End-Stage Renal Disease (2024)

Continuing Education Activity

More than 500,000 people in the United States live with end-stage renal disease (ESRD). The development of chronic kidney disease (CKD) and its progression to this terminal disease remains a significant source of reduced quality of life and premature mortality. The Kidney Disease Improving Global Outcomes (KDIGO) define CKD using markers of kidney damage, specifically the ones that determine proteinuria and glomerular filtration rate. Many chronic diseases can cause end-stage renal disease. In many developed and developing countries, diabetes mellitus is the leading cause. This activity explains when this condition should be considered in the differential diagnosis and how to evaluate this condition properly. Furthermore, it highlights the interprofessional team's role in caring for patients with this condition.

Objectives:

• Describe the causes of end-stage renal disease.

• Outline the presentation of a patient with end-stage renal disease.

• Summarize the treatment options for end-stage renal disease.

• Outline interprofessional team strategies for improving care coordination and communication to ensure improvement and best outcomes in end-stage renal disease.

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Introduction

More than 500,000 people in the United States live with end-stage renal disease (ESRD). The development of chronic kidney disease (CKD) and its progression to this terminal disease remains a significantcause of reduced quality of life and premature mortality.[1] Chronic kidney disease (CKD) is a debilitating disease, and standards of medical care involveaggressive monitoring for signs of disease progression and early referral to specialists for dialysis or possible renal transplant. The Kidney Disease Improving Global Outcomes (KDIGO) foundation guidelines define CKD using kidney damage markers, specifically markers that determine proteinuria and glomerular filtration rate. By definition, the presence ofboth factors (glomerular filtration rate [GFR] less than 60 mL/min and albumin greater than 30 mg per gram of creatinine) along with abnormalities of kidney structure or function for greater than three months signifies chronic kidney disease. End-stage renaldisease is defined as a GFR of less than 15 mL/min.[2][3]

According to KDIGO 2012 clinical practice guideline, CKD is classified into five stages considering the GFR level.[4]

• Stage 1: Kidney damage with normal GFR (greater than 90 ml/min)

• Stage 2: Mild reduction in GFR (60-89 mL/min)

• Stage 3a: Moderate reduction in GFR (45to 59 mL/min)

• Stage 3b: Moderate reduction in GFR (30to 44 mL/min)

• Stage 4: Severe reduction in GFR (15to 29 mL/min)

• Stage 5: Renal failure (GFR less than 15 mL/min)

Etiology

Many chronic diseases can cause end-stage renal disease. In many developed and developing countries, diabetes mellitus is the leading cause.[5] Other causes include:[6][7]

• Hypertension

• Vascular disease

• Glomerular disease (primary or secondary)

• Cystic kidney diseases

• Tubulointerstitial disease[8]

• Urinary tract obstruction or dysfunction

• Recurrent kidney stone disease[9]

• Congenital (birth) defects of the kidney or bladder

• Unrecovered acute kidney injury

• Certain medications, including non-steroidal anti-inflammatory drugs (NSAIDs), calcineurin inhibitors, and antiretrovirals[10]

1. Vascular Diseases

   • Renal artery stenosis

   • Cytoplasmic pattern antineutrophil cytoplasmic antibody (C-ANCA)–positive and perinuclear pattern antineutrophil cytoplasmic antibody (P-ANCA)–positive vasculitides

   • ANCA-negative vasculitides

   • Atheroemboli

   • Hypertensive nephrosclerosis

   • Renal vein thrombosis[11]

2. Primary Glomerular Diseases

   • Membranous nephropathy

   • Alport syndrome

   • Immunoglobulin A (IgA) nephropathy

   • Focal and segmental glomerulosclerosis (FSGS)

   • Minimal change disease

   • Membranoproliferative glomerulonephritis (MPGN)

   • Complement-related diseases (atypical hemolytic-uremic syndrome [HUS], dense deposit disease)

   • Rapidly progressive (crescentic) glomerulonephritis[12][13]

3. Secondary Causes of Glomerular Disease

   • Diabetes mellitus

   • Systemic lupus erythematosus

   • Rheumatoid arthritis

   • Mixed connective tissue disease

   • Scleroderma

   • Granulomatosis with polyangiitis (formerly known as Wegener granulomatosis)

   • Mixed cryoglobulinemia

   • Endocarditis

   • Hepatitis B and C

   • Syphilis

   • Human immunodeficiency virus (HIV) infection

   • Parasitic infection

   • Heroin use

   • Gold

   • Penicillamine

   • Amyloidosis

   • Light-chain deposition disease

   • Neoplasia

   • Thrombotic thrombocytopenic purpura (TTP)

   • Shiga-toxin orStreptococcus pneumoniae– related HUS

   • Henoch-Schönlein purpura

   • Reflux nephropathy[14][15][16][17]

4. Causes of Tubulointerstitial Disease

   • Drugs (eg, sulfonamides, allopurinol)

   • Infection (viral, bacterial, parasitic)

   • Sjögren syndrome

   • Tubulointerstitial nephritis and uveitis (TINU) syndrome

   • Chronic hypokalemia

   • Chronic hypercalcemia

   • Sarcoidosis

   • Multiple myeloma cast nephropathy

   • Heavy metals

   • Radiation nephritis

   • Polycystic kidneys

   • Cystinosis and other inherited diseases[18][19]

5. Urinary Tract Obstruction

   • Benign prostatic hypertrophy

   • Urolithiasis (kidney stones)

   • Urethral stricture

   • Tumors

     See Also

     The Tragic Real-Life Story Of Leif Garrett - GrungeExcess Death Estimates in Patients with End-Stage Renal Disease ...Leif Garrett Has Never Had a Wife Yet Dated a Lot of WomenVascular Disease, ESRD, and Death: Interpreting Competing Risk Analyses

   • Neurogenic bladder

   • Congenital (birth) defects of the kidney or bladder

   • Retroperitoneal fibrosis[20]

Epidemiology

According to the United States Renal Data System, in 2015, there were 124,411 new ESRD diagnoses, reflecting an increasing burden of kidney failure. The prevalence of the disease has been rising at a stable number of about 20,000 cases per year.[21][22]Kidney disease is the ninth leading cause of death in the United States.

Race/Ethnicity

The degree of kidney failure varies widely by race in the US. In 2015, the rate of ESRD was three times higher in African Americans compared to Whites (393.5 versus 139.9 per million population). That same year, the ESRD prevalence was about ten times higher in American Indians or Alaska Natives and twice as high in Native Hawaiians or Pacific Islanders. Prevalence rates were 1.3 times higher in Asian Americans, as well. Of note, incidence rates in the African American population have decreased each year since 2006, leading to an overall decrease of 21%. This reduction has been even more pronounced in American Indians/Alaska Natives.[23]

Age

The prevalence of CKD increases with age, with the most rapid growth in people aged 60 years or older. For example, the prevalence is 6.0% at ages 18to 44 years and 38.1% at ages more than 65 years.

Sex

The cumulative incidence of end-stage renal disease is higher in males than females.

Pathophysiology

Each nephron in a normal kidney contributes to the total glomerular filtration rate (GFR). The decline of kidney function is gradual and may initially present asymptomatically. The natural history of renal failure depends on the etiology of the disease but ultimately involves early homeostatic mechanisms involving hyperfiltration of the nephrons. The kidney maintains GFR, despite the progressive destruction of nephrons because the remaining normal nephrons develop hyperfiltration and compensatory hypertrophy. As a result, the patient with mild renal impairment can show normal creatinine values, and the disease can go undetected for some time.[24]

This nephron adaptability allows for continued normal clearance of plasma solutes. This adaptive mechanism will run its course and eventually cause damage to the glomeruli of the remaining nephrons. At this point, antihypertensives such as ACEs or ARBs may be beneficial in slowing the progress of the disease and preserving renal function. Plasma levels of substances such as urea and creatinine start to show measurable increases only after total GFR has decreased by 50%. For example, a rise in plasma creatinine from 0.6 mg/dL to 1.2 mg/dL in a patient, although within the normal range, actually represents a loss of 50% of functioning nephron mass.

Although hyperfiltration and hypertrophy of residual nephrons are beneficial for maintaining GFR, it is found to be a major cause of progressive renal dysfunction.[25] The increased glomerular capillary pressure may damage the capillaries, leading to focal and segmental glomerulosclerosis (FSGS) and eventually to global glomerulosclerosis.

Factors that may worsen renal injury include:

• Nephrotoxins (NSAIDs)

• Systemic hypertension

• Proteinuria

• Dehydration

• Smoking[26]

• Hyperlipidemia

• Uncontrolled diabetes

• Hyperphosphatemia

Hyperkalemia

Potassium excretion at near-normal levels is generally maintained in CKD as long as aldosterone secretion and distal flow are maintained. Hyperkalemia develops when GFR falls to less than 20-25 mL/min/1.73 m²; at this point, the kidneys have decreased ability to excrete potassium.[27]

Metabolic Acidosis

Metabolic acidosis in stage 5 CKD is high anion gap metabolic acidosis but with the anion gap generally not higher than 20 mEq/L. In CKD, the kidneys cannot produce enough ammonia in the proximal tubules to excrete endogenous acid into the urine in the form of ammonium. In stage 5 CKD, the accumulation of phosphates, sulfates, and other organic anions is the cause of the increase in the anion gap.[28]

Metabolic acidosis has deleterious effects on protein balance, leading to the following:

• Negative nitrogen balance

• Increased protein degradation

• The increased essential amino acid oxidation

• Reduced albumin synthesis

• Lack of adaptation to a low-protein diet

Metabolic acidosis also plays a role in the development of renal osteodystrophy because bones are buffers for excess acid, with a resultant loss of minerals. Acidosis also interferes with vitamin D metabolism.

Salt and Water Handling Abnormalities

Salt and water handling by the kidney are affected in CKD. Volume overload results from the failure of sodium and free-water excretion and occur when the GFR falls to less than 10-15 mL/min/1.73 m². This leads to peripheral edema, pulmonary edema, and hypertension. Tubulointerstitial renal diseases often cause fluid loss rather than overload. Thus, despite severe reductions in GFR, tubulointerstitial renal diseases may manifest as polyuria and volume depletion, with the inability to concentrate the urine.[29]

Anemia

Normochromic normocytic anemia develops from the decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production.[30] Other causes of anemia in CKD include the following:

• Chronic blood loss: Uremia-induced platelet dysfunction enhances the bleeding tendency

• Secondary hyperparathyroidism

• Inflammation

• Nutritional deficiency

Bone Disease

Renal bone disease is a common complication of CKD. Different types of bone disease occur with CKD, as follows:

• High-turnover bone disease from high parathyroid hormone (PTH) levels

• Low-turnover bone disease (adynamic bone disease)[31]

• Defective mineralization (osteomalacia)

• Mixed disease

• Beta-2-microglobulin–associated bone disease

Secondary hyperparathyroidism develops in CKD because of the following factors:

• Hyperphosphatemia

• Hypocalcemia

• Decreased renal synthesis of 1,25-dihydroxycholecalciferol (1,25-dihydroxyvitamin D, or calcitriol)

• Intrinsic alteration in the parathyroid glands gives rise to increased PTH secretion and increased parathyroid growth[32]

• Skeletal resistance to PTH

Hyperphosphatemia develops from the inability of the kidneys to excrete excess phosphate. Hyperphosphatemia suppresses the renal hydroxylation of inactive 25-hydroxyvitamin D to calcitriol. Increased phosphate concentration also affects PTH concentration by directly affecting the parathyroid glands (posttranscriptional effect). Hypocalcemia results from decreased intestinal calcium absorption because of low plasma calcitriol levels.

Hypocalcemia, hyperphosphatemia, and low serum calcitriol levels stimulate PTH synthesis and secretion. With persistent stimulus in advanced CKD, parathyroid glands become hypertrophic and then hyperplastic.

History and Physical

End-stage renal disease can present with a constellation of signs and symptoms. Some include volume overload refractory to diuretics, hypertension poorly responsive to medication, anemia, mineral and bone disorders, and metabolic derangements including hyperkalemia, hyponatremia, metabolic acidosis, hypo/hypercalcemia, and hyperphosphatemia.[33] Metabolic acidosis in stage 5 CKD presents protein-energy malnutrition, muscle weakness, and loss of lean body mass. Salt and water retention can cause peripheral edema, pulmonary edema, and hypertension. Anemia manifests as fatigue, impaired cognitive function, and reduced quality of life. Anemia can also lead to heart failure.

Other manifestations of uremia in end-stage renal disease (ESRD) are:

• Pericarditis

• Encephalopathy

• Peripheral neuropathy

• Restless leg syndrome

• Anorexia, nausea, vomiting, diarrhea

• Dry skin, pruritus, ecchymosis

• Malnutrition

• Erectile dysfunction, decreased libido, amenorrhea

• Platelet dysfunction

Uremic toxicity is an indication of urgent dialysis.[34]ESRD symptoms generally appear in stages 4 and 5 when the GFR is less than 30 ml/min. Some patients with nephrotic syndrome and cystic renal disease may present earlier. Depression is ubiquitous in patients with ESRD and should be screened for on presentation.[35]

Evaluation

Chronic kidney disease is diagnosed when there is evidence of kidney damage for at least three months or in any patient with a GFR of less than 60 mL/min for that same amount of time.[36][37]

To calculate GFR, three equations are commonly used (the MDRD [Modification of Diet in Renal Disease Study], CKD-EPI, and co*ckcroft-Gault formula). However, the best estimate of GFR is the CKD-EPI(Chronic Kidney DiseaseEpidemiology Collaboration) equation, which adjusts for age, race, and gender. However, it is important to note that the formula underestimates the actual GFR at a GFR more significant than 60 mL/min.[38]

Further evaluation of kidney disease can include a renal ultrasound, complete blood count (CBC), basic metabolic panel (BMP), urinalysis,and/or kidney biopsy.

Complete Blood Count

CBC shows normochromic normocytic anemia.[39]

Basic Metabolic Panel (BMP)

The blood urea nitrogen (BUN) and serum creatinine levels are elevated. Hyperkalemia or low bicarbonate levels are usually present. Serum albumin levels are low due to urinary protein loss or malnutrition. Serum phosphate, 25-hydroxyvitamin D, alkaline phosphatase, and intact parathyroid hormone (PTH) levels are obtained to look for evidence of renal bone disease.[40] A lipid profile should be obtained because of the risk of cardiovascular disease.

Urinalysis

A spot urine protein/creatinine ratio can be used to quantitate albuminuria. A value higher than 30 mg of albumin per gram of creatinine is considered abnormal, while valuesgreater than 300 mg/g are considered severely impaired renal function. Additionally, a 24-hour urine protein can also be performed. A valuegreater than 3.5 g is concerning for nephrotic range proteinuria.

Renal Ultrasonography

Renal ultrasonography should be done to look for hydronephrosis or involvement of the retroperitoneum with fibrosis, tumor, or diffuse adenopathy. Small, echogenic kidneys are observed in advanced renal failure. While indiabetic nephropathy, kidneys are normal in size. Structural abnormalities like polycystic kidneys also may be observed on ultrasonograms.An ultrasound can provide data estimating size, obstructions, stones, echogenicity, and cortical thinning.[41]

Radiology

Plain abdominal radiography can detect radio-opaque stones or nephrocalcinosis, while a voiding cystourethrogram (VCUG) is diagnostic for vesicoureteral reflux.[42]

Computed tomography (CT) scanning can help better describe renal masses and cystsand is also sensitive for identifying renal stones.

Magnetic resonance angiography (MRA) can accurately diagnose renal artery stenosis.

A renal radionuclide scan with captopril administration can diagnose renal artery stenosis, and it also quantitates differential renal contribution to the total glomerular filtration rate (GFR).

Renal Biopsy

Percutaneous ultrasound-guided renal biopsy is indicated when the diagnosis is unclear after an appropriate workup.[43]

Specific Tests

• Serum and urine protein electrophoresis for multiple myeloma

• Antinuclear antibodies (ANA), double-stranded DNA antibody levels for systemic lupus erythematosus

• Serum complement levels

• Cytoplasmic and perinuclear pattern antineutrophil cytoplasmic antibody (C-ANCA and P-ANCA) levels for granulomatosis with polyangiitis (Wegener granulomatosis) and microscopicpolyangiitis

• Anti–glomerular basem*nt membrane (anti-GBM) antibodies forGoodpasture syndrome

• Hepatitis B and C,human immunodeficiency virus (HIV), and venereal disease research laboratory (VDRL) serology

Treatment / Management

Treatment of end-stage renal disease involves correcting parameters at the level of the patient's presentation.[44] Interventions aimed at slowing the rate of kidney disease should be initiated and can include:

• Treating the underlying cause and managing blood pressure and proteinuria. Blood pressure should be targeted to a systolic blood pressure of less than 130 mmHg, and diastolic blood pressure of less than 80 mmHg in adults with or without diabetes mellituswhose urine albumin excretion exceeds 30 mg for 24 hours. For diabetic patients with proteinuria, an angiotensin-converting-enzyme inhibitor (ACEI) or angiotensin 2 receptor blocker (ARB) should be started in caseswhere urine albumin values range between 30 and 300 mg in 24 hours and greater than 300 mg in 24 hours. These drugs slow the disease progression, particularly when initiated before the GFR decreases to less than 60 mL/min or before plasma creatinine concentration exceeds 1.2 and 1.5 in women and men, respectively.[45]

• Other targets in preventive care and monitoring should include tight glycemic control, cardiovascular risk reduction, and general lifestyle recommendations such as smoking cessation and dietary restriction. Glycemic control is critical. A hemoglobin A1C of less than 7% is generally recommended to prevent or delay microvascular complications in this population. Management with sodium-glucose transporter 2 (SGLT-2) inhibitors may reduce the disease burden in those with type 2 diabetes mellitus.[46]

• Treatment of chronic metabolic acidosis with supplemental renal bicarbonatealsomay slow the progression of end-stage renal disease.[47]

• Patients with CKD tend tohave dyslipidemia, particularly hypertriglyceridemia. Monitoring fasting lipid panels and initiation of cholesterol-lowering agents such as HMG-CoA reductase inhibitors should be done early in the course of the disease.[48]

• Volume overload or pulmonary edema should be treated with loop diuretics or ultrafiltration.

• For uremic manifestations, long-term renal replacement therapy (hemodialysis, peritoneal dialysis, or kidney transplantation) is needed.

• Anemia is treated with an erythropoiesis-stimulating agent (ESA) such as erythropoietin.

• Hyperphosphatemia is treated with phosphate binders (calcium acetate, sevelamer carbonate, or lanthanum carbonate) and dietary phosphate restriction.

• Lifestyle modification and dietary restrictions are routinely recommended. For example, adhering to a low salt diet (less than 2 g/day), a renal diet (avoiding foods that arehigh in phosphorus), and restricting daily protein to 0.8 g per kg body weight per day is essential to managing disease burden.

• Hypocalcemia should also be monitored. A 25-OH vitamin D level less than 10 ng/mL warrants initiation of ergocalciferol 50,000 IU weekly for 6 to 8 weeks before switching to cholecalciferol 800 to 1000 IU daily.[49]

• Hyperparathyroidism should be treated with calcitriol, vitamin D analogs, or calcimimetics.

Planning for Long-term Renal Replacement Therapy

Early patient education should be initiated regarding natural disease progression, different modalities for dialysis, and renal transplantation. For patients in whomtransplantation is not imminent, a primary arteriovenous fistula should be created in advance of the anticipated date of dialysis.[50] Every patient with end-stage renal disease should be timely referred for renal transplantation.

Indications for renal replacement therapy in patients with CKD include the following:

• Severe metabolic acidosis

• Hyperkalemia

• Pericarditis

• Encephalopathy

• Intractable volume overload

• Failure to thrive and malnutrition

• Peripheral neuropathy

• Intractable gastrointestinal symptoms

• Glomerular filtration rate (GFR) of 5to 9 mL/min/1.73 m^2, irrespective of the symptoms or the presence or absence of other comorbidities

Differential Diagnosis

The clinical features of end-stage renal disease mimic many other disorders, and many diseases lead to end-stage renal disease.[51][52] Therefore the following differentials should be considered whenever assessing a patient with end-stage renal disease.

• Chronic glomerulonephritis

• Chronic pyelonephritis

• Rapidly progressive glomerulonephritis

• Nephropathy of pregnancy/pregnancy toxemia

• Unclassifiable nephritis

• Polycystic kidney disease

• Nephrosclerosis

• Malignant hypertension

• Diabetic nephropathy

• Systemic lupus erythematosus nephritis

• Amyloidal kidney

• Gouty kidney

• Renal failure due to a congenital abnormality of metabolism

• Renal/urinary tract tuberculosis

• Renal/urinary tract calculus

• Renal/urinary tract tumor

• Obstructive urinary tract disease

• Myeloma

• Renal hypoplasia

Prognosis

End-stage renal disease is a progressive disorder, and timely renal replacement therapy is necessary to prevent death. The disorder is associated with numerous hospitalizations, increased healthcare costs, and metabolic changes. The mortality rates for patients with end-stage renal disease are significantly higher than those without the disease. Even with timely dialysis, the death rates vary from 20% to 50% over 24 months. The most common cause of death is hyperkalemia, followed by adverse cardiac events.[53]Mortality rates are higher for men than women; similarly, Blacks are more prone to death due to ESRD than Whites. The highest mortality rate is within the first six months of starting dialysis. The 5-year survival rate for a patient undergoing long-term dialysis in the United States is approximately 35% and about 25% in patients with diabetes.

In children, puberty is delayed in both genders, and low vitamin D levels are common, an independent risk factor for death.[54]

Complications

Complications of end-stage renal disease are divided into two groups—complications due to ESRD and complications due to vascular access or dialysis.

Complications due to ESRD

• Coronary heart disease is a significant complication of chronic kidney disease and is the most common cause of death in this population. Patients on dialysis have a 10 to 30 times higher cardiovascular mortality risk than the general population.[55]

• Peripheral vascular disease is also commonly seen[56]

• Hypertension

• Mineral and bonedisorders (secondary to hyperparathyroidism, vitamin D deficiency)

• Hyperuricemia

• Metabolic acidosis

• Hyperphosphatemia

• Hypoalbuminemia

• Anemia

• Decreased libido, erectile dysfunction

Complications due to Vascular Access/Dialysis

• Bleeding

• Local or disseminated intravascular infection

• Graft occlusion

• Electrolyte abnormalities after dialysis

• Dialysis dementia

• Dialysis disequilibrium syndrome

Consultations

The management of end-stage renal disease requires a dedicated interprofessional healthcare team comprised of the following:

• Nephrologist

• Intensivist

• Renal transplant surgeon

• Nurse educator

• Pharmacist

• Nutritionist

Deterrence and Patient Education

The U.S. Preventive Services Task Force (USPSTF) does not recommend screening asymptomatic individuals for CKD.[57] However, for those at higher risk for the disease, such as those with diabetes or hypertension, USPSTF recommends ongoing screening for CKD with proteinuria testing. However, it is essential to note that screening for proteinuria is not necessary for a patient who is already on ACEI or ARB therapy.

Patients with end-stage renal disease should be educated about the following:

• Avoidance of nephrotoxic drugs like non-steroidal anti-inflammatory drugs

• Advanced counseling for renal replacement modalities, including peritoneal dialysis, hemodialysis, and transplantation

• Timely placement of vascular access for hemodialysis

• Pregnancy could be fatal in ESRD

• Avoid phosphate-rich foods[58]

• Potassium restriction in diet

• Sodium and water restriction to avoid volume overload

• Protein restriction to delay the onset of uremic symptoms[59]

• Reduction in salt intake may slow the progression of diabetic CKD

Pearls and Other Issues

• End-stage renal disease is a terminal illness with a glomerular filtration rate of less than 15 mL/min.

• The most common cause of ESRD in the US is diabetic nephropathy, followed by hypertension.

• Other etiologies can include glomerulonephritis, cystic kidney disease, recurrent kidney infection, chronic obstruction, etc.

• The disease can present with nausea, vomiting, metabolic, hematologic, electrolyte derangements, seizures, coma, bleeding diathesis, refractory fluid overload, hypertension unresponsive to pharmacotherapy, uremic pericarditis, etc.

• Vigilant monitoring of GFR and proteinuria in diabetics and non-diabetics is essential for managing disease progression in patients with chronic kidney disease.

• Early referral to specialists is necessary for timely dialysis or renal transplant planning.

Enhancing Healthcare Team Outcomes

Once a patient has been diagnosed with end-stage renal disease, a significant number of patients will require dialysis, and the lucky few may be eligible for a renal transplant. Unfortunately, end-stage renal failure significantly increases morbidity and mortality; it also leads to enormous costs to the healthcare system. Thus, the disorder is best managed by an interprofessional team dedicated to adequate disease control and improving outcomes for these patients.

There is no cure for end-stage renal disease, and all the available treatments are short-term. Thus, the key to improving long-term outcomes is preventing the disease's progression.

A dedicated interprofessional healthcare team should comprise a nurse educator, a specialized pharmacist, a nutritionist, a social worker, and a couple of clinical providers, including a primary care provider and a trained nephrologist.

The specialized nurse educator plays a vital role in educating the patient about lifestyle modifications necessary to prevent the progression of CKD. In patients with advanced CKD, the dedicated nurse's role become crucial in protecting an arm for future fistula placement. During hospitalizations, the clinical nurse should place limb restrictions on that arm to ensure venipunctures and blood pressure readings are not taken on that arm.

The pharmacist should identify those patients who carry a diagnosis of CKD and provide specialized instructions to these patients, particularly concerning avoiding nephrotoxic agents and medications. In addition, the pharmacist plays a crucial role in communicating and guiding the providers about the patient's medications to limit those that can adversely affect the kidneys.

A trained nutritionist should also be involved in the care of these patients to guide an appropriate diet plan specific to their needs.[60]

A social worker should be involved in the care to ensure that the patient has a support system and financial resources to continue therapy.

To improve outcomes, each interprofessional team member should maintain accurate and updated patient records, communicate with the other team members, and act collaboratively to ensure that the patient receives optimal care resulting in the best outcomes. [Level 5]

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Disclosure: Muhammad Hashmi declares no relevant financial relationships with ineligible companies.

Disclosure: Onecia Benjamin declares no relevant financial relationships with ineligible companies.

Disclosure: Sarah Lappin declares no relevant financial relationships with ineligible companies.