25-hydroxyvitamin D | Calcium/phosphate: CKD stage G3: every half dozen–12 months CKD stage G4: every 3–half dozen months CKD stage G5: every 1–3 months Parathyroid hormone: CKD stage G3: at baseline, so as needed CKD stage G4: every six–12 months CKD phase G5: every 3–six months Vitamin D: CKD stages iii–5: at baseline, then as needed | Consider phosphate-lowering therapy (eg, calcium acetate, sevelamer, iron-based binders) and vitamin D supplementation |
| Hyperkalemia | Serum potassium | At baseline and as needed | Depression-potassium diet, correction of hyperglycemia and acidemia, consider potassium binders |
| Metabolic acidosis | Serum bicarbonate | At baseline and as needed | Oral bicarbonate supplementation (eg, sodium bicarbonate, baking soda, or sodium citrate/citric acrid) for values persistently <22 mmol/L |
| Cardiovascular disease | Lipid panel | At baseline and equally needed | Low- to moderate-dose statin therapy for patients anile ≥50 years with CKD Statin therapy for patients anile eighteen–49 years with CKD and coronary artery disease, diabetes, prior ischemic stroke, or loftier risk of myocardial infarction or cardiovascular death |
Anemia and the Role of Erythropoietin in CKD
Anemia is among the most common complications of CKD. In a study that included 19 CKD cohorts from beyond the world, 41% of the 209 311 individuals had low levels of hemoglobin (defined equally <thirteen g/dL in men and <12 g/dL in women).92 The initial workup of anemia should include assessment of iron stores: those who are atomic number 26 deficient may benefit from oral or intravenous iron repletion. Patients with hemoglobin levels persistently below 10 thousand/dL despite addressing reversible causes can be referred to a nephrologist for consideration of additional medical therapy, including erythropoietin-stimulating agents; yet, erythropoietin-stimulating agents take been associated with increased risk of death, stroke, and venous thromboembolism, and these risks must be weighed against whatever potential benefits.93
Electrolyte, Mineral, and Bone Abnormalities in CKD
Electrolyte abnormalities are present in iii% to eleven% of patients with CKD.92 Initial treatment strategies unremarkably involve dietary restrictions and prescription of supplements. For example, primary care clinicians should recommend low-potassium diets for patients with hyperkalemia and depression-phosphorus diets for patients with hyperphosphatemia.5,18,94,95 For patients with a serum bicarbonate level persistently below 22 mmol/L, oral bicarbonate supplementation should be considered, as studies have suggested that chronic metabolic acidosis is associated with faster CKD progression.5,18,96–99
Mineral and bone disorders are likewise common. In a report that included 42 985 patients with CKD, 58% had intact parathyroid hormone levels greater than 65 pg/mL.92 Although the optimal intact parathyroid hormone level for CKD remains unclear, well-nigh nephrologists agree that concomitant hyperphosphatemia, hypocalcemia, and vitamin D deficiency should be addressed, such as with a low-phosphate diet, phosphate binders, adequate elemental calcium intake, and vitamin D supplementation (Table).94,95
Prognosis of CKD
The incidence of ESKD varies by the presence of hazard factors and geographical location. For example, in North America, the incidence amidst individuals with eGFR less than 60 mL/min/1.73 mii ranged from 4.9 to 168.3 ESKD events per 1000 patient-years in 16 cohorts; in 15 non–North American cohorts, the incidence ranged from one.two to 131.iii ESKD events per 1000 patient-years.100 Near patients with CKD do not require kidney replacement therapy during their lifetime.101 Simple online tools are available to aid with risk stratification. For example, the Kidney Failure Risk Equation (KFRE; https://kidneyfailurerisk.com/) predicts the two-year and 5-twelvemonth probabilities of requiring dialysis or transplant among individuals with eGFR less than 60 mL/min/1.73 gtwo.100,102 The KFRE, which has been validated in more than than 700 000 individuals from more than 30 countries, uses readily bachelor clinical and laboratory variables. The 4-variable equation includes age, sexual practice, eGFR, and urine ACR, whereas the 8-variable equation further incorporates serum albumin, phosphate, calcium, and bicarbonate levels.100,102 Some health systems have tested the implementation of KFRE in clinical practice: nephrology referrals based on a 5-year KFRE greater than 3% led to shorter expect times,103 and a 2-year KFRE greater than x% was used to guide referrals to multidisciplinary CKD clinics.104 An ongoing trial is evaluating whether a KFRE take a chance-based approach improves CKD management.105 For patients with eGFR less than 30mL/min/1.73mtwo, the CKD G4+ adventure estimator (https://www.kdigo.org/equation/) may provide additional information on the risks of cardiovascular disease and expiry.106,107 Importantly, risk prognostication may be helpful in not simply identifying individuals at loftier risk of disease progression but besides providing reassurance to those with mild CKD such as stage G3a A1.
Referral to a Nephrologist and Timing of Kidney Replacement Therapy
The KDIGO guidelines recommend that patients with CKD be referred to a nephrologist when eGFR falls below 30 mL/min/1.73 grand2 (stage G4) and/or urine ACR increases above 300 mg per 24 hours (stage A3).5 The presence of albuminuria greater than 2200 mg per 24 hours should prompt expedited evaluation by a nephrologist and consideration of nephrotic syndrome. Additional indications for referral include the following: presence of greater than 20 red claret cells per high-ability field of unclear etiology, scarlet blood prison cell casts on urine microscopy or other indication of glomerulonephritis, CKD with uncontrolled hypertension despite 4 or more than antihypertensive medications, persistent hypokalemia or hyperkalemia, anemia requiring erythropoietin replacement, recurrent or extensive kidney stones, hereditary kidney disease, acute kidney injury, and rapid CKD progression (a decrease in eGFR ≥25% from baseline or a sustained reject in eGFR >5 mL/min/ane.73 m2).5 In persons without CKD, even modest changes in serum creatinine (eg, from 0.7 mg/dL to 1.ii mg/dL) reflect big declines in eGFR, and primary intendance clinicians should attempt to identify reversible causes. Indications for kidney biopsy may include merely are not limited to unexplained persistent or increasing albuminuria, presence of cellular casts or dysmorphic red blood cells on urine sediment, and unexplained or rapid decline in GFR.5 Specific thresholds vary depending on patient characteristics and past institution. Patients with polycystic kidney affliction, sure types of glomerulonephritis, and nephrotic-range albuminuria are at particularly high risk of progressing to ESKD.5,39,102
Referral to nephrology is important for planning kidney replacement therapy and transplant evaluation. The conclusion to begin kidney replacement therapy is based on the presence of symptoms and non solely on level of GFR.108 Urgent indications include encephalopathy, pericarditis, and pleuritis due to severe uremia.109 Otherwise, initiation of dialysis should exist individualized and considered when patients have uremic signs or symptoms (eg, nausea, vomiting, poor appetite, metallic taste, pericardial rub or effusion, asterixis, or altered mental condition), electrolyte abnormalities (eg, hyperkalemia or metabolic acidosis), or book overload (eg, pulmonary or lower extremity edema) refractory to medical management.5,18,109 A shared controlling arroyo is best. Patients should exist educated about treatment options and actively contribute to decision-making. Early on instruction should include information on the potential complications of CKD every bit well equally the unlike modalities of kidney replacement therapy. Kidney transplantation is considered the optimal therapy for ESKD, with living donor kidney transplantations performed earlier or shortly after dialysis initiation having the best outcomes.110,111 As such, early on referral (eg, eGFR <30 mL/min/one.73 mtwo and an elevated 2-yr hazard of ESKD) for transplant evaluation is important.112,113 Alternative therapies for ESKD may include in-heart hemodialysis, home hemodialysis, peritoneal dialysis, or bourgeois care without dialysis.107 Patient preference should be taken into consideration when selecting dialysis modality; however, patients with multiple abdominal surgeries with resultant peritoneal scarring or unstable housing are likely poor candidates for peritoneal dialysis.107,109 Patients planning for hemodialysis who showroom rapid decline in eGFR should be referred to an experienced vascular surgeon for arteriovenous fistula placement. The KDOQI guidelines recommend that access cosmos should occur when eGFR is between 15 and 20 mL/min/1.73 m2.114 Of notation, dialysis initiation has been associated with accelerated functional decline and high brusque-term mortality among older patients with poor functional condition.115,116 Patient preferences for conservative approaches to medical management should be discussed and honored.
Conclusions
Chronic kidney disease affects 8% to sixteen% of the population worldwide and is a leading crusade of death. Optimal management of CKD includes cardiovascular take a chance reduction, handling of albuminuria, avoidance of potential nephrotoxins, and adjustments to drug dosing. Patients also crave monitoring for complications of CKD, such as hyperkalemia, metabolic acidosis, anemia, and other metabolic abnormalities. Diagnosis, staging, and appropriate referral of CKD by primary care clinicians are important in reducing the burden of CKD worldwide.
Funding/Support:
Dr Chen was supported by a Clinician Scientist Career Development Award from Johns Hopkins University and is supported by a George M. O'Brien Heart for Kidney Inquiry Pilot and Feasibility Grant from Yale University and award K08DK117068 from the National Institutes of Health/NIDDK. Dr Grams is supported past NIDDK grants DK1008803, DK100446, and DK115534.
Function of the Funder/Sponsor: The supporting institutions had no function in the pattern and bear of the study; collection, direction, assay, and interpretation of the data; training, review, or approval of the manuscript; or decision to submit the manuscript for publication.
Footnotes
Conflict of Interest Disclosures: Dr Chen reported receipt of grants from the National Found of Diabetes and Digestive and Kidney Diseases (NIDDK) and Yale Academy. Dr Grams reported receipt of grants from the NIDDK and the National Kidney Foundation and travel support from Dialysis Clinics Inc for an invited speakership at a directors' meeting in May 2019. No other disclosures were reported.
Submissions: We encourage authors to submit papers for consideration equally a Review. Delight contact Edward Livingston, Doc, at Edward. gro.krowtenamaj@notsgnivil or Mary McGrae McDermott, Medico, at ude.nretsewhtron@806mdm.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7015670/
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