Chronic Kidney Disease NCLEX Review

This NCLEX review will discuss chronic kidney disease (also called chronic renal failure).

As a nursing student, you must be familiar with chronic kidney disease along with how to care for patients who are experiencing this condition.

These type of questions may be found on NCLEX and definitely on nursing lecture exams.

Don’t forget to take the chronic kidney disease quiz.

You will learn the following from this NCLEX review:

• Definition of chronic kidney disease
• Causes
• Pathophysiology
• Stages of CKD
• Signs and Symptoms
• Nursing Interventions
• Treatment

NCLEX Lecture on Chronic Kidney Disease

Chronic Kidney Disease

What is CKD? It is a significant decline in kidney function that happens over a long period of time that leads to the build up of waste, water, and electrolyte imbalances in the body. CKD is irreversible.

Role of the Kidneys:

The kidneys receive fresh blood from the heart and filters the blood via the nephrons (glomerulus), which creates a filtrate/urine that will progress through the rest of the nephron (renal tubule). The renal tubule will fine-tune the filtrate by pulling out water and ions. Then the substances left over will be excreted in the urine.

Remember the glomerulus does NOT normally filter blood cells or proteins (just water, urea, creatinine, ions). In addition, creatinine is the only substance filtered by the glomerulus that is solely filtered from the bloodstream that is NOT reabsorbed within the renal tubule. Therefore, measuring creatinine levels in the urine/blood help us to determine the functionality of the kidneys, specifically the nephron.

The creatinine level along with the patient’s gender, race, weight, and age can help the physician determine the patient’s glomerular filtration rate (GFR).

In CKD, the filtering structure of nephron (GLOMERULUS) is unable to filter properly. Therefore, the patient’s glomerular filtration rate (GFR) is decreased.

There are various stages of CKD. A normal GFR is 90 mL/min or higher. This is the rate the glomerulus filters waste, ions, and water.

Stages of Chronic Kidney Disease

Be familiar with the GFR for each stage, especially stage 5, which represents ESRD (end-stage renal disease).

Stage 1: Kidney damage with normal renal function GFR >90 ml/min but with proteinuria (3 months or more)

Stage 2: Kidney damage with mild loss of renal function GFR 60-89 ml/min with proteinuria (3 months or more)

Stage 3: Mild-to-severe loss of renal function GFR 30-59 mL/min

Stage 4: Severe loss renal function GFR 15-29 mL/min

Stage 5: end stage renal disease GFR less 15 mL/min

*Source: “Kidney Disease Statistics For The United States | NIDDK”

When GFR decreases dramatically it leads to many problems (in the early stages the patient may be asymptomatic):

• Increased waste in the body: Uremia (Increased BUN and Creatinine levels, neuro changes, itching, metabolic acidosis)
• Hypervolemia (edema, HTN, pulmonary and cardiac problems)
• Electrolyte Imbalances: hyperkalemia, hypocalcemia, hyperphosphatemia (high phosphate levels cause low calcium levels, which stimulates the parathyroid gland to produce PTH. This causes calcium to leak out of the bones…hence bone problems), hypermagnesemia
• Oliguria (less than 400 ml/day) or Anuria (less than 100 mL/day)
• Proteinuria and Hematuria: glomerulus is damaged so it is allowing blood cells and proteins to leak through. The patient may have lower albumin levels (more swelling) and further anemia.

Kidneys also produce hormones:

EPO (erythropoietin): helps create RBCs in the bone marrow. In CKD, the EPO decreases, which leads to anemia.

Renin: plays a role in increasing blood pressure. In CKD the glomerulus is filtering less water and the kidneys think the blood pressure is low, so it releases renin, which in turn increases blood pressure even more.

Kidneys activate Vitamin D

Vitamin D: plays a role in helping the body reabsorb calcium from the food we eat. In CKD, the activation of vitamin D is diminished and this leads to lower calcium levels (hypocalcemia).

Causes of CKD

• *High blood pressure (hypertension): constant high pressure on the artery wall that supplies the kidneys causes damage. Therefore, less blood reaches the kidneys and the nephrons can’t function properly.
• *Diabetes Mellitus: uncontrolled hyperglycemia causes glucose to stick to arteries walls, which damages the blood supply to the kidneys.
• Acute kidney injury
• Polycystic kidney disease: genetic condition where cysts grow in the kidneys
• Infection
• Nephrotoxic drugs: NSAIDS, aminoglycosides, chemo therapy drugs, contrast dyes for testing procedures

*most common causes of chronic renal failure

Treatment for Chronic Kidney Disease:

Early stages with normal GFR:

• Controlling blood pressure and glucose level
• Medications for hypertension that help protect the kidneys, such as ACE inhibitors “pril” or ARBs “sartan”
• Monitoring GFR and blood pressure regularly

Advanced stages where GFR is abnormal:

• Dialysis
• Kidney transplant
• Diet changes

Nursing Interventions for Chronic Kidney Disease

What is going on with this patient? Remember waste build up (uremia and metabolic acidosis), anemia, electrolyte imbalances, low urinary output, and fluid overload.

Uremia (build up of waste in the blood)

• Safety: patient may be confused, assess neuro status
• Itching: due to deposits of urea crystals on the skin via the sweat glands. It looks like frost on the skin and is called “uremic frost”

• Low protein diet: urea is a waste product of protein breakdown (patient doesn’t need any more urea). However, patient needs some protein to prevent muscle wasting.
• Assess for kussmaul breathing was is deep/rapid breaths from the acid building up in the blood (metabolic acidosis). This type of breathing is a compensatory mechanism by the respiratory system to increase the blood’s pH.

Anemia: low red blood cells in the blood. RBCs help transport oxygen throughout the body so it can function.

• Why is anemia presenting? Due to low amounts of EPO being produced by the kidneys and possible deficiency in other minerals that help with hemoglobin production (which acts a transporter for RBCs). These minerals include: iron, folic acid, and vitamin B12
• Patient signs and symptoms: pale, extremely tired, dyspnea, confused
• Treatment: Supplements of Iron (IV form if patient on dialysis rather than PO), Erythropoietin (subq injections), or blood transfusions per MD order

Electrolyte Imbalances:

Hyperkalemia (>5.1 mEq/L): (normal level 3.5 – 5.1 mEq/L) at risk for significant cardiac event due to the nephrons decreased ability to excrete potassium.

• Nursing Role:
  • restrict potassium-rich foods (potatoes, avocados, strawberries, tomatoes, spinach, oranges, bananas), monitor EKG for changes (tall peaked T-waves, Wide QRS and prolonged PR interval)
  • monitor lab values
  • may be ordered to give Kayexalate orally or rectally to remove extra potassium out of the blood
  • place on cardiac monitor to watch rhythm

Hyperphosphatemia (>4.5 mg/dL): normal level 2.7-4.5 mg/dL

Hypocalcemia (<8.6 mg/dL): normal level 8.6-10 mg/dL

• Phosphate builds up in the blood because it cannot be excreted out of the kidney due to a damaged nephron, which leads to the decrease of calcium “hypocalcemia”. WHY? Because phosphate binds to the calcium and when there are high amounts of phosphate in the blood it depletes calcium from the blood due to this binding. In addition, calcium levels decrease due to the inactivation of vitamin d by the kidneys.
• In addition, high phosphate levels stimulate the parathyroid gland to release PTH (parathyroid hormone), which causes the bones to leak calcium in the blood stream to increase the level. This can cause bone problems.
• Nursing Role:
  • Administer phosphate binders, such as calcium carbonate or “PhosLo (calcium acetate)” to decrease phosphate levels. These medications works by excreting phosphate in the stool found in food. Give with meals or immediately after eating.
  • Diet low in phosphate: Restrict foods high is phosphate: poultry, fish, dairy, nuts, sodas, oatmeal.
  • Safety due to weak bones.

Hypermagnesemia (>2.6 mg/dL): normal 1.6-2.6 mg/dL

• Patient is at risk for EKG changes, tendon reflexes diminished or absent, lethargy.
• Nursing role:
  • Avoid administering magnesium based antacids or laxatives
  • Low magnesium foods
  • MD may order IV calcium to help decrease level

LOW UOP and Fluid Overload:

• Monitor intake and output (strict)
• Daily weights
• Assess swelling and lung sounds “crackles”
• Monitor blood pressure
• Low sodium diet

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