Chronic renal failure

Prepared by:
Under supervision:
Ahmed Adel Shaban
Dr. Marwa AbdElrahman. Aya Hamdy Mohamed
Dr. Samar Hussien. Aya Ayman AbdElmonem

Bilal Taha Hussien

Hossam Mahmoud Mohamed

Khalid Mostafa Atta

Habiba Elsayed Fahmy

Alaa Osama Mohamed

Mostafa Bayomi Mohamed

Internship year
2024/2025
Outlines:
➢ Introduction.
➢ Definition.
➢ Risk factors.
➢ Causes.
➢ Signs and symptoms.
➢ Complications.
➢ Diagnosis.
➢ Lab investigation.
➢ Treatment.
➢ Medical management.
➢ Nursing management.
 Introduction
Your kidneys are like a filter in your body. Filter out wastes, toxins
and extra water from your blood. They also help with other functions
like bone and red blood cell health. When your kidneys begin to lose
their function, they can’t filter waste, which means the waste builds
up in your blood.
Kidney disease is called “chronic” because kidney function slowly
decreases over time. CKD can lead to kidney failure, which is also
called end-stage kidney disease. Not everyone with CKD will
develop kidney failure, but the disease will often worsen without
treatment. There’s no cure for chronic kidney disease. But there are
steps you can take to slow kidney damage. Treatments like dialysis
and transplantation are options for kidney failure.

Definition:
Chronic kidney disease (CKD):
- When the kidneys have become damaged over time (for at least 3
months) and have a hard time doing all their important jobs.
- Gradual loss of kidney function. Your kidneys filter waste and
excess fluids from your blood, which are then removed in your
urine. Advanced chronic kidney disease can cause dangerous levels
of fluid, electrolytes and waste to build up in your body.
 Risk factors:
Anyone can develop CKD - at any age. However, some
people are at a higher risk than others. The most common
CKD risk factors are:
➢ Diabetes.
➢ High blood pressure.
➢ Heart disease or heart failure.
➢ Obesity.
➢ Age over 60 years old.
➢ Family history of CKD or kidney failure.
➢ Personal history of acute kidney injury (AKI).
➢ Smoking and/or use of tobacco products.
For many people, CKD is not caused by just one reason.
Instead, it is a result of many physical, environmental, and
social factors. Early detection is important – CKD often begins
without causing any noticeable symptoms. Knowing the risk
factors can help you know your level of risk and if you should
get checked for CKD.
Causes:
1. Diabetes Mellitus (Diabetic Nephropathy): High blood sugar
levels damage kidney filtration units, leading to CKD Most
common cause of CKD worldwide.
2. Hypertension (Hypertensive Nephrosclerosis): Chronic high
blood pressure damages the small blood vessels in the kidneys,
reducing their ability to filter blood.
3. Glomerulonephritis: Inflammation of the glomeruli, the kidney's
filtering units, often due to autoimmune diseases, infections, or
other systemic conditions.
4. Polycystic Kidney Disease (PKD): A genetic disorder
characterized by the growth of cysts in the kidneys, leading to their
enlargement and dysfunction.
5. Chronic Pyelonephritis: Recurrent urinary tract infections (UTIs)
or kidney infections that cause scarring and damage over time.
6. Obstructive Uropathy: Blockages in the urinary tract (e.g., due to
kidney stones, tumors, or an enlarged prostate) can lead to long-
term kidney damage.
7. Autoimmune Diseases: Conditions like systemic lupus
erythematosus (SLE) or vasculitis can damage the kidneys.
8. Chronic Use of Nephrotoxic Drugs: Long-term use of
medications such as NSAIDs, some antibiotics, or contrast agents
can damage kidneys.
9. Chronic Kidney Infections: Persistent infections, such as
tuberculosis of the kidney, may cause gradual kidney damage.
10. Other causes:
• Toxins or heavy metals (e.g., lead or cadmium exposure).
• Congenital malformations.
• Rare genetic or metabolic disorders (e.g., Alport syndrome,
Fabry disease).
• Pathophysiology Overview
• CKD progresses through stages:
• Initial damage (e.g., inflammation, high blood sugar, or
pressure).
• Compensatory hyperfiltration in remaining nephrons.
 Signs and symptoms:
General symptoms:
❖ Fatigue and weakness: Caused by anemia (due to reduced
erythropoietin production) and toxin buildup.
❖ Nausea and vomiting: Resulting from uremia (accumulation of
waste products in the blood).
❖ Loss of appetite: Often related to nausea and metabolic
disturbances.
❖ Weight loss: Due to poor appetite and muscle wasting.
❖ Swelling: Swelling in the legs, ankles, feet, or face due to fluid
retention.
Urinary symptoms:
❖ Change in urinary output: Increased urination (especially at
night, nocturia) or reduced urine production.
❖ Foamy urine: Indicates proteinuria (excess protein in the urine).
❖ Blood in urine (Hematuria): May occur in some cases.
Cardiovascular symptoms:
❖ Hypertension: Both cause and symptom of CKD.
❖ Shortness of breath: Due to fluid overload in the lungs or anemia.
❖ Chest pain: Caused by pericarditis (inflammation of the
pericardium) or fluid retention.
Neurological symptoms:
❖ Confusion: Caused by toxin buildup in the blood (uremic
encephalopathy).
❖ Muscle cramps: Due to electrolyte imbalances, particularly low
calcium or high potassium.
❖ Prepheral neuropathy: Tingling or numbness in hands and feet.
 Skin symptoms:
❖ Itchy skin: Due to uremia or calcium-phosphorus imbalance.
❖ Dry yellowish skin: Caused by anemia and toxin accumulation
Other symptoms:
❖ Bone pain: Resulting from secondary hyperparathyroidism and
mineral imbalance.
❖ Bad breath: Ammonia-like odor due to urea breakdown in the
saliva.
❖ Cold intolerance: Caused by anemia.
❖ Bleeding easily: Due to platelet dysfunction in uremia.
Late stage symptoms:
❖ Severe fluid retention.
❖ Severe electrolyte imbalances (e.g., hyperkalemia causing
arrhythmias).
❖ Seizures or coma due to uremic encephalopathy.

Complications:
❖ Salt/fluid balance: Salt and fluid balance abnormalities are common
in CKD, becoming more apparent in stages 4 and 5. These patients
often respond to sodium restriction and loop diuretics.
❖ Hypertension: Hypertension in CKD can be a manifestation of volume
expansion, although patients with CKD do not always have edema to
suggest volume expansion. Many patients with CKD benefit from
using a loop diuretic before escalating the doses of other
antihypertensives.
❖ Hyperkalemia: Hyperkalemia in CKD can occur particularly in
oliguric patients and those with distal renal tubular dysfunction.
Contributing factors include dietary potassium intake, tissue
breakdown, and aldosterone resistance. Additionally, medications such
as angiotensin-converting enzyme (ACE) inhibitors and nonselective
beta-blockers can also lead to hyperkalemia
❖ Metabolic acidosis: Metabolic acidosis is a common complication of
advanced CKD due to the retention of acidic compounds. Chronic
metabolic acidosis can lead to osteopenia in these patients. Treatment
typically involves bicarbonate supplementation to maintain a serum
bicarbonate level of 23 mEq/L.
❖ Hyperphosphatemia: Hyperphosphatemia is a common complication
of CKD due to a decreased filtered phosphorous load. This leads to
increased secretion of PTH and causes secondary hyperparathyroidism.
While hyperparathyroidism aims to normalize phosphorus and calcium
levels, it often leads to hyperphosphatemia at the expense of bone
health.
❖ Anemia: Anemia of CKD is typically normocytic normochromic and
results from reduced erythropoietin production due to decreased
functioning renal mass, abnormal iron metabolism, and reduced red
blood cell survival. Hemoglobin levels should be checked annually in
stage 3 CKD, every 6 months in stages 4 and 5, and monthly in dialysis
patients. Erythropoiesis-stimulating agents should be considered when
hemoglobin is below 10 g/dL, with iron saturation at least 20% to 30%
and ferritin greater than 200 ng/mL. For dialysis patients, the target
hemoglobin concentration is 10 to 11.5 g/dL.
 Diagnosis:
When evaluating a patient for CKD, it is crucial to consider other
potential diagnoses that may present similar symptoms and clinical
findings. The differential diagnoses include:
➢ Acute kidney injury.
➢ Alport syndrome.
➢ Anti glomerular basement membrane disease.
➢ Diabetic nephropathy.
➢ Multiple myeloma.
➢ Nephrolithiasis.
➢ Rapidly progressive glomerulonephritis.
➢ Renal artery stenosis.
Staging:
The 6 categories of CKD staging include:
1. G1: GFR 90 mL/min/1.73 m2 and above with urinary abnormalities
suggesting kidney disease such as hematuria or
2. G2: GFR 60 to 89 mL/min/1.73 m2
3. G3a: GFR 45 to 59 mL/min/1.73 m2
4. G3b: GFR 30 to 44 mL/min/1.73 m2
5. G4: GFR 15 to 29 mL/min/1.73 m2
6. G5: GFR less than 15 mL/min/1.73 m2 or ESRD
The 3 levels albuminuria include:
A1: ACR less than 30 mg/g (<3.4 mg/mmol).
A2: ACR 30 to 299 mg/g (3.4-34 mg/mmol).
A3: ACR greater than 300 mg/g (>34 mg/mmol).
 Laboratory investigations:
1- Basic renal function test:
• Serum Creatinine: Elevated in CKD due to reduced kidney clearance.
• Estimated Glomerular Filtration Rate (eGFR): (Calculated using
creatinine, age, gender, and race - Defines CKD stages).
• Blood Urea Nitrogen (BUN): Elevated in CKD, indicating impaired
excretion.
2- Urine test:
• Urinalysis: Detects proteinuria, hematuria, and casts (e.g., red blood cell
casts in glomerulonephritis).
• Spot Urine Protein-to-Creatinine Ratio (UPCR): Quantifies
proteinuria.
• 24-Hour Urine Collection: Measures protein and creatinine clearance.
• Urine Albumin-to-Creatinine Ratio (ACR): Detects microalbuminuria
in early CKD, especially in diabetics.
3- Electrolyte and Acid-base status:
• Serum Potassium: Elevated in advanced CKD (hyperkalemia).
• Serum Sodium: May be high or low, depending on fluid balance.
• Serum Bicarbonate: Low in metabolic acidosis.
• Chloride Levels: Can help assess acid-base imbalances.
4- Bone and mineral metabolism:
• Serum Calcium: Often low in CKD due to reduced vitamin D activation.
• Serum Phosphate: Elevated due to impaired renal excretion.
• Parathyroid Hormone (PTH): Elevated in secondary
hyperparathyroidism.
• Vitamin D Levels: Often deficient in CKD.
5- Hematology:
• Complete blood count (CBC): Detects anemia (low hemoglobin and
hematocrit) due to reduced erythropoietin.
• Iron Studies: Serum iron, ferritin, and transferring saturation to assess
iron deficiency.
6- Cardiovascular risk assessment:
• Lipid Profile: Dyslipidemia is common in CKD.
• C-Reactive Protein (CRP): May indicate inflammation.
7- Imaging and special tests:
• Renal Ultrasound: Evaluates kidney size, structure, and presence of
cysts, stones, or obstructions.
• Renal Biopsy: Done if glomerulonephritis or other specific diseases are
suspected.
8- Tests for underlying causes:
• Blood Glucose and HbA1c: To check for diabetes.
• Antibody Tests: (ANA, anti-DNA for lupus nephritis - ANCA for
vasculitis).
• Serum Complement Levels (C3, C4): Low in certain glomerulonephritis
types.
• Urine Culture: To rule out chronic infections.
9- Monitoring:
• Regular Creatinine and eGFR: To track CKD progression.
• Electrolytes and Acid-Base Levels: To manage complications.
• Albumin-to-Creatinine Ratio (ACR): To assess proteinuria trends.
Treatment:
1- Treat underlying cause:
❖ Diabetes management:
- Control blood glucose with insulin or oral antidiabetic agents.
- Use SGLT2 inhibitors or GLP-1 receptor agonists to protect kidneys.
❖ Hypertension management:
- Target BP <130/80 mmHg.
- Use ACE inhibitors or ARBs to reduce proteinuria and protect renal
function.
❖ Treat glomerulonephritis:
- Use corticosteroids or immunosuppressants (e.g., cyclophosphamide) if
autoimmune.
 2- Lifestyle modification:
❖ Dietary changes:
- Restrict sodium (≤2g/day) to control blood pressure and reduce edema.
- Limit protein intake (0.6-0.8 g/kg/day) to reduce kidney workload.
- Avoid high-potassium and high-phosphorus foods in advanced CKD.
❖ Hydration:
- Maintain adequate hydration but avoid fluid overload in later stages.
- Quit Smoking and Alcohol.
- Reduce cardiovascular and kidney damage.
❖ Exercise:
- Regular moderate exercise improves cardiovascular health and overall
well-being.

3- Manage complications:
❖ Anemia:
- Treat with erythropoiesis-stimulating agents (e.g., epoetin alfa) and iron
supplements.
❖ Electrolyte imbalance:
- Hyperkalemia: Low-potassium diet, potassium binders, or dialysis if
severe.
- Hyperphosphatemia: Phosphate binders (e.g., sevelamer, calcium
acetate).
- Hypocalcemia: Calcium supplements and activated vitamin D (calcitriol).
- Metabolic Acidosis: Sodium bicarbonate supplementation.
❖ Bone disorders:
- Treat secondary hyperparathyroidism with vitamin D analogs or calcimine.

4- Slow CKD progression:

❖ Proteinuria management: Use ACE inhibitors or ARBs even in non-
hypertensive patients with proteinuria.
❖ Control lipids: Stations to manage dyslipidemia and reduce
cardiovascular risk.
 5- Renal replacement therapy (Advanced CKD or
ESRD):
❖ Dialysis: Hemodialysis or peritoneal dialysis to remove waste products
and excess fluid.
❖ Kidney transplantation: Ideal option for suitable candidates, restoring
normal kidney function.
6- Palliative care (if dialysis / transplant is not
feasible):
Focus on symptom control (e.g., pain, itching, fatigue) and improving quality
of life.
❖ Monitoring and follow-up:
- Regular monitoring of renal function (e.g., GFR, creatinine).
- Monitor and address complications like anemia, electrolyte imbalances, and
cardiovascular risk.
- Goal: Delay progression, manage complications, and enhance patient well-
being. Early referral to a nephrologist is crucial for optimal care.
Medical management:
Ten ways to manage kidney disease:
➢ Control your blood pressure.
➢ Control your blood glucose if you have diabetes.
➢ Work with your health care team to monitor your kidney health.
➢ Take medicines as prescribed.
➢ Work with a dietitian to develop a meal plan.
➢ Make physical activity part of your routine.
➢ Aim for a healthy weight.
➢ Get enough sleep.
➢ Stop smoking if you smoke.
➢ Find healthy ways to cope with stress and depression.
 Nursing management:
❖ Impaired Urinary Elimination Related to Chronic
kidney disease as evidenced by Oliguria, Dysuria and
Urinary retention.
Assessment:
1. Assess the patient’s urinary elimination patterns and problems.
2. Assess urine characteristics (Assess the amount, color, clarity, and odor of
urine for additional complications such as infection).
Interventions:
1. Administer diuretics as indicated.
2. Administer fluids with caution.
3. Educate on expectations: With CRF, urine production may increase and
decrease. Educate the patient that as the disease progresses urine production
will slow and may stop completely.
4. Prevent infections: Patients who are receiving dialysis due to severe CFR
are at risk of infections from dialysis catheters and fistulas. Monitor for
fever and abdominal pain.

❖ Excess Fluid Volume Related to Kidney dysfunction as

evidenced by Edema.
Interventions:
1. Assess lung sound
2. Assess and monitor the patient’s intake and output.
3. Assess laboratory values.
4. Monitor the patient’s weight daily.
5. Restrict fluids as indicated.
6. Administer medications as indicated.
7. Provide care to edematous extremities as needed.
8. Prepare the patient for dialysis as indicated.
❖ Imbalanced Nutrition: Less Than Body Requirements
Related to disease process and Metabolic acidosis As
evidence by weight loss.
Interventions:
1. Assess the patient’s eating pattern and factors contributing to imbalanced
nutrition.
2. Assess and review laboratory results. (If Decreased serum albumin is
present).
3. Assess the patient’s hydration status and daily weight.
4. Encourage the patient to avoid foods high in potassium, sodium, and
phosphorus such as cola, brown rice, bananas, processed meats
5. Encourage the patient to eat the right amount and type of protein.
6. Increase fiber.

❖ Risk for Decreased Cardiac Output Related to Fluid

imbalance affecting circulating volume and myocardial
workload.
Interventions:
1. Assess and monitor the patient’s blood pressure.
2. Assess chest pain, its location, severity, and intensity.
3. Assess for signs and symptoms of decreased cardiac output. (Decreased
cardiac output can be manifested as fatigue, dyspnea, orthopnea, edema,
and decreased peripheral pulses).
4. Administer medications as indicated.
5. Closely monitor fluid status and restrict fluids as indicated.
6. Assist and prepare the patient for dialysis.
❖ Risk for Electrolyte Imbalance Related to Renal failure.

Interventions:
1. Assess laboratory data.
2. Assess and monitor vital signs.
3. Administer lactulose in case of Hyperkalemia
4. Administer loop diuretics. Loop diuretics are potassium-wasting and will
rid the body of potassium.
5. Provide or restrict nutrition based on lab work. Electrolytes are found in
many foods and fluids. Restrict intake when levels are high or provide
additional sources if deficient.
6. Educate the patient about signs of high potassium and other risks
(Hyperkalemia can cause muscle weakness, restlessness, cramping, and a
slow heart rate. Hyponatremia can cause muscle cramps, nausea,
disorientation, and alterations in mental status).
 References:
➢ Chapter 1: Definition and classification of CKD. Kidney Int Suppl
(2021). 2023 Jan;3(1):19-62.
➢ Inker LA, Astor BC, Fox CH, Isakova T, Lash JP, Peralta CA, Kurella
Tamura M, Feldman HI. KDOQI US commentary on the 2012 KDIGO
clinical practice guideline for the evaluation and management of CKD. Am
J Kidney Dis. 2024 May;63(5):713-35.
➢ Webster AC, Nagler EV, Morton RL, Masson P. Chronic Kidney
Disease. Lancet. 2019 Mar 25;389(10075):1238-1252.
➢ National Kidney Foundation. K/DOQI clinical practice guidelines for
chronic kidney disease: evaluation, classification, and stratification. Am J
Kidney Dis. 2022 Feb;39(2 Suppl 1):S1-266.
➢ https://en.wikipedia.org/wiki/Chronic_kidney_disease
➢ https://my.clevelandclinic.org/health/diseases/15096-chronic-kidney
disease
➢ https://www.kidney.org/kidney-topics/chronic-kidney-disease-ckd.