Renal System Notes

Urostomies

• Some types of urostomies can keep patients continent, unlike regular urostomies where urine constantly flows out.

Indiana Pouch

• An Indiana pouch is created using a piece of the colon and ileum to form a reservoir with a valve.
• Patients with an Indiana pouch self-catheterize to empty the reservoir, similar to emptying the urethra; this avoids constant incontinence.
• Self-catheterization is required to empty the bladder, ensuring continence.

Neobladder

• A neobladder allows patients to void through their urethra like a regular person.
• Patients may experience a small degree of incontinence, but generally, continence is maintained, and urination occurs through the urethra.

Traditional Urostomy

• Traditional urostomies involve a bag to collect urine.

Post-Operative Care for Ostomies

• For any ostomy, consult the wound care team, specifically a wound ostomy nurse.
• Monitor urine output to detect any obstructions in the new bladder or reservoir.
• Educate patients with an Indiana pouch on how to self-catheterize, emphasizing cleanliness and signs/symptoms of infections (UTIs, bladder infections).

Cancer of the Kidneys

• After a kidney biopsy, monitor patients for bleeding.

Signs and Symptoms of Bleeding

• Signs include tachycardia and hypertension.
• Blood collection may be observed in the back where the kidneys are located, indicating a retroperitoneal bleed.

Nephrectomy

• A nephrectomy involves the removal of one kidney; patients can live with a single kidney.

Post-operative Monitoring

• Monitor for potential complications with a focus on anticipation and preparation.
• Assess both the patient and the environment for possible complications, ensuring all necessary equipment is readily available.

Potential Complications

• Bleeding: Monitor for signs of hemorrhage.
• Infection: Watch for signs of post-operative infection.
• Pneumothorax: There is a high risk of pneumothorax due to the proximity of the kidneys to the lungs.

Assessing for Pneumothorax

• Breathing: Assess for labored breathing.
• Vital Signs: Monitor for low oxygen saturation and elevated heart rate.
• Breathing Patterns: Look for hyperventilation and the use of accessory muscles, such as retractions.
• Lung Sounds: Assess for diminished or absent breath sounds on the affected side.
• Be cautious, as sounds from the unaffected side may be louder due to increased breathing effort.

Post-Anesthesia Considerations

• Expect slightly lower oxygen saturation post-anesthesia (e.g., 92-93%).
• Encourage deep breaths; if the patient struggles, suspect a problem.

Renal Trauma

• Renal trauma can result from falls or direct blows to the back.

Signs of Renal Trauma

• Retroperitoneal bruising, swelling, pain, and hematuria (bloody urine).
• Testing and Treatment:
• Urinalysis to detect hematuria.
• IV pyelogram, ultrasound, or CT scan for diagnosis.
• Treatment includes addressing the injury, monitoring input and output, administering IV fluids, and managing pain.
• Monitor kidney enzymes to ensure they decrease, indicating recovery.

Polycystic Kidney Disease

• Polycystic kidney disease is a hereditary disorder leading to chronic kidney disease, characterized by multiple cysts forming on the kidneys.
• These cysts replace healthy kidney tissue, leading to impaired function.

Signs and Symptoms

• Dull heaviness in the flank or back, hematuria, hypertension, and recurrent UTIs.

Diagnosis and Treatment

• Cysts can be visualized on ultrasound.
• There is no cure for polycystic kidney disease; treatment focuses on managing symptoms.
• Patients typically require dialysis or kidney replacement and are advised to undergo genetic counseling due to the hereditary nature of the disease.

Diabetic Nephropathy

• Diabetic patients have a high risk of developing kidney disease, often leading to dialysis.

Cause

• High glucose levels in the blood damage the kidneys over time.

Physiological Changes

• Atherosclerotic changes decrease blood flow to the kidneys.
• Damaged blood vessels impede blood flow, harming the kidneys. Decreased blood flow is damaging to the kidneys.

Interventions

• Early interventions include controlling blood glucose and blood pressure.
• Protein restriction in the diet can reduce the workload on the kidneys.
• Later stages may require dialysis or a kidney transplant.

Patient Education

• Reinforce the importance of controlling blood glucose to prevent damage to other systems (e.g., kidneys).
• Uncontrolled diabetes can cause hypertension and affect the heart, leading to multi-organ issues.

Nephrotic Syndrome

• Nephrotic syndrome involves the loss of large amounts of protein in the urine due to increased glomerular membrane permeability.

Mechanism

• Decreased albumin levels increase permeability, allowing proteins to leak out.
• Low protein levels cause fluid to leak from blood vessels into tissues, leading to edema, ascites, and anasarca (generalized edema).

Compensatory Response

• The liver increases lipoprotein production, resulting in foamy urine.
• Foamy urine indicates the liver is releasing lipoproteins in response to decreased albumin levels.

Nursing Implications

• Assess albumin levels when foamy urine is observed and recognize the compensatory mechanisms.

Potential Complications

• Loss of immunoglobulins increases susceptibility to infection.
• Loss of clotting inhibitors can lead to bleeding.

Treatment

• Treatment focuses on managing symptoms.

Symptom Management

• ACE inhibitors or ARBs to reduce pressure in the glomerulus and slow down protein excretion.
• Loop diuretics and sodium restriction to reduce edema.
• Protein restriction is determined on a case-by-case basis, balancing the need to limit protein loss with the need for adequate intake.
• Statins to decrease cholesterol and triglyceride levels, which increase during this syndrome.
• Anticoagulants may be necessary to prevent reclotting, as the body may compensate for the loss of clotting inhibitors by increasing coagulation factors.

Nephrosclerosis

• Nephrosclerosis involves sclerotic changes due to hypertension, damaging the kidneys.

Mechanism

• Hypertension damages the kidneys, causing cirrhotic changes in small arteries.

Treatment

• Antihypertensives to manage hypertension and prevent ischemia and further kidney damage.

Glomerulonephritis

• Glomerulonephritis is the inflammation of the glomeruli, the filtering units of the kidneys, often due to an immune response.

Mechanism

• Proteins, white blood cells, and red blood cells leak into the urine.

Common Cause

• Frequently caused by a streptococcal infection (group A beta-hemolytic strep) 6-10 days after a throat or skin infection.

Assessment

• Inquire about recent sore throat or strep infections.

Pathophysiology

• Antibodies form complexes with the strep antigen, depositing in the glomeruli and causing inflammation.

Symptoms

• Edema, oliguria (decreased urine output), and hypertension.

Hallmark Sign

• Periorbital edema (edema around the eyes). The swelling starts in the face, around the eyes, and then progresses down through the body.

Additional Signs

• Hematuria, proteinuria, electrolyte imbalances, edema, and hypertension.

Treatment

• Elevated creatinine and BUN levels.
• Dark, foamy urine.

Management

• Most cases resolve spontaneously within a week, but kidney damage may require treatment.
• Antibiotics for strep infections, temporary dialysis if severe.

Prevention

• Take antibiotics completely for strep infections.
• Follow fluids, sodium, and protein restrictions as appropriate.

Acute Kidney Injury (AKI)

• Acute kidney injury is the sudden loss of kidney function, leading to a rapid accumulation of toxic waste (azotemia).
• Azotemia results from the kidneys failure, causing elevated creatinine and BUN levels.
• Most cases can be corrected before progressing to chronic injury.

Causes:

• Hypoperfusion: Decreased blood flow to the kidneys (e.g., dehydration).
• Direct Tissue Injury: Toxins or mechanical injuries.
• Hypersensitivity: Inflammatory responses to medications or substances.

Phases of AKI

Initiating Phase

• The event occurs, potentially lasting hours to days, until symptoms appear.

Oliguric Phase

• Urine output decreases to less than 400 mL in 24 hours, typically lasting 24 hours to 7 days.
• Fluid retention, electrolyte imbalances, and increased waste products occur.
• Metabolic acidosis due to the failure to eliminate hydrogen ions.

Diuretic Phase

• Urine production increases to 1-3 liters per day, but the kidneys cannot concentrate the urine.
• Leads to dehydration, hypovolemia, and hypotension.
• Electrolytes are depleted, but BUN and creatinine levels remain high.

Recovery Phase

• Can last up to a year, with kidney function gradually returning.

Etiology of AKI

Prerenal Failure

• Occurs before blood reaches the kidneys.
• Caused by dehydration, blood loss, shock, or NSAID use.

Mechanism of NSAIDs

• Impair autoregulatory responses of the kidneys, decreasing perfusion by blocking prostaglandins.

Diagnosis

• Evaluate possible causes.
• Assess if the patient is dehydrated, and test with IV hydration and reassess creatinine levels.

Intrarenal Failure

• Actual damage to the nephrons in the kidney and the most common causes are toxins and ischemia.
• Such as a clot in the kidney.
• Causes necrosis of tissue and glomerular nephritis.
• Contrast dye is intrarenal.

Postrenal Failure

• Occurs after blood leaves the kidneys.
• Caused by obstructions, tumors, or an enlarged prostate.

Nephrotoxins

• Medications that are caustic to the kidneys such as certain antibiotics.
• For example if vanco levels are too high then the vanco is toxic and could be dangerous to the patient.

Prevention

• Check GFR, follow protocols for contract induced neuropathy, and hydrate before/after contrast media.
• Peak and trough levels tested for CRRT in the ICU.

Chronic Kidney Disease

• Chronic kidney disease is a progressive, irreversible deterioration in kidney function.
• It results in the accumulation of nitrogen waste product and uremia and is caused by hypertension, diabetic nephropathy, nephrosclerosis, or glomerulonephritis.

Genetic Factors

• Autoimmune diseases or genetic disorders can be inherited that cause the kidneys to attack themselves.

Complications

• Edamatous and shortness of breath.
• A progressive loss of function.

Focus of transplant

• Focus on infection and anti-rejection drugs after a transplant.

Stages

Renal Insufficiency

• Up to 75% of nephrons are damage and loss.

End Stage Chronic Kidney Disease

• At least 90% of the nephrouns are lost.

Symptoms

• Fluid Accumulation, EDEMA, SOB, electrolyte imbalances, and Anemia.

Complication Signs

• prone to fractures, dry skin, coma, Edema, fluid accumulation, infection, heart failure, and hypertension.

Diet

• Low protein and calorie restricitons.
• A low sodium, potassium and phosphorus diet and a fluid restriction.

Axalate

• Binded in what? Gi tract