|
| A) | rash. | ||
| B) | hematuria. | ||
| C) | proteinuria. | ||
| D) | bacteremia. |
A common marker of CKD is proteinuria, which is first detectable as microalbuminuria (i.e., >30 mg albumin in a 24-hour urine collection). Due to the difficulty of measuring 24-hour urine protein excretion, proteinuria is usually screened using dipstick or a spot urine albumin-creatinine ratio. Other indicators include abnormal urine sediment or abnormal imaging studies.
| A) | allergies and diabetes. | ||
| B) | infection and diabetes. | ||
| C) | diabetes and hypertension. | ||
| D) | infection and hypertension. |
The two leading causes of ESRD are diabetes (38% of new patients) and hypertension (27% of new cases) [12]. New cases of ESRD with diabetes or hypertension listed as the primary cause had been rising rapidly since 1980, but each has declined from 2000 to 2016 [13,14]. Other less common causes of ESRD include glomerulonephritis, interstitial nephritis, autosomal dominant polycystic kidney disease (the leading genetic cause), and collagen vascular disease. Due to the prevalence of kidney transplantation, post-transplantation kidney disease has become the fourth largest cause of ESRD in the United States; however, these patients are reported within their original disease category for epidemiologic purposes [15]. New cases of diabetic ESRD are expectedly higher with increasing age in all racial groups, but generally lower among younger individuals [11]. Statistically, non-whites are four times more likely to require dialysis. Adjusted ESRD prevalence increases with advancing age, with 7,048 cases per million people 65 to 74 years of age and 7,380cases per million people 75 years of age and older. Adjusted ESRD prevalence in Black, White, and Asian individuals was essentially unchanged between 2021 and 2022. However, adjusted ESRD prevalence in Black Americans was 23 times higher than in White Americans in 2022; 14 years earlier, that ratio was 3.8, highlighting the slow progress in addressing the disparity in ESRD prevalence [11].
| A) | diabetes. | ||
| B) | Alport syndrome. | ||
| C) | autosomal recessive polycystic kidney disease. | ||
| D) | autosomal dominant polycystic kidney disease. |
The two leading causes of ESRD are diabetes (38% of new patients) and hypertension (27% of new cases) [12]. New cases of ESRD with diabetes or hypertension listed as the primary cause had been rising rapidly since 1980, but each has declined from 2000 to 2016 [13,14]. Other less common causes of ESRD include glomerulonephritis, interstitial nephritis, autosomal dominant polycystic kidney disease (the leading genetic cause), and collagen vascular disease. Due to the prevalence of kidney transplantation, post-transplantation kidney disease has become the fourth largest cause of ESRD in the United States; however, these patients are reported within their original disease category for epidemiologic purposes [15]. New cases of diabetic ESRD are expectedly higher with increasing age in all racial groups, but generally lower among younger individuals [11]. Statistically, non-whites are four times more likely to require dialysis. Adjusted ESRD prevalence increases with advancing age, with 7,048 cases per million people 65 to 74 years of age and 7,380cases per million people 75 years of age and older. Adjusted ESRD prevalence in Black, White, and Asian individuals was essentially unchanged between 2021 and 2022. However, adjusted ESRD prevalence in Black Americans was 23 times higher than in White Americans in 2022; 14 years earlier, that ratio was 3.8, highlighting the slow progress in addressing the disparity in ESRD prevalence [11].
| A) | White race. | ||
| B) | low income. | ||
| C) | female sex. | ||
| D) | BMI. |
The two leading causes of ESRD are diabetes (38% of new patients) and hypertension (27% of new cases) [12]. New cases of ESRD with diabetes or hypertension listed as the primary cause had been rising rapidly since 1980, but each has declined from 2000 to 2016 [13,14]. Other less common causes of ESRD include glomerulonephritis, interstitial nephritis, autosomal dominant polycystic kidney disease (the leading genetic cause), and collagen vascular disease. Due to the prevalence of kidney transplantation, post-transplantation kidney disease has become the fourth largest cause of ESRD in the United States; however, these patients are reported within their original disease category for epidemiologic purposes [15]. New cases of diabetic ESRD are expectedly higher with increasing age in all racial groups, but generally lower among younger individuals [11]. Statistically, non-whites are four times more likely to require dialysis. Adjusted ESRD prevalence increases with advancing age, with 7,048 cases per million people 65 to 74 years of age and 7,380cases per million people 75 years of age and older. Adjusted ESRD prevalence in Black, White, and Asian individuals was essentially unchanged between 2021 and 2022. However, adjusted ESRD prevalence in Black Americans was 23 times higher than in White Americans in 2022; 14 years earlier, that ratio was 3.8, highlighting the slow progress in addressing the disparity in ESRD prevalence [11].
| A) | diabetic. | ||
| B) | prerenal. | ||
| C) | postrenal. | ||
| D) | intrarenal. |
The pathophysiology of AKI depends on the site of occurrence. Prerenal AKI, the most common type, is caused by renal hypoperfusion (most likely from dehydration) [16]. Intrarenal or intrinsic AKI, the result of damage to the renal parenchyma, may be a result of prolonged prerenal AKI (leading to acute tubular necrosis), toxins, interstitial disease, vascular disease, or acute glomerular disease [16]. Postrenal (obstructive) AKI results from physical obstruction of urine outflow and may be caused by neoplasm, prostatic enlargement, bladder dysfunction, or nephrolithiasis [3,16,17].
| A) | the presence of proteinuria. | ||
| B) | clinical signs and symptoms. | ||
| C) | patient physical examination. | ||
| D) | recognition of the primary pathologic mechanism responsible for renal injury. |
The clinical presentation of CKD is often subtle, and symptoms are uncommon with a GFR greater than about 35 mL/min/1.73 m2. Therefore, suspicion for mild renal disease should be based on recognition of the primary pathologic mechanism responsible for renal injury, particularly in patients with diabetes and/or hypertension. It is equally important to begin early screening for the complications of renal disease to prevent morbidity and to establish a credible baseline for the individual patient.
| A) | dipstick urinalysis. | ||
| B) | kidney ultrasound. | ||
| C) | auscultation of lung sounds. | ||
| D) | serum creatinine measurements. |
The most important tool in monitoring patients with suspected and diagnosed renal failure or those at risk for developing renal disease is dipstick urinalysis, which should be performed at virtually every office visit. Urine dipstick testing is highly specific (although false positives do occur) but less sensitive than quantitative testing. The presence of proteinuria should alert the clinician to perform a full 24-hour urine analysis for protein and creatinine clearance (Table 3). All patients with diabetes who are negative for macroscopic proteinuria on dipstick testing should have laboratory testing for microalbuminuria, as early identification and treatment can improve prognosis. This testing should be initiated at the time of diagnosis for patients with type 2 diabetes and within two years of diagnosis for patients with type 1 diabetes [19].
| A) | orthostatic hypotension. | ||
| B) | edema of the extremities. | ||
| C) | very high urine osmolality. | ||
| D) | brownish, muddy appearance of urine. |
Urinalysis is highly diagnostic in differentiating between AKI and CKD. Prerenal AKI is usually accompanied by urine osmolality of more than 500 mOsm/kg, specific gravity of more than 1.020, and hyaline casts. Intrarenal AKI results in a urine osmolality of approximately 300 mOsm/kg, with a specific gravity of around 1.010, tubular casts, tubular cells, and a distinctive brownish, muddy appearance of the urine due to brown granular casts [18,26].
| A) | Proteinuria | ||
| B) | Increasing GFR | ||
| C) | Older age at diagnosis | ||
| D) | Hematuria of nonrenal origin |
Almost all patients with stage 1 and stage 2 CKD are managed in primary care. Stage 1 CKD is kidney disease with normal kidney function. Kidney function in stage 2 is 60% to 90% [27]. The emphasis for these patients is identifying and managing risk factors, monitoring progression of renal impairment, and beginning patient education. It is important to remember that the risk of cardiovascular events is higher in patients with early CKD than advancement to dialysis or kidney transplantation [27]. Therefore, interventions to address cardiovascular risk factors are warranted, including increased physical activity, dietary changes, smoking cessation, and possibly pharmacologic treatment of hyperlipidemia or hypertension. Factors that indicate an increased risk of advancement to higher stages of kidney disease include [27]:
Proteinuria (albumin-to-creatinine ratio >70 mg/mmol or protein-to-creatinine ratio >100 mg/mmol)
Hematuria of renal origin
Declining GFR (Loss of 5 mL/min/1.73 m2 over one year or less or loss of 10 mL/min/1.73 m2 over five years or less)
Young age at diagnosis
Family history of renal failure
Hypertension that is difficult to control
| A) | monthly. | ||
| B) | every six months. | ||
| C) | annually. | ||
| D) | every two years. |
Cardiovascular risk should also be assessed and addressed annually. Patients should be counseled regarding smoking, exercise, and lifestyle. Cholesterol-lowering therapy should be considered in patients with evidence of macrovascular disease or with an estimated 10-year risk of cardiovascular events ≥20% [27].
| A) | uremia. | ||
| B) | anemia. | ||
| C) | liver failure. | ||
| D) | cardiovascular complications. |
While cardiovascular complications are recognized as the leading cause of death among patients with ESRD, accounting for more than 50% of deaths in the first year of dialysis, studies have shown that even mild-to-moderate renal disease (defined as an elevated serum creatinine between 1.2 mg/dL and 1.4 mg/dL) is an independent risk factor for cardiovascular events [5,6,38]. A meta-analysis of 38,000 patients revealed a 19% to 21% increase in the need for thrombolytic therapy in patients with a GFR less than 70 mL/min/1.73 m2 compared to patients with normal GFR [5]. A GFR less than 60 mL/min/1.73 m2 is an independent risk factor for heart failure. The mortality rate for patients with ESRD is more than 20% per year, making the prevention of cardiovascular complications the utmost priority [38].
| A) | lupus. | ||
| B) | hypotension. | ||
| C) | renal artery stenosis. | ||
| D) | diabetic nephropathy. |
Adequate blood pressure control has been proven beneficial in patients diagnosed with CKD [38]. Ideally, blood pressure should be reduced to less than 130/85 mm Hg [9]. The United Kingdom Prospective Diabetes Study showed benefit of even lower systolic pressures, with reduction in macrovascular complications in patients with diabetes continuing to systolic pressures as low as 114 mm Hg [40]. The use of ACE inhibitors and ARBs has also been shown to be beneficial in patients with diabetic nephropathy and for those with nondiabetic renal disease and proteinuria [40,41,42,43,44,45,46]. A meta-analysis suggested that ACE inhibitor therapy may provide superior benefit over ARB therapy, with a 10% reduction in all-cause mortality [47]. However, the selection of one agent over another will also take into account patient-specific factors (e.g., cost, potential for side effects). Simultaneous treatment with an ACE inhibitor and an ARB is not recommended, as this has been shown to worsen kidney function [6,48,49,50,51]. ACE inhibitors and ARBs should be used cautiously in patients at risk for hyperkalemia and should be avoided in patients with renal artery stenosis unless prescribed by a renal specialist, in which case close monitoring of renal function is absolutely essential [18,32].
| A) | 50 mg/dL. | ||
| B) | 70 mg/dL. | ||
| C) | 100 mg/dL. | ||
| D) | 130 mg/dL. |
Hyperlipidemia is both a complication of CKD and a potential factor in the progression of the disease [9]. Lowering LDL cholesterol to achieve National Cholesterol Education Program goals (i.e., LDL less than 70 mg/dL) in patients with CKD is recommended [60]. The LDL target for any patient with diabetes and CKD is the same as for a patient without diabetes. A number of agents are available for the treatment of lipid disorders, although most have dosing limitations dependent on the degree of renal impairment present.
| A) | 0.8–1.2 g. | ||
| B) | 3–5 g. | ||
| C) | 8–12 g. | ||
| D) | less than 60 g. |
DIETARY RECOMMENDATIONS FOR ADULT PATIENTS WITH CHRONIC RENAL FAILURE WHO ARE NOT ON DIALYSIS
| Nutrient | Recommendation |
|---|---|
| Protein | 0.6–0.8 g/kg/day |
| Calories | 35 kcal/kg/day |
| Phosphorus | 0.8–1.2 g/day |
| Calcium | 1.2–1.6 g/day |
| Sodium | 1–3 g/day |
| Potassium | <60 mEq/day (restricted if serum potassium level is elevated or urinary output is <1 L/day) |
| A) | Digoxin | ||
| B) | Opioids | ||
| C) | Antifungals | ||
| D) | All of the above |
| A) | anemia. | ||
| B) | neutropenia. | ||
| C) | pancytopenia. | ||
| D) | thrombocytopenia. |
Erythropoietin production is usually normal in patients with GFR rates greater than 20 mL/min/1.73 m2. However, the CBC should be monitored. If the hematocrit level falls to less than 32% (the level at which erythropoietin production is stimulated), serum erythropoietin levels should be assessed to determine the cause of the anemia. If serum erythropoietin stays low, exogenous erythropoietin should be given. To avoid transfusion-related hepatitis B (as well as the need for increased infection control precautions during hemodialysis), immunization should be given to patients who are antibody negative. Follow-up serology (i.e., hepatitis B surface antibody and hepatitis B surface antigen) should also be obtained, as many uremic patients seem to have problems mounting a demonstrable immune response after immunization [76].
| A) | 15 mL/min/1.73 m2. | ||
| B) | 25 mL/min/1.73 m2. | ||
| C) | 35 mL/min/1.73 m2. | ||
| D) | 45 mL/min/1.73 m2. |
ESRD is commonly defined as a GFR of less than 15 mL/min/1.73 m2, and the basic hallmark of ESRD is uremia [5,88]. Uremic toxins are the byproducts of protein metabolism; in patients with ESRD, the toxins are not eliminated by the kidneys and begin to accumulate [5]. Severe uremia necessitates the use of dialysis to remove uremic toxins and prevent or control complications.
| A) | 0.1–0.4 g/kg. | ||
| B) | 0.6–0.8 g/kg. | ||
| C) | 1.1–1.4 g/kg. | ||
| D) | 11–14 g/kg. |
DIETARY RECOMMENDATIONS FOR ADULTS WITH END-STAGE RENAL DISEASE ON DIALYSIS
| Nutrient | Recommendation for Hemodialysis | Recommendation for Peritoneal Dialysis |
|---|---|---|
| Protein | 1.1–1.4 g/kg/day | 1.2–1.5 g/kg/day |
| Calories | 30–35 kcal/kg/day | 25–35 kcal/kg/day |
| Phosphorus | <17 mg/kg/day | <17 mg/kg/day |
| Calcium | 1.0–1.8 g/day | 1.0–1.8 g/day |
| Fluid | Daily urinary output + 500–750 mL/day | 2–3 L/day based on weight and blood pressure |
| Sodium | 2–3 g/day | 3–4 g/day based on weight |
| Potassium | 40 mg/kg | Unrestricted unless elevated |
| A) | arteriovenous graft. | ||
| B) | arteriovenous fistula. | ||
| C) | temporary venous catheter. | ||
| D) | All of the above |
Hemodialysis can be provided via three major different types of access: an AV fistula, an AV graft, or a temporary venous catheter. In its 2006 guideline for vascular access, the NKF endorsed a goal for at least 65% of all patients on hemodialysis to have a working AV fistula by 2009 [95]. In the 2019 update of the guideline, the vascular access Work Group emphasizes a more patient-focused approach that takes into account each patient's needs and preferences when choosing access type [96]. From 2012 to 2022, the percentage of institutions initiating hemodialysis with an AV fistula fell from 16.5% to 12.5% [11].
| A) | palpating a thrill. | ||
| B) | auscultating a bruit. | ||
| C) | taking a blood pressure of the fistula. | ||
| D) | Both A and B |
Fistula patency can be assessed by palpation of "thrill" and auscultation of bruit. A palpable motion in the surface of the fistula and a bruit when a stethoscope is placed over the fistula should both be present. The bruit should be loudest at the arterial side of the fistula. Patients found to have nonpatent grafts should be referred immediately to interventional radiology, as patency can often be restored by the use of antithrombotics (e.g., tissue plasminogen activators) and/or balloon angioplasty. Unfortunately, the use of contrast medium is usually necessary in order to restore patency. In these cases, the patient should be dialyzed within 24 hours of receiving the contrast. If the patient is to receive dialysis immediately after angioplasty, catheters may be left in place so it is not necessary to recannulate immediately after the procedure. If the patient is to return the following day for dialysis, temporary catheters should be removed to prevent potentially deadly hemorrhage. At no point should any patient with ESRD receive gadolinium-based contrast dye due to the risk of nephrogenic systemic fibrosis [96]. Postexposure dialysis does not decrease the risk of developing nephrogenic systemic fibrosis in at-risk patients.
| A) | Hypertension | ||
| B) | HIV infection | ||
| C) | Metastatic cancer | ||
| D) | Age older than 50 years |
The indication for transplantation is ESRD, or a GFR of <15 mL/min/1.73 m2 [9]. In recent years, the process for selection of kidney transplant has liberalized, with larger numbers of elderly patients being accepted for transplantation. In 1991, 30% of kidney transplant recipients were older than 50 years of age. In 2021, the rate of kidney transplantation is 42.3 per 100 person-years among individuals 0 to 17 years of age, 9.8 among individuals 18 to 44 years of age, 5.0 among individuals 45 to 64 years of age, 2.9 among individuals 65 to 74 years of age, and 0.5 among individuals 75 years of age or older. This distribution represented a slightly younger mix of transplant recipients compared to 2017 [11]. Guidelines for selection of patients for transplantation vary from program to program. Generally, metastatic disease or severe pulmonary or heart disease are exclusionary factors. Human immunodeficiency virus (HIV) is no longer considered an absolute contraindication, and studies have shown that patients with ESRD and HIV nephropathy have an increased life expectancy when treated with transplantation versus dialysis [109].
| A) | 1 year. | ||
| B) | 2.3 years. | ||
| C) | 4 years. | ||
| D) | 10.6 years. |
Allocation of all transplants in the United States is managed by the United Network for Organ Sharing (UNOS). Kidney transplant guidelines place the highest considerations on histocompatibility and time spent on the transplant list [110]. Children suffering from ESRD will lose growth (and possibly other milestones) while on dialysis, so they are given priority. The median adult wait time for a cadaver kidney is just over four years [108].
| A) | Mannitol | ||
| B) | Furosemide | ||
| C) | ACE inhibitors | ||
| D) | Sodium bicarbonate infusion |
The use of sodium bicarbonate infusion pre- and postexposure to contrast medium has also been shown to help prevent the incidence of CIN. In a 2004 study, 119 patients were randomized to receive either sodium bicarbonate or sodium chloride at a rate of 3 mL/kg for one hour prior to their procedure followed by 1 mL/kg for six hours postprocedure [119]. The study was ultimately halted early due to a lower rate of acute renal failure in the sodium bicarbonate group, and remaining patients all received sodium bicarbonate. Follow-up analysis showed that 8.4 patients needed to be treated with sodium bicarbonate to prevent one case of CIN [119]. Absolute data from the study showed that 13.6% of patients in the sodium chloride group developed acute contrast-induced nephropathy; in the bicarbonate infusion group, only 1.7% of patients developed acute contrast nephropathy [119]. A 2018 randomized, placebo-controlled trial assessed the efficacy of intravenous NAC for prevention of CIN following diagnostic and/or interventional procedures requiring administration of contrast medium [120]. A total of 222 patients were randomly assigned to receive either NAC or placebo. All patients received IV hydration with normal saline before and after catheterization. CIN occurred in 30 of the 222 patients (13.5%), including 9 of 108 (8.3%) in the NAC group and 21 of 114 patients (18.4%) in the control group. Elevated serum creatinine 10 to 15 days after administration of the contrast medium was associated with an increased risk of adverse events [120]. A retrospective cohort study conducted at the Mayo Clinic assessed the risk of CIN with the use of sodium bicarbonate, NAC, or a combination of the two [121]. Compared with no treatment, sodium bicarbonate alone was associated with an increased risk of CIN, while NAC alone or in combination with sodium bicarbonate did not significantly affect the incidence of CIN [121]. Other therapies being investigated for the prevention of CIN include the use of vitamins C and E and prostaglandin E1 (PGE1), but additional research is needed [122,123].
| A) | nephropathy. | ||
| B) | pre-eclampsia. | ||
| C) | lupus nephritis. | ||
| D) | glomerulonephritis. |
While most clinicians do not generally think of renal failure as a consequence of HIV, in fact nephropathy is the most common form of renal disease in HIV-positive individuals [131]. Kidney disease is a fairly common complication of HIV disease, ranging from nephropathy to kidney injury due to antiretroviral therapy and prerenal AKI due to dehydration [131].
| A) | Increased GFR | ||
| B) | Decreased kidney size | ||
| C) | Decreased renal plasma flow | ||
| D) | Fewer urinary tract infections |
In even a typical, uncomplicated pregnancy, renal dynamics are affected. Renal plasma flow increases dramatically, and by the second trimester, GFRs can reach 150% of normal [147,148]. Accordingly, BUN and serum creatinine normally decrease. Blood pressure should fall in the first 24 weeks by approximately 10 mm Hg and return to normal levels by term [147]. Glucosuria also occurs in normal pregnancy due to changes in tubular function and decreased serum sodium levels (by approximately 5 mEq/L). Overall kidney size increases by approximately 1–1.5 cm, and the ureters dilate. This, coupled with changes in the pelvis, can lead to urinary stasis and an increase in urinary tract infections. Proteinuria up to 300 mg/day may occur even in normal pregnancy [147,148].
| A) | late-term seizures. | ||
| B) | hypotension and hematuria. | ||
| C) | hypertension and proteinuria. | ||
| D) | hyperglycemia and hemorrhage. |
Pre-eclampsia is a syndrome of proteinuria and hypertension that affects up to 5% of all pregnancies, while eclampsia is the occurrence of seizures in a patient with pre-eclampsia [147]. Pre-eclampsia does not usually develop until after the 32nd week of pregnancy, but it may develop much earlier in patients with CKD or hypertension. Risks factors include prepregnancy hypertension, diabetes, and CKD. Management of pre-eclampsia begins with bed rest but can include use of antihypertensives. Methyldopa, labetalol, and hydralazine are generally used, although this indication is off label. ACE inhibitors are contraindicated in pregnancy and can cause fetal loss, and diuretics are usually avoided in euvolemic patients. Intravenous magnesium sulfate can be used to prevent seizures. After 32 weeks' gestation, worsening pre-eclampsia warrants early delivery; eclampsia always mandates immediate delivery [147,148].
| A) | 25%. | ||
| B) | 50%. | ||
| C) | 75%. | ||
| D) | 90%. |
Since 1958, more than 5,000 women have given birth post-transplant [152]. Women who previously were unable to conceive while undergoing dialysis often have a return of fertility after transplant, and up to 12% of all women of childbearing age may become pregnant [151]. Outcomes are generally quite good, with up to a 90% fetal survival rate [148]. Patients should be counseled that a properly planned and monitored pregnancy is possible, including preconception counseling by the transplant team. Recommendations for patients considering pregnancy include changing immunosuppressive regimens to limit dosages of prednisone and azathioprine and stopping mycophenolate mofetil and sirolimus six weeks prior to conception. Ideally, the patient should be two years post-transplant and in good health, with a serum creatinine level less than 2.0 mg/dL. There should be no recent or ongoing rejection, and patients should be normotensive and have minimal or no proteinuria [147,148].
| A) | be increased. | ||
| B) | be decreased. | ||
| C) | remain the same. | ||
| D) | be adjusted according to renal clearance. |
Treatment of nonsuicidal patients who are found to be appropriate for outpatient care usually begins with a selective serotonin reuptake inhibitor. These medications are preferred in renal disease due to their relatively benign side effect profile and their lack of renal clearance resulting in no need to modify dosage.
| A) | of sense of self. | ||
| B) | without accompanying grief, sorrow, or mourning. | ||
| C) | experienced by those with no close relationship to the patient. | ||
| D) | without the finality of death but also with no certainty of returning to previous levels of functioning. |
Chronic illness can be the source of ambiguous loss, which is defined as loss without the finality of death but also with no certainty that the person will return to his or her previous level of functioning [158]. The goal is not necessarily to eliminate this sense of loss, but rather to increase family tolerance and coping. After identifying the loss, the family would work collaboratively to make decisions regarding day-to-day care and activities. Depression, which is commonly experienced among caregivers, may also be viewed as symptomatic of ambiguous loss. Therefore, practitioners can help encourage caregivers to not assume all the burden of responsibility, but rather to delegate and distribute the work. This may mean obtaining respite assistance [158].
| A) | are candidates for dialysis. | ||
| B) | have a serum creatinine level less than 15 mg/dL. | ||
| C) | have a creatinine clearance less than 15 mL/minute. | ||
| D) | All of the above |
An end-of-life discussion is recommended in the presence of stage 4 or 5 CKD or ESRD [171,172,173]. Hospice is generally approved when patients with ESRD are not candidates for dialysis, have a creatinine clearance less than 15 mL/minute, and/or have a serum creatinine level greater than 8 mg/dL (or 6 mg/dL in patients with diabetes) [174]. Guidelines from the Renal Physicians Association note that prognosis should be fully discussed with all patients who have stage 4 or 5 disease or ESRD [172]. Clinicians should carefully prepare for the discussion of prognosis by reviewing the patient's medical record and talking to other healthcare professionals involved in the care of the patient [175]. Because there is variation among patients with regard to their desire for information, clinicians should follow the "ask-tell-ask" approach: ask the patient if he or she is willing to discuss prognosis; if yes, discuss the prognosis and then ask the patient to confirm his or her understanding [171,176]. When discussing prognosis, quantitative estimates are more understandable for patients and family than qualitative ones (e.g., "poor"), and general timeframes for survival should be given [171,176,177,178]. In addition, clinicians should emphasize that prognosis is determined by looking at large groups of patients and that it is harder to predict survival for an individual [171,172]. The discussion of prognosis is often not documented in the patient's record, but it should be [175].