CHRONIC KIDNEY DISEASE

INTRODUCTION
Chronic kidney disease (CKD) is a major public health problem with a high global incidence and prevalence, with
important multi-systemic complications leading to poor outcomes and high-cost treatments
Chronic kidney disease, also known as chronic renal disease or CKD, is the progressive irreversible loss of kidney
function.
DEFINITION
The Kidney Disease Outcomes Quality Initiative [KDOQI] of the national kidney foundation defines CKD as either
the presence of kidney damage or a decreased GFR less than 60Ml/min/1.73m2 for longer than 3 months.
STAGES OF CKD

Description GFR

Stage 1 with normal or high GFR GFR > 90 mL/min

Stage 2 Mild CKD GFR = 60-89 mL/min
Stage 3A Moderate CKD GFR = 45-59 mL/min
Stage 3B Moderate CKD GFR = 30-44 mL/min
Stage 4 Severe CKD GFR = 15-29 mL/min
Stage 5 End Stage CKD GFR <15 mL/min

ETIOLOGY
The leading causes of CKD are diabetes (50%), Hypertension (about 25%).

 Diabetes occurs when blood sugar remains too high. Over time, unmanaged blood sugar can cause damage
to many organs in your body, including the kidneys and heart and blood vessels, nerves, and eyes.
 High blood pressure occurs when blood pressure against the walls of blood vessels increases. If
uncontrolled or poorly controlled, high blood pressure can be a leading cause of heart attacks, strokes, and
chronic kidney disease. Also, chronic kidney disease can cause high blood pressure.
 Age above 60 years
 Cardiovascular diseases
 Family history of CKD
 Exposure to nephrotoxic drugs.
Less common etiologies are glomerulo CKD, cystic diseases and urologic diseases.
PATHOPHYSIOLOGY
CKD can be caused by a multitude of underlying conditions; however, once about half of the total nephrons are
lost, CKD progresses similarly, regardless of etiology.
• Underlying etiology: ↓ total number of nephrons (nephron mass), which leads to:
o ↑ Glomerular permeability → ↑ filtration of proteins, which are lost in the urine (i.e., proteinuria)
o Activation of the RAAS
o Cytokine release
o ↑ Growth factors
• These changes lead to adaptive hyperfiltration:
o GFR may actually ↑ during this time.
o Occurs as a compensatory mechanism
o Leads to ↑ intraglomerular capillary pressure (i.e., glomerular hypertension)
• ↑ Intraglomerular capillary pressure and inflammatory mediators cause damage to the remaining nephrons.
• Damage to the remaining nephrons continues the positive feedback loop, and CKD progresses.

CLINICAL FEATURES
Often, CKD disease remains asymptomatic until the late stages, despite a significant decrease in GFR during the
earlier stages. Also, CKD is often either found incidentally on labs or it presents with complications.
• Incidentally discovered on lab work:

 Routine monitoring of serum creatinine

 Routine albuminuria screening for diabetics
 Hematuria and/or proteinuria found on urinalysis for other reasons (e.g., urinary tract infection)
• Hypertension: 80%–85% prevalence in CKD regardless of etiology
• Signs of volume overload:

 Lower-extremity edema
 Elevated jugular venous pressure
 S3 gallop on cardiac auscultation
 Crackles on pulmonary auscultation
 New or increasing requirement for supplemental oxygen
 Ascites
• Signs of uremia:

 Nausea, vomiting, and anorexia

 Altered mental status
 Asterixis (“flapping tremor” of the hands)
 Friction rub on cardiac auscultation (sign of pericardial effusion)
 Skin excoriations from pruritus
 Uremic frost (urea crystals deposited in the skin)
• Specific exam findings by etiology:

 Retinopathy (hypertensive nephrosclerosis, diabetes)

 Abdominal bruit (renal artery stenosis)
 Livedo reticularis rash, particularly on the toes (cholesterol emboli)
 Easily palpable kidneys (PKD)
 Periorbital edema (nephrotic syndrome)
 Gross hematuria (IgA nephropathy)
 Other characteristic signs of autoimmune diseases (e.g., malar rash in SLE)
• Complications:

 Cardiovascular disease (clinically most important): chest pain, dyspnea on exertion

 Mineral and bone disease (secondary hyperparathyroidism): bone pain, fractures
 Anemia: fatigue, dyspnea on exertion, pallor
 Hyperkalemia: muscle weakness, cardiac arrhythmias
DIAGNOSTIC TESTS
• History collection
• Physical examination
• Serum creatinine and BUN level
• Serum electrolytes
• Urinalysis- urine sediment containing abundant cells, casts or proteins suggest intrarenal disorders.
• Renal ultrasound- A kidney ultrasound is often the first test done, since it provides imaging without
exposure to potentially nephrotoxic contrast agents. It is useful for evaluating for possible kidney
disease and obstruction of the urinary collection system.
• Renal scan - A renal Scan can assess abnormalities in kidney blood flow, tubular function, and the
collecting system.
• CT scan - A computed tomography (CT) scan can identify lesions, masses, obstructions, and vascular
anomalies.
• Renal biopsy -
MANAGEMENT
The overall goal of CKD therapy is
• to preserve existing kidney function,
• reduce the risk of CV diseases
• prevent complications
• provide for patient’s comfort
Early recognition, diagnosis, and treatment can deter the progression of CKD. It is important that patients with
CKD receive appropriate referral and follow up by the nephrologist early in the course of disease.
DRUG THERAPY
Hyperkalemia
• Restriction of potassium rich food and drugs.
• Acute hyperkalemia may be treated with IV glucose and insulin or 10% calcium gluconate.
 • Sodium polystyrene sulfonate is commonly used to lower potassium levels in stage 4.
• Dialysis may be required to remove excess potassium.
Hypertension
It is recommended that the TARGET BP be less than 130/80mm Hg for CKD patients and 125/75 mm Hg for
patients with significant proteinuria.
Treatment for hypertension includes
• Weight loss
• Therapeutic lifestyle changes(e.g., exercise, avoidance of alcohol, smoking cessation)
• Diet recommendations- DASH diet
• Administration of antihypertensive drugs- commonly used drugs are diuretics, ACE inhibitors,
angiotensin receptor blocker agents.
CKD-MBD
Limiting dietary phosphorus intake – phosphate intake is not restricted until the patient requires RRT. The intake
is limited to 1g/day, but dietary control alone is not sufficient.
Administering phosphate binders – It include calcium based binders: calcium acetate and calcium carbonate. To
be effective, administer phosphate binders with each meal.
Supplementing vitamin D- Assess vitamin D levels to determine the need for supplementation. If levels are
low(less than 30 ng/dl), supplementation is given. Recommended in the form of cholecalciferol. Active vitamin is
available as oral or IV Calcitriol, IV paricalcitol, oral or IV doxercalciferol
Controlling hyperparathyroidism- treatment of secondary hyperparathyroidism in ESKD patients requires the
activated form of vitamin D because the kidney no longer possess the ability of activate vitamin D.
Cinacalcet, a calcimimetic agent, is used to control secondary hyperparathyroidism. Calcimimetics mimic calcium
and increase the sensitivity of the calcium receptors in the parathyroid glands. As a result, the parathyroid glands
detect calcium at lower serum levels and decrease PTH secretion. lf hyper parathyroid disease becomes severe
despite medical management, a subtotal or total parathyroidectomy may be performed to decrease the synthesis and
secretion of PTH.
Anemia
The most important cause of anemia is decreased production of erythropoietin.
• Exogenous erythropoietin (EP0) is used in the treatment.
It is available as epoetin alfa, which can be administered IV or subcutaneously, usually two or three
times per week. Darbepoetin alfa is longer acting and can be administered weekly or biweekly.
A significant increase in hemoglobin and hematocrit levels is usually not seen for 2 to 3 weeks. Higher
hemoglobin levels (more than 12 g/dL) and higher doses of EPO are associated with a higher rate of
thromboembolic events and increased risk of death from serious CV events (heart attack, HE stroke).
The recommendation is to use the lowest possible dose of EPO to treat anemia.
• Most patients receiving HD are prescribed IV sucrose injection and sodium ferric gluconate complex in
sucrose injection.
• Supplemental folic acid[1mg/day]
Dyslipidemia
SATINS [HMG CoA reductase inhibitors], such as atorvastatin, are used to lower LDL levels.
DIETARY MANAGEMENT
As nutritional management of patients with CKD is thought to control uremic symptoms and provide beneficial
effects on the progression of kidney dysfunction, the diet of patients with CKD should be an important
consideration in their care.
PROTIEN
A high-protein diet, defined as intake of > 1.2 g protein per kilogram of body weight per day (g/kg/day), has been
shown to cause significant deterioration in kidney function. High protein intake increases kidney blood flow and
elevates intraglomerular pressure, which leads to higher GFR and more efficient excretion of protein-derived
nitrogen products.
Although most international guidelines support a low-protein diet in patients with CKD, the protein requirements
vary
• Most guidelines recommend 0.6 to 0.8 g/kg/day protein or very-low-protein diet with keto acid analogs
for patients with moderate-to-advanced kidney disease (eGFRcr < 45 mL/min/1.73 m2) and those with
substantial proteinuria (urinary protein excretion > 0.3 g/day).
• Higher protein intake (1.0 to 1.2 g/kg/day) is recommended for patients with KF with replacement
therapy, as additional protein is needed to prevent PEW.
• Patients with nephrotic syndrome may benefit from a low-protein diet (0.8 g/kg/day plus 1 g/day
protein for each 1 g urinary protein excretion over 5 g/day), while ensuring adequate caloric intake.
• Furthermore, the target of protein intake should be individualized according to each patient’s clinical
condition and disease severity.
SODIUM
High sodium intake has deleterious effects on blood pressure, cardiovascular health, kidney function, and CKD
progression. In patients with CKD, dietary sodium restriction is strongly recommended to control fluid retention,
lower blood pressure, and reduce cardiovascular risk.
“Guidelines recommend lowering sodium intake to 2 to 2.3 g/day in adults.”
POTASSIUM
The 2015 American Dietary Guidelines Advisory Committee report recommends a daily potassium intake of 4,700
mg (121 mmol) for healthy adults. The National Kidney Foundation Kidney Disease Outcomes Quality Initiative
guidelines recommend a potassium intake of 2 to 4 g/day (51 to 102 mmol/day) for patients with CKD G3, G4, but
no restrictions (> 4 g/day or > 102 mmol/day) for those with earlier-stage CKD.
FLUID RESTRICTION
The recommended fluid intake depends on daily urine output.
NURSING MANAGEMENT
Nursing Assessment
• Assess fluid status (daily weight, intake and output, skin turgor, distention of neck veins, vital signs,
and respiratory effort).
• Assess nutritional dietary patterns (diet history, food preference, and calorie counts).
• Assess nutritional status (weight changes, laboratory values).
• Assess understanding of cause of renal failure, its consequences and its treatment.
• Assess patient’s and family’s responses and reactions to illness and treatment.
• Assess for signs of hyperkalemia.
Nursing diagnosis
•  Excess fluid volume related to impaired kidney function
•  Impaired renal tissue perfusion related to
•  Impaired Urinary Elimination R/T failing glomerular filtration AEB Impaired excretion of
nitrogenous products secondary to Renal Failure
•  Risk for electrolyte imbalance related to impaired kidney function
•  Imbalanced nutrition less than body requirement related to restriction intake of nutrients [especially
protein], nausea, vomiting, and anorexia.
Nursing interventions
 •  Monitor and record vital signs.
•  Note condition of skin and mucous membranes, color of urine.
•  Review lab data like BUN, Creatinine, and Serum electrolyte.
•  Record I&O accurately and calculate fluid volume balance
•  Restrict sodium and fluid intake if indicated
•  Encourage quiet, restful atmosphere.
•  Emphasize the need to adhere with prescribe diet
•  Emphasize importance of having good hygiene
CONCLUSION
Chronic kidney disease (CKD) is a long-term condition where the kidneys don't work as well as they should. It's a
common condition often associated with getting older. It can affect anyone, but it's more common in people who
are black or of south Asian origin. CKD can get worse over time and eventually the kidneys may stop working
altogether, but this is uncommon. Many people with CKD are able to live long lives with the condition.