kidney disease presentation pdf

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Chronic Kidney Disease Diagnosis and Management

Author Contributions: Dr Grams had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Acquisition, analysis, or interpretation of data: Chen, Grams.

Drafting of the manuscript: Chen.

Critical revision of the manuscript for important intellectual content: All authors.

Statistical analysis: Grams.

Administrative, technical, or material support: Chen, Knicely.

Supervision: Grams.

Additional Contributions: We thank Andrew S. Levey, MD, Tufts Medical Center, and Natalie Daya, MS, Johns Hopkins University, for helpful input on the manuscript (uncompensated).

Chronic kidney disease (CKD) is the 16th leading cause of years of life lost worldwide. Appropriate screening, diagnosis, and management by primary care clinicians are necessary to prevent adverse CKD-associated outcomes, including cardiovascular disease, end-stage kidney disease, and death.

OBSERVATIONS

Defined as a persistent abnormality in kidney structure or function (eg, glomerular filtration rate [GFR] <60 mL/min/1.73 m 2 or albuminuria ≥30 mg per 24 hours) for more than 3 months, CKD affects 8% to 16% of the population worldwide. In developed countries, CKD is most commonly attributed to diabetes and hypertension. However, less than 5% of patients with early CKD report awareness of their disease. Among individuals diagnosed as having CKD, staging and new risk assessment tools that incorporate GFR and albuminuria can help guide treatment, monitoring, and referral strategies. Optimal management of CKD includes cardiovascular risk reduction (eg, statins and blood pressure management), 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 risk of CKD progression (eg, estimated GFR <30 mL/min/1.73 m 2 , 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 appropriate referral of CKD by primary care clinicians are important in reducing the burden of CKD worldwide.

Chronic kidney disease (CKD) affects between 8% and 16% of the population worldwide and is often underrecognized by patients and clinicians. 1 – 4 Defined by a glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m 2 , 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 3 months, 5 CKD is more prevalent in low- and middle-income than in high-income countries. 6 Globally, CKD is most commonly attributed to diabetes and/or hypertension, but other causes such as glomerulonephritis, infection, and environmental exposures (such as air pollution, herbal remedies, and pesticides) are common in Asia, sub-Saharan Africa, and many developing countries. 4 Genetic risk factors may also contribute to CKD risk. For example, sickle cell trait and the presence of 2 APOL1 risk alleles, both common in people of African ancestry but not European ancestry, may double the risk of CKD. 4 , 7 – 10

In the United States, the average rate of GFR decline is approximately 1 mL/min/1.73 m 2 per year in the general population, 11 , 12 and the lifetime risk of developing a GFR of less than 60 mL/min/1.73 m 2 is more than 50%. 13 Early detection and treatment by primary care clinicians is important because progressive CKD is associated with adverse clinical outcomes, including end-stage kidney disease (ESKD), cardiovascular disease, and increased mortality. 14 – 17 Recent professional guidelines suggest a risk-based approach to the evaluation and management of CKD. 5 , 18 – 20 This review includes discussion of new calculators for determining risk 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 primary care clinicians. Considerations for referral to a nephrologist and dialysis initiation are also covered.

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-language, 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 expanded to include review articles and observational studies, including cross-sectional studies, and more recent publications contained in reference lists of identified articles. All clinical trials for treatment or prevention of CKD were included without regard to study size or age of patient population.

Clinical Presentation

Chronic kidney disease is typically identified through routine screening with serum chemistry profile and urine studies or as an incidental finding. Less commonly, 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 advanced, patients may report fatigue, poor appetite, nausea, vomiting, metallic taste, 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 about additional symptoms that might suggest a systemic cause (eg, hemoptysis, rash, lymphadenopathy, hearing loss, neuropathy) or urinary obstruction (eg, urinary hesitancy, urgency, or frequency or incomplete bladder emptying). 21 Moreover, patients should be assessed for risk factors of kidney disease, including prior exposure to potential nephrotoxins (eg, nonsteroidal anti-inflammatory drugs [NSAIDs], phosphate-based bowel preparations, herbal remedies such as those containing aristolochic acid, antibiotic therapies such as gentamicin, and chemotherapies), history of nephrolithiasis or recurrent urinary tract infections, presence of comorbidities (eg, hypertension, diabetes, autoimmune disease, chronic infections), family history of kidney disease, and, if available, other known genetic risk factors such as sickle cell trait. 9 , 18 , 21 – 24

A detailed physical examination may provide additional clues regarding the underlying cause of CKD and should include careful evaluation of a patient’s volume status. Signs of volume depletion may reflect poor oral intake, vomiting, diarrhea, or overdiuresis, whereas signs of volume overload may be due to decompensated heart failure, liver failure, or nephrotic syndrome. The presence of arterial-venous nicking or retinopathy on retinal examination suggests long-standing 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, skin excoriations, muscle wasting, asterixis, myoclonic jerks, altered mental status, and pericardial rub. 21

CKD Definition and Staging

Chronic kidney disease is defined as the presence of an abnormality in kidney structure or function persisting for more than 3 months. 5 , 25 This includes 1 or more of the following: (1) GFR less than 60 mL/min/1.73 m 2 ; (2) albuminuria (ie, urine albumin ≥30 mg per 24 hours or urine albumin-to-creatinine ratio [ACR] ≥30 mg/g); (3) abnormalities in urine sediment, histology, or imaging suggestive of kidney damage; (4) renal tubular disorders; or (5) history of kidney transplantation. 5 If the duration of kidney disease is unclear, repeat assessments should be performed to distinguish CKD from acute kidney injury (change in kidney function occurring within 2–7 days) and acute kidney disease (kidney damage or decreased kidney function present for ≤3 months). 25 Evaluation for the etiology of CKD should be guided by a patient’s clinical history, physical examination, and urinary findings ( Figure 1 ). 5 , 18 , 21

a Other imaging modalities or urine studies may also be considered.

b A variety of scores are available, eg, https://kidneyfailurerisk.com/ .

Once a diagnosis of CKD has been made, the next step is to determine staging, which is based on GFR, albuminuria, and cause of CKD ( Figure 2 ). 5 Staging of GFR is classified as G1 (GFR ≥90 mL/min/1.73 m 2 ), G2 (GFR 60–89 mL/min/1.73 m 2 ), G3a (45–59 mL/min/1.73 m 2 ), G3b (30–44 mL/min/1.73 m 2 ), G4 (15–29 mL/min/1.73 m 2 ), and G5 (<15 mL/min/1.73 m 2 ). 5 Although GFR can be directly measured by clearance of agents such as iohexol or iothalamate, 26 – 28 the development of estimating equations (eg, the Chronic Kidney Disease 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 metabolism 25 and one for which laboratory assays have been standardized since 2003. 32 The preferred estimating equation in the United States and much of the world is the CKD-EPI 2009 creatinine equation, which is more accurate than the earlier MDRD equation, particularly for eGFR values greater than 60 mL/min/1.73 m 2 ( https://www.kidney.org/professionals/kdoqi/gfr_calculator). 29 , 30 In situations requiring additional accuracy and precision, cystatin C can 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, high-protein diet, use of creatinine supplements, or use of drugs affecting tubular secretion of creatinine). 5 , 25

GFR indicates glomerular filtration rate; KDIGO, Kidney Disease Improving Global Outcomes. Categories are grouped by risk of progression, which includes chronic kidney disease progression, defined by a decline in GFR category (accompanied by a ≥25% decrease in estimated GFR from baseline) or sustained decline in estimated GFR greater than 5 mL/min/1.73 m 2 per year. Green indicates low risk (if no other markers of kidney disease and no CKD); yellow, moderately increased risk; orange: high risk; and red, very high risk. Reproduced with permission from Kidney International Supplements . 5

Albuminuria should ideally be quantified by a urine ACR. Albuminuria staging is classified as A1 (urine ACR <30 mg/g), A2 (30–300 mg/g), and A3 (>300 mg/g). 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 likely to be standardized and have better precision at lower values of albuminuria. 5 , 33 The most precise measurements come from a first morning 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, however, 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 marker of glomerular pathology 5 since some urine proteins such as uromodulin are present (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 protein can be pursued (eg, immunoglobulin heavy and light chains, α 1 -microglobulin, and β 2 -microglobulin). 5 Imaging by kidney ultrasound to assess morphology and to rule out urinary obstruction should be considered in all patients diagnosed as having CKD. 5

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 not the only organ affected. Anatomic locations are divided into glomerular, tubulointerstitial, vascular, and cystic/congenital diseases. 5 Determining the cause of CKD may have important implications on prognosis and treatment. For example, polycystic kidney disease 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 , 40 Patients with unexplained causes of CKD should be referred to a nephrologist.

Screening for CKD

Given that most patients with CKD are asymptomatic, screening may be important to early detection of disease. 18 The National Kidney Foundation has developed a kidney profile test that includes measuring both serum creatinine for estimating GFR and urine ACR. 41 A risk-based approach to screening is suggested by many clinical practice guidelines, with screening recommended in those older than 60 years or with a history of diabetes or hypertension. 18 – 20 Screening should also be 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 acute kidney injury, among others ( Box ). 9 , 18 , 42 – 45 However, no randomized clinical trials have demonstrated that screening asymptomatic patients for CKD improves outcomes.

Clinical, Sociodemographic, and Genetic Risk Factors for Chronic Kidney Disease

Hypertension

Autoimmune diseases

Systemic infections (eg, HIV, hepatitis B virus, hepatitis C virus)

Nephrotoxic medications (eg, nonsteroidal anti-inflammatory drugs, herbal remedies, lithium)

Recurrent urinary tract infections

Kidney stones

Urinary tract obstruction

Reduced kidney mass (eg, nephrectomy, low birth weight)

History of acute kidney injury

Intravenous drug use (eg, heroin, cocaine)

Family history of kidney disease

Sociodemographic

Age >60 years

Nonwhite race

Low education

APOL1 risk alleles

Sickle cell trait and disease

Polycystic kidney disease

Alport syndrome

Congenital anomalies of the kidney and urinary tract

Other familial causes

Other Risk Factors for CKD

There are several sociodemographic factors that contribute to increased risk of CKD, including nonwhite race, low education, low income, and food insecurity. 18 , 43 , 46 Compared with whites, African Americans and Pacific Islanders have a substantially greater risk of ESKD. 47 This is in part due to an increased prevalence of hypertension, diabetes, and obesity. 11 However, genetic factors likely also contribute. More specifically, risk alleles in the gene encoding apolipoprotein L1 ( APOL1 ) may increase risk of kidney disease in a recessive genetic manner 7 , 8 : individuals with 2 APOL1 risk alleles (present in approximately 13% of African Americans) have a 2-fold risk of CKD progression and up to a 29-fold risk of specific CKD etiologies (eg, focal-segmental glomerulosclerosis and HIV-associated nephropathy) compared with those with 0 or 1 risk allele. 11 , 44 , 45 , 48 , 49 Sickle cell trait (present in approximately 8% of African Americans) has also been associated with an increased risk of kidney disease. Compared with noncarriers, individuals with sickle cell trait have a 1.8-fold odds of incident CKD, 1.3-fold odds of eGFR decline greater than 3 mL/min/1.73 m 2 , and 1.9-fold odds of albuminuria. 9

Management of Patients With CKD

Reducing risk of cardiovascular disease.

The prevalence of cardiovascular disease is markedly higher among individuals with CKD compared with those without CKD. For example, in a Medicare 5% 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 same population, the presence of CKD was associated with lower 2-year survival in people with coronary artery disease (77% vs 87%), acute myocardial infarction (69% vs 82%), heart failure (65% vs 76%), atrial fibrillation (70% vs 83%), and cerebrovascular accident/transient ischemic attack (73% vs 83%). 47

Therefore, a major component of CKD management is reduction of cardiovascular risk. 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 be encouraged. 5 , 53 Both the Eighth Joint National Committee (JNC 8) 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 opinion. 5 , 54 The KDIGO guidelines further recommend that adults with urine ACR of at least 30 mg per 24 hours (or equivalent) have systolic and diastolic blood pressures maintained below 130 mm Hg and 80 mm Hg, respectively. 5 More recently, the Systolic Blood Pressure Intervention Trial (SPRINT) demonstrated that among individuals with increased risk of cardiovascular disease but without diabetes, more intensive blood pressure control (goal systolic blood pressure <120 mm Hg) was associated with a 25% lower (1.65% vs 2.19% per year) risk of a major cardiovascular event and a 27% lower risk of all-cause mortality compared with standard blood pressure control (goal systolic blood pressure <140 mm Hg). 55 The intensive treatment group had a greater risk of at least a 30% decline in eGFR to a level below 60 mL/min/1.73 m 2 ; 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 be used to treat hypertension in people with CKD. 54 , 58 Presence and severity of albuminuria should be evaluated. Blockade of the renin-angiotensin-aldosterone system with either an angiotensin-converting enzyme inhibitor (ACE-I) or an angiotensin II receptor blocker (ARB) is recommended for adults with diabetes and a urine ACR of at least 30 mg per 24 hours or any adult with a urine ACR of at least 300 mg per 24 hours. 5 , 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 also 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 general, drugs that are largely cleared by the kidneys (eg, glyburide) should be avoided, whereas drugs metabolized by the liver and/or partially excreted by the kidneys (eg, metformin and some dipeptidyl peptidase 4 [DPP-4] and sodium-glucose cotransporter-2 [SGLT-2] inhibitors) may require dose reduction or discontinuation, particularly when eGFR falls below 30 mL/min/1.73 m 2 . 18 , 19 Third, use of specific medication classes such as SGLT-2 inhibitors in those with severely increased albuminuria should be considered. The Canagliflozin and Renal Events in Diabetes with Established Nephropathy Clinical Evaluation (CREDENCE) trial demonstrated that, among 4401 patients with type 2 diabetes and CKD stage G2-G3/A3 (baseline eGFR 30 to <90 mL/min/1.73 m 2 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 also suggested cardiovascular benefit with this class of medications, which may extend to patients with CKD who have 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 not recommended, especially among individuals who are taking ACE-I or ARB therapy. 5 , 18 Herbal remedies are not regulated by the US Food and Drug Administration, and some (such as those containing aristolochic acid or anthraquinones) have been reported to cause a myriad of kidney abnormalities, including acute 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 can lead to acute phosphate nephropathy. 23 , 24 Proton pump inhibitors are widely used and have been associated with acute interstitial nephritis in case reports and incident CKD in population-based studies. 71 – 73 In the population-based Atherosclerosis Risk in Communities cohort, the incidence of CKD was 14.2 events in those taking proton pump inhibitors and 10.7 per 1000 events in people who did not take them. 71 Uniform discontinuation of proton pump inhibitors in CKD is not necessary. However, indications for use should be addressed at each primary care visit.

Drug Dosing

Adjustments in drug dosing are frequently required in patients with CKD. Of note, the traditional Cockcroft-Gault equation often poorly reflects measured GFR, whereas estimation of GFR using the CKD-EPI equation likely correlates better with drug clearance by the kidneys. 74 , 75 Common medications that require dose reductions include most antibiotics, direct oral anticoagulants, gabapentin and pregabalin, oral hypoglycemic agents, insulin, chemotherapeutic agents, and opiates, among others. 5 , 18 In general, use of medications with low likelihood of benefit should be minimized because patients with CKD are at high risk of adverse drug events. 76 – 79 Gadolinium-based contrast agents are contraindicated in individuals with acute kidney injury, eGFR less than 30 mL/min/1.73 m 2 , or ESKD given the risk of nephrogenic systemic fibrosis, a painful and debilitating disorder characterized by marked fibrosis of the skin and occasionally other organs. 5 , 18 , 80 , 81 Newer macrocyclic chelate formulations (eg, gadoteridol, gadobutrol, or gadoterate) are much less likely to cause nephrogenic systemic fibrosis, but the best prevention may still 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. 5 , 18 , 80 – 82

Dietary Management

Dietary management to prevent CKD progression is controversial since large trials have had equivocal results. 83 – 85 For example, the MDRD study evaluated 2 levels of protein restriction in 840 patients, finding that a low-protein diet compared with usual protein intake resulted in slower GFR decline only after the initial 4 months, and that a very low-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 g per day, although this group was small. 83 Other, smaller trials have suggested a benefit of protein 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 education) in adults with CKD stages G4-G5 and to less than 1.3 g/kg per day in other adult patients with CKD at risk of progression. 5 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 also help protect against kidney injury. 90 , 91 Low-sodium diets (generally <2 g per day) are recommended for patients with hypertension, proteinuria, or fluid overload. 5

Monitoring of Established CKD and Treatment of Complications

Once CKD is established, the KDIGO guidelines recommend monitoring eGFR and albuminuria at least once 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 year ( Figure 2 ). 5 Patients with moderate to severe CKD are at increased risk 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 complete blood count, basic metabolic panel, serum albumin, phosphate, parathyroid hormone, 25-hydroxyvitamin D, and lipid panel ( Table ). 5 , 50 , 93 , 94

Screening, Monitoring, and Management of the Complications of Chronic Kidney Disease (CKD)

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 across the world, 41% of the 209 311 individuals had low levels of hemoglobin (defined as <13 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 iron deficient may benefit from oral or intravenous iron repletion. Patients with hemoglobin levels persistently below 10 g/dL despite addressing reversible causes can be referred to a nephrologist for consideration of additional medical therapy, including erythropoietin-stimulating agents; however, erythropoietin-stimulating agents have been associated with increased risk of death, stroke, and venous thromboembolism, and these risks must be weighed against any potential benefits. 93

Electrolyte, Mineral, and Bone Abnormalities in CKD

Electrolyte abnormalities are present in 3% to 11% of patients with CKD. 92 Initial treatment strategies usually involve dietary restrictions and prescription of supplements. For example, primary care clinicians should recommend low-potassium diets for patients with hyperkalemia and low-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 also common. In a study 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, most 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 risk factors and geographical location. For example, in North America, the incidence among individuals with eGFR less than 60 mL/min/1.73 m 2 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 1.2 to 131.3 ESKD events per 1000 patient-years. 100 Most patients with CKD do not require kidney replacement therapy during their lifetime. 101 Simple online tools are available to help with risk stratification. For example, the Kidney Failure Risk Equation (KFRE; https://kidneyfailurerisk.com/ ) predicts the 2-year and 5-year probabilities of requiring dialysis or transplant among individuals with eGFR less than 60 mL/min/1.73 m 2 . 100 , 102 The KFRE, which has been validated in more than 700 000 individuals from more than 30 countries, uses readily available clinical and laboratory variables. The 4-variable equation includes age, sex, 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 wait times, 103 and a 2-year KFRE greater than 10% was used to guide referrals to multidisciplinary CKD clinics. 104 An ongoing trial is evaluating whether a KFRE risk-based approach improves CKD management. 105 For patients with eGFR less than 30mL/min/1.73m 2 , the CKD G4+ risk calculator ( https://www.kdigo.org/equation/ ) may provide additional information on the risks of cardiovascular disease and death. 106 , 107 Importantly, risk prognostication may be helpful in not only identifying individuals at high risk of disease progression but also 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 m 2 (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 blood cells per high-power field of unclear etiology, red blood cell casts on urine microscopy or other indication of glomerulonephritis, CKD with uncontrolled hypertension despite 4 or more 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 decline in eGFR >5 mL/min/1.73 m 2 ). 5 In persons without CKD, even small changes in serum creatinine (eg, from 0.7 mg/dL to 1.2 mg/dL) reflect large declines in eGFR, and primary care clinicians should attempt to identify reversible causes. Indications for kidney biopsy may include but 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 by institution. Patients with polycystic kidney disease, certain 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 decision to begin kidney replacement therapy is based on the presence of symptoms and not solely on level of GFR. 108 Urgent indications include encephalopathy, pericarditis, and pleuritis due to severe uremia. 109 Otherwise, initiation of dialysis should be 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 status), electrolyte abnormalities (eg, hyperkalemia or metabolic acidosis), or volume overload (eg, pulmonary or lower extremity edema) refractory to medical management. 5 , 18 , 109 A shared decision-making approach is best. Patients should be educated about treatment options and actively contribute to decision-making. Early education should include information on the potential complications of CKD as well as the different modalities of kidney replacement therapy. Kidney transplantation is considered the optimal therapy for ESKD, with living donor kidney transplantations performed before or shortly after dialysis initiation having the best outcomes. 110 , 111 As such, early referral (eg, eGFR <30 mL/min/1.73 m 2 and an elevated 2-year risk of ESKD) for transplant evaluation is important. 112 , 113 Alternative therapies for ESKD may include in-center hemodialysis, home hemodialysis, peritoneal dialysis, or conservative 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 exhibit rapid decline in eGFR should be referred to an experienced vascular surgeon for arteriovenous fistula placement. The KDOQI guidelines recommend that access creation should occur when eGFR is between 15 and 20 mL/min/1.73 m 2 . 114 Of note, dialysis initiation has been associated with accelerated functional decline and high short-term mortality among older patients with poor functional status. 115 , 116 Patient preferences for conservative approaches to medical management should be discussed and honored.

Conclusions

Chronic kidney disease affects 8% to 16% of the population worldwide and is a leading cause of death. Optimal management of CKD includes cardiovascular risk reduction, treatment of albuminuria, avoidance of potential nephrotoxins, and adjustments to drug dosing. Patients also require 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 Center for Kidney Research Pilot and Feasibility Grant from Yale University and award K08DK117068 from the National Institutes of Health/NIDDK. Dr Grams is supported by NIDDK grants DK1008803, DK100446, and DK115534.

Role of the Funder/Sponsor: The supporting institutions had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; or decision to submit the manuscript for publication.

Conflict of Interest Disclosures: Dr Chen reported receipt of grants from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and Yale University. 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 as a Review. Please contact Edward Livingston, MD, at Edward. gro.krowtenamaj@notsgnivil or Mary McGrae McDermott, MD, at ude.nretsewhtron@806mdm .

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XORTX Announces Presentation at American Society of Nephrology – Kidney Week 2024

Health consequences of over active xanthine oxidase may accelerated pkd progression.

CALGARY, Alberta , Aug. 20, 2024 (GLOBE NEWSWIRE) -- XORTX Therapeutics Inc. ("XORTX" or the “Company”) (NASDAQ: XRTX | TSXV: XRTX | Frankfurt: ANUA), a late-stage clinical pharmaceutical company focused on developing innovative therapies to treat progressive kidney disease, is pleased to announce the acceptance of an abstract submitted to the American Society of Nephrology (the “ASN”).  The abstract entitled "Xanthine oxidase in rats, mice and humans with polycystic kidney disease" was reviewed by the ASN review panel for scientific merit and novel discoveries.  The study was conducted at the University of Colorado in the independent laboratory of Dr. Charles Edelstein and was sponsored by XORTX and will be presented during the Session Title: Genetic Diseases: Cystic - Therapeutic Investigations and Prognosis.

About this study

The xanthine oxidase (“XO”) enzyme is an essential enzyme within the uric acid pathway, and is required for the breakdown of purine nucleotides. Uric acid as well as reactive oxygen species released during the enzymatic reaction may also play a detrimental role in the circulatory system and within tissue during disease. Recent pioneering discoveries in rodent models of polycystic kidney disease (“PKD”) implicate over expression or over activity of XO. It is currently unknown if XO over expression or over activity in humans is associated with PKD or more rapid progression of disease.   The aim of the study was to gain insight into whether increased XO activity results in cyst growth, XO activity was measured in PCK1 rats, PKD1RC/RC (RC) mice and 34 patients from the HALT-PKD Clinical study.

The abstract outlines study results from mouse, rat and human studies of PKD. The purpose of the study was to gain an understanding of serum xanthine oxidase activity (XOa) in PKD during varied stages of disease and further to relate that activity to total kidney volume, and decline of glomerular filtration rate (GFR).  The results of the study provide understanding of where aberrant purine metabolism in PKD tissue due to sources XO enzyme may contribute to circulating uric acid levels, expansion rate of kidney and cyst and functional GFR decline.  Prior study results suggested over expression of XO in PKD kidney tissue may be a feature of cystic disease. XORTX will provide a further update on the results of the study during the first week of November.

Dr. Allen Davidoff , CEO of XORTX, stated, “We are pleased to once again be presenting pioneering studies in PKD due to ADPKD at the American Society of Nephrology annual meeting during Kidney Week 2024 with this poster presentation. Most importantly, results of this study deepen our understanding of how increased serum uric acid or aberrant kidney tissue expression of XO contribute to accelerate injury using data from mouse, rat and human studies of PKD. The XRx-008 program continues to pioneer our understanding of how too much or too active xanthine oxidase may result in a health consequence in PKD.”

About the American Society of Nephrology – Kidney Week

ASN represents more than 21,000 kidney health professionals working to help people with kidney diseases and their families. ( Source: https://www.asn-online.org/ )

The Kidney Week Conference is attended by approximately 10,000 other kidney professionals from across the globe at Kidney Week 2024 in Orlando, Florida . The world's premier nephrology meeting, Kidney Week provides participants with exciting and challenging opportunities to exchange knowledge, learn the latest scientific and medical advances, and listen to engaging and provocative discussions with leading experts in the field. ( Source: https://www.asn-online.org/education/kidneyweek/American Society of Nephrology - Program and Abstracts)

The Kidney Week program is available on the ASN website . Abstracts will be available on the ASN website by October 14, 2024 .

About ADPKD

ADPKD is a rare disease that affects more that 10 million individuals worldwide.1,2 ADPKD is typically diagnosed based upon expansion of fluid-filled cysts in the kidneys. Over time, the increasing number and size of cysts can contribute to structural and functional changes to kidneys and is frequently accompanied by chronic pain which is a common problem for patients with ADPKD.3 Expansion of cysts is thought to compress healthy functioning tissue surrounding the cysts and contribute to further loss of kidney function, fibrosis, impaired nutrient exchange and impaired kidney function, accompanied later by end-stage renal disease.1 Health consequences of high uric acid have been reported to be increased in ADPKD individuals, including increased incidence of kidney stones5 and gout.6,7 For individuals with progressing ADPKD, treatment recommendations include anti-hypertensive treatment, dietary restrictions, and, for a limited percentage of suitable patients, pharmacotherapy.4 New, more broadly applicable therapies to effectively slow decline of kidney function in ADPKD are needed.

References:

• Wiley C., Kamat S., Stelhorn R., Blais J., Analysis of nationwide date to determine the incidence and diagnosis of autosomal dominant polycystic kidney disease in the USA , Kidney Disease, 5(2): 107-117, 2019
• Bergmann C., Guay-Woodford L.M ., Harris P.C. , Horie S., Peters D.J., Torres V.E., Polycystic Kidney Disease, Nat Rev Dis Primers. 4(1): 50, 2018
• https://pkdcure.org/living-with-pkd/chronic-pain-management
• Gimpel C., Bergmann C., Bockenhauer D., et al., International consensus statement of the diagnosis and management of autosomal dominant polycystic kidney disease in children and young people, Nat Rev Nephrol 15(11):713-726, 2019
• Torres VE, et al, The association of nephrolithiasis and autosomal dominant polycystic kidney disease, Am J Kidney Dis, 1988, vol 11, 318-325
• Newcombe, DS. Letter Gouty Arthritis and polycystic kidney disease, Ann Intern Med, 1973 vol 79, pg 605
• Rivera JV Martinez, et al, Association of hyperuricemia and polycystic kidney disease, Bol Asoc Med P R, 1965 vol 7 251-263

About XORTX Therapeutics Inc.

XORTX is a pharmaceutical company with two clinically advanced products in development: 1) our lead, XRx-008 program for ADPKD; and 2) our secondary program in XRx-101 for acute kidney and other acute organ injury associated with Coronavirus / COVID-19 infection. In addition, XRx-225 is a pre-clinical stage program for Type 2 Diabetic Nephropathy. XORTX is working to advance its clinical development stage products that target aberrant purine metabolism and xanthine oxidase to decrease or inhibit production of uric acid. At XORTX, we are dedicated to developing medications to improve the quality of life and future health of patients. Additional information on XORTX is available at www.xortx.com .

Neither the TSX Venture Exchange nor Nasdaq has approved or disapproved the contents of this news release. No stock exchange, securities commission or other regulatory authority has approved or disapproved the information contained herein.

Forward Looking Statements

This press release contains express or implied forward-looking statements pursuant to applicable securities laws. These forward-looking statements include, but are not limited to, the Company's beliefs, plans, goals, objectives, expectations, assumptions, estimates, intentions, future performance, other statements that are not historical facts and statements identified by words such as "expects", "anticipates", "intends", "plans", "believes", "seeks", "estimates" or words of similar meaning.  These forward-looking statements and their implications are based on the current expectations of the management of XORTX only, and are subject to a number of factors and uncertainties that could cause actual results to differ materially from those described in the forward-looking statements. Such risks, uncertainties, and other factors include, but are not limited to, our ability to obtain additional financing; the accuracy of our estimates regarding expenses, future revenues and capital requirements; the success and timing of our preclinical studies and clinical trials; the performance of third-party manufacturers and contract research organizations; our plans to develop and commercialize our product candidates; our plans to advance research in other kidney disease applications; and, our ability to obtain and maintain intellectual property protection for our product candidates.  Except as otherwise required by applicable law and stock exchange rules, XORTX undertakes no obligation to publicly release any revisions to these forward-looking statements to reflect events or circumstances after the date hereof or to reflect the occurrence of unanticipated events. More detailed information about the risks and uncertainties affecting XORTX is contained under the heading “Risk Factors” in XORTX’s Annual Report on Form 20-F filed with the SEC , which is available on the SEC's website, www.sec.gov (including any documents forming a part thereof or incorporated by reference therein), as well as in our reports, public disclosure documents and other filings with the securities commissions and other regulatory bodies in Canada , which are available on www.sedarplus.ca .

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• Disease activity of rheumatoid arthritis and kidney function decline: a large prospective registry study
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• http://orcid.org/0000-0002-3082-1374 Sho Fukui 1 , 2 , 3 ,
• Wolfgang C Winkelmayer 4 ,
• http://orcid.org/0000-0001-9475-1363 Sara K Tedeschi 1 ,
• http://orcid.org/0000-0001-9157-4269 Javier Marrugo 1 ,
• Hongshu Guan 1 ,
• Leslie Harrold 5 , 6 ,
• Heather J Litman 6 ,
• Tomohiro Shinozaki 7 ,
• http://orcid.org/0000-0001-8202-5428 Daniel H Solomon 1
• 1 Division of Rheumatology, Inflammation, and Immunity , Brigham and Women's Hospital and Harvard Medical School , Boston , Massachusetts , USA
• 2 Department of Emergency and General Medicine , Kyorin University , Tokyo , Japan
• 3 Immuno-Rheumatology Center , St. Luke’s International Hospital , Tokyo , Japan
• 4 Selzman Institute for Kidney Health, Section of Nephrology , Baylor College of Medicine , Houston , Texas , USA
• 5 Medicine , University of Massachusetts Medical School , Worcester , Massachusetts , USA
• 6 CorEvitas LLC , Waltham , Massachusetts , USA
• 7 Department of Information and Computer Technology, Faculty of Engineering , Tokyo University of Science , Katsushika-ku , Tokyo , Japan
• Correspondence to Dr Sho Fukui; sfukui{at}bwh.harvard.edu ; Professor Daniel H Solomon; dsolomon{at}bwh.harvard.edu

Introduction Chronic kidney disease (CKD) is a common comorbidity of rheumatoid arthritis (RA). The association of longitudinal RA disease activity with long-term kidney function has remained uncertain.

Method We analysed a multicentre prospective RA registry in the USA from 2001 to 2022. The exposure was updated time-averaged Clinical Disease Activity Index (TA-CDAI) categories from study enrolment. The primary outcome was a longitudinal estimated glomerular filtration rate (eGFR) change. Secondary outcomes included developments of CKD stage G3a (eGFR<60 mL/min/1.73 m 2 ) and stage G3b (eGFR<45 mL/min/1.73 m 2 ). Results were adjusted for relevant time-fixed and time-varying covariates.

Results 31 129 patients (median age: 58.0 years, female: 76.3%, median eGFR: 90.7 mL/min/1.73 m 2 ) contributed 234 973 visits and 146 778 person-years of follow-up. Multivariable mixed-effect linear model showed an average annual eGFR decline during follow-up in the TA-CDAI-remission group of −0.83 mL/min/1.73 m 2 and estimated additional annual declines (95% CI) of –0.09 (–0.15 to –0.03) in low, –0.17 (−0.23 to –0.10) in moderate and −0.18 (–0.27 to –0.08) mL/min/1.73 m 2 in high disease activity patients. Compared with TA-CDAI remission, adjusted HRs (95% CI) for CKD stage G3a during follow-up were 1.15 (1.01 to 1.30) in low, 1.22 (1.06 to 1.40) in moderate and 1.27 (1.05 to 1.52) in high disease activity; for CKD stage G3b, 1.22 (0.84 to 1.76) in low, 1.66 (1.12 to 2.45) in moderate and 1.93 (1.16 to 3.20) in high disease activity.

Conclusions Higher RA disease activity was associated with accelerated eGFR decline and increased risk of clinically relevant kidney dysfunction. Future intervention studies should attempt to replicate the association between RA disease activity and eGFR.

• Rheumatoid Arthritis
• Epidemiology
• Arthritis, Rheumatoid
• Atherosclerosis

Data availability statement

No data are available. Data are not available publicly.

https://doi.org/10.1136/ard-2024-226156

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Handling editor Josef S Smolen

Contributors SF and DHS contributed to the original conception and design of this study, which WCW, SKT, JM, LH, HJL and TS reviewed and corrected. SF and HG collected data. SF performed data analysis with supervision from LH, HJL, TS and DHS. SF, WCW, SKT, JM and DHS initially interpreted the data, and other authors advised on the interpretation. SF drafted the original manuscript, which was critically reviewed and revised by all other authors. All authors have read and approved the final version of the manuscript. The corresponding author attests that all listed authors meet authorship criteria and that no others meeting the criteria have been omitted. SF is the guarantor.

Funding This study was supported by funding from National Institute of Arthritis and Musculoskeletal and Skin Diseases P30 AR072577 (PI: DHS).

Competing interests WCW reports having served as a scientific advisor or consultant to Actos, Akebia, Ardelyx, AstraZeneca, Bayer, Cadrenal, GlaxoSmithKline, Lilly, Merck, Natera, Pharmacosmos, Unicycive, Vera and Zydus. SKT reports consulting fees from Novartis. LH reports employment of CorEvitas, consultant to AbbVie, Bristol Myers Squibb, Pfizer, Roche and speakers bureau for Bristol Myers Squibb. DHS reports salary support through research contracts to his institution from CorEvitas, Janssen and Novartis.

Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

Provenance and peer review Not commissioned; externally peer reviewed.

Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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Anemia and Chronic Kidney Disease

What is anemia.

Anemia happens when your red blood cells are in short supply. Red blood cells carry oxygen from your lungs to all parts of your body, giving you the energy you need for your daily activities.

What are the symptoms of anemia?

Anemia can cause you to:

• Have little energy for your daily activities
• Have a poor appetite
• Have trouble sleeping
• Have trouble thinking clearly
• Feel dizzy or have headaches
• Have a rapid heartbeat
• Feel short of breath
• Feel depressed or "down in the dumps"

Why do people with kidney disease get anemia?

Your kidneys make an important hormone called erythropoietin (EPO) . Hormones are chemical messengers that travel to tissues and organs to help you stay healthy. EPO tells your body to make red blood cells. When you have kidney disease, your kidneys cannot make enough EPO. Low EPO levels cause your red blood cell count to drop and anemia to develop.

Most people with kidney disease will develop anemia. Anemia can happen early in the course of kidney disease and grow worse as kidneys fail and can no longer make EPO. Anemia is especially common if you:

• Have diabetes
• Are African-American/Black
• Have moderate or severe loss of kidney function ( CKD stage 3 or 4)
• Have kidney failure (stage 5)

Check out our online communities to connect, learn more and hear from others going through similar experiences.

How do i know if i have anemia.

Not everyone with anemia has symptoms. If you have kidney disease, you should have a blood test to measure your hemoglobin level at least once a year to check for anemia. Hemoglobin is the part of red blood cells that carries oxygen throughout your body. If your hemoglobin is too low, it is likely you have anemia. In that case, your healthcare provider will check to find the exact cause of your anemia and plan a treatment that is right for you.

How do you treat anemia?

Your treatment will depend on the exact cause of your anemia.

If your anemia is due to kidney disease, your healthcare provider will treat you with:

• Drugs called erythropoiesis stimulating agents (ESAs) ESAs help your body make red blood cells. Your healthcare provider will give the ESA to you as an injection under the skin.
• Extra iron Your body also needs iron to make red blood cells—especially when you are receiving ESAs. Without enough iron, your ESA treatment will not work as well. Your healthcare provider may give you iron to take as a pill. Another way to receive iron is directly into a vein in your doctor's office or clinic.

For more information please view our full PDF brochures or request a free copy by calling 855.NKF.CARES ( 855.653.2273 ) or email [email protected] .

• Anemia and Iron Needs in Dialysis

If you would like more information, please contact us .

© 2015 National Kidney Foundation. All rights reserved. This material does not constitute medical advice. It is intended for informational purposes only. Please consult a physician for specific treatment recommendations.

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