TRIPASS XR تري باس

 

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p. 596

Chronic kidney disease (CKD) is progressive, irreversible kidney

damage characterized by decreased estimated glomerular filtration rate

(eGFR) or evidence of kidney damage for at least 3 months.

Case 28-1 (Question 1)

Classification of CKD staging should be determined on the basis of

kidney function, defined by the Kidney Disease: Improving Global

Outcomes (KDIGO). Each stage is associated with certain action plans.

Case 28-1 (Question 1)

Many equations exist for calculating creatinine clearance (CrCl) or

eGFR. The Modification of Diet in Renal Disease (MDRD) equation is

used to quantify GFR, to detect or stage the degree of CKD, and to

follow progression. The Cockcroft–Gault (CG) equation is used to

adjust the doses of medications that are eliminated by the kidneys.

Equations 28-3–28-5

Diabetes is the number one cause of CKD in the United States. Optimal

control of blood glucose levels is essential to slow the progression of

CKD and reduce morbidity and mortality.

Case 28-1 (Questions 2–4)

Fluid accumulation and electrolyte abnormalities secondary to CKD

often complicate the treatment of hypertension and can have cardiotoxic

effects.

Case 28-1 (Questions 5–9)

Metabolic acidosis presents in late stages of CKD from reduced

hydrogen ion excretion and bicarbonate production. Metabolic acidosis

can worsen bone disease and other metabolic processes.

Case 28-1 (Question 8)

Treating anemia of CKD is essential to reducing cardiovascular disease

(CVD) complications. Management of anemia includes administration

of iron supplementation and erythropoiesis-stimulating agents.

Case 28-1 (Questions 10–12)

CVD is the number one cause of morbidity and mortality in CKD.

Cardioprotective measures should be addressed at allstages.

Case 28-2 (Question 1)

Hypertension is the second leading cause of CKD in the United States.

Treating hypertension to target goals is necessary to slow the

progression of CKD and reduce mortality.

Case 28-2 (Question 2)

Mineral and bone disorders (MBD) characterized by biochemical

abnormalities, renal osteodystrophy, and vascular calcification become

more common as CKD progresses. Biochemical abnormalities lead to

Case 28-3 (Questions 1, 2)

the development of vascular calcifications and increase the risk for

cardiovascular mortality.

Hyperphosphatemia is managed with dietary phosphorus restriction and

phosphate-binding agents.

Case 28-3 (Question 2)

Activated forms of vitamin D (calcitriol, paricalcitol, and doxercalciferol)

or a calcimimetic agent (cinacalcet) may be necessary to achieve

proper biochemical balance and bone metabolism.

Case 28-3 (Question 2)

Glomerulonephropathies (GN) are a collection of glomerular diseases

caused by a variety of immunologic mechanisms and the third leading

cause of CKD. Patients with GN may present with nephrotic syndrome

and require treatment with immunosuppressant therapy.

Case 28-4 (Questions 1, 2),

Case 28-5 (Questions 1, 2)

p. 597

p. 598

INTRODUCTION

Chronic kidney disease (CKD) describes the continuum of kidney dysfunction from

early to late-stage disease. Estimated glomerular filtration rates (eGFR) range from

90 mL/minute/1.73 m2

in the early stages to less than 15 mL/minute/1.73 m2

in the late

stages of disease. The most advanced stage of CKD, known as end-stage renal

disease (ESRD), occurs when chronic renal replacement therapy in the form of

dialysis or kidney transplantation is necessary to sustain life.

1 Complications

associated with CKD that increase the complexity of this condition include fluid and

electrolyte abnormalities, anemia, cardiovascular disease (CVD), mineral and bone

disorders (MND), and malnutrition. Optimal treatment of patients with CKD is best

achieved using a multidisciplinary approach to address the concurrent medical

problems and complex pharmacotherapeutic regimens. Alterations in drug

disposition that occur with kidney impairment and the subsequent need for dosage

adjustments are additional considerations when determining rational

pharmacotherapy in this population.

Implementation of clinical practice guidelines leads to improved patient outcomes

and reduced variability in patient care.

2 As a result many countries have developed

evidence-based clinical practice guidelines for the treatment of kidney disease. In the

United States, the National Kidney Foundation (NKF) established the Kidney

Disease Outcomes Quality Initiative (K/DOQI) to provide evidence-based treatment

guidelines for all stages of kidney disease and related conditions. However, because

kidney disease is a worldwide public health issue and the problems faced by kidney

disease around the world are universal, the Kidney Disease: Improving Global

Outcomes (KDIGO) was established in 2003. The mission of KDIGO is to improve

the care and outcomes of kidney disease patients worldwide by promoting

coordination, collaboration, and integration of initiatives. KDIGO is managed by the

NKF. Contact information for K/DOQI and KDIGO and corresponding web

addresses for clinical practice guidelines can be found in Table 28-1.

Definition and Classification of CKD

CKD is characterized by a progressive deterioration in kidney function with time

characterized by irreversible structural damage to existing nephrons. The KDIGO

2012 Clinical Practice Guideline for the Evaluation and Management of Chronic

Kidney Disease defines CKD as abnormalities in kidney structure or damage (e.g.,

albuminuria) or function (e.g., decreased glomerular filtration rate or GFR) present

for at least 3 months with implications for the patient’s health (Table 28-2). CKD is

classified by CGA categories (cause of kidney disease, GFR, albuminuria) in the

KDIGO guidelines. (Table 28-3 and Table 28-4).

1 The presence of the protein

albumin in urine (defined as albuminuria) is an early and sensitive marker of kidney

damage (Table 28-4). Unlike previous K/DOQI guidelines, KDIGO divides category

three into two subcategories, 3a (GFR 45–59 mL/min/1.73 m2

) and 3b (GFR 30–44

mL/min/1.73 m2

), to better stratify patients based on the different outcomes and risks

associated with these levels of GFR. Kidney damage is indicated by pathologic

abnormalities of the kidneys or markers of kidney injury, including abnormalities in

blood or urine tests and imaging studies.

1 Table 28-5 provides etiologic examples of

CKD staging.

Table 28-1

Resources for Kidney Disease Clinical Practice Guidelines

National Kidney Foundation Kidney Disease Outcomes Quality Initiative

30 East 33rd Street

New York, New York 10016

Phone: 1-800-622–9010

Website: https://www.kidney.org/professionals/guidelines

Kidney Disease: Improving Global Outcomes

30 East 33rd Street, Suite 900

New York, New York 10016

Phone: 212-889-2210 x288

Website: http://kdigo.org/home/

Table 28-2

Criteria for CKD1

Markers of Kidney Damage Decreased GFR

Albuminuria (AER ≥30 mg/24 hours; ACR ≥30 mg/g [≥3 mg/mmol])

Urine sediment abnormalities

Electrolyte and other abnormalities due to tubular disorders

Abnormalities detected by histology

Structural abnormalities detected by imaging

History of kidney transplantation

GFR<60 mL/minute/1.73 m

2

Must be at the defined GFR range or damage persisting for 3 months or greater.

AER, albumin excretion rate; ACR, albumin-to-creatinine ratio; CKD, chronic kidney disease; GFR, glomerular

filtration rate.