Chapter 49: Management of Pts w/Kidney Disorders

Volume Status Monitoring

Patient Weight: This is the most accurate indicator of volume status and is essential for determining daily fluid allowances.

I&O Records: Used to document fluid intake, urine excretion, and other losses, though considered less accurate than weight for indicating fluid volume excess or deficit

Fluid Overload

Occurs when intake exceeds the kidney's excretion capacity

Volume Depletion

Occurs when intake is inadequate, leading to fluid volume deficit

Fluid Volume Deficit Manifestations

Weight loss >5% decreased skin turgor, oliguria/anuria, increased hct/BUN

Fluid Volume Deficit Management Strategies

IV fluid challenge, oral/parenteral replacement

Fluid Volume Excess Manifestations

Weight gain >5%, edema, crackles, SOB, JVD

Fluid Volume Excess Management Strategies

fluid/sodium restriction, diuretics, dialysis

Hyponatremia Manifestations

Nausea, malaise, lethargy, headache, seizures

Hyponatremia Management Strategies

Normal saline or 3% IV hypertonic saline 

Hyperkalemia Manifestations

Muscle weakness, ECG changes, arrhythmias, abd cramping 

Hyperkalemia Management Strategies

Dietary restriction, diuretics, IV glucose/insulin, cation exchange resins, dialysis

Metabolic Acidosis Manifestations

Headache, confusion, increased RR, flushed skin

Metabolic Acidosis Management Strategies

 IV/oral bicarbonate, dialysis

Hypoalbuminemia Manifestations

Chronic weight loss, fatigue, oft flabby muscles, edema

Hypoalbuminemia Management Strategies

 High–biologic protein diet, IV albumin 

Chronic Kidney Disease (CKD)

Definition: Kidney damage or a decreased GFR lasting ≥3 months.

The Impact: Associated with decreased quality of life and premature death, often from cardiovascular disease.

Health Disparities: There is a higher prevalence in Black Americans.

The "Silent" Issue: 9 out of 10 adults with CKD are unaware they have it

Most common causes of kidney failure is diabetes and hypertension

Risk Factors of CKD

Diabetes, hypertension, cardiovascular disease, obesity, and advanced age

Pathophysiology of CKD- Early Stages

Diverse etiology: systemic (diabetes), primary(kidney stones)

Pathophysiology of CKD- Glomerular Damage Mechanism

Healthy glomerulus:

Healthy capillary walls

Large proteins, albumin, globulin

Damaged Glomerulus in CKD:

Increased capillary in CKD

Inflammation 

Large plasma, globulins

Increased glomerular permeability

Pathophysiology of CKD- Protein Leakage and Functional Markers

Albuminuria: elevated: <10 mg

Proteinuria: normal massive: >3.5 g/d

Functional Decline: <15

Pathophysiology of CKD- Cycle of Damage

Protein leakage (urotein: albuminuria and proteinuria) → structural damage, inflammation, and cellular injury → protein leakage 

Urinary albumin excretion is what causes damage to kidney structures and decreased GFR

Untreated proteins cause further injury

Persistent albuminuria and decreased GFR for > 3 months = CKD diagnosis

Stage 1 of CKD

GFR: >90

Kidney damage w/normal or increased GFR

Stage 2 of CKD

60-89

Mild decrease in GFR

Stage 3a of CKD

45-59

Mild to moderately decreased GFR

Stage 3b of CKD

30-44

Moderately to severely decreased GFR

Stage 4 of CKD

25-29

Severe decrease in GFR

Stage 5 of CKD

<15 

End stage kidney disease (ESKD); kidney replacement therapy (KRT) required

Assessment and Diagnostic Findings of CKD

GFR= amount of plasma filtered through glomeruli

Creatinine clearance= measure amount of creatinine kidneys clear in 24 hrs

Medical Management of CKD

Treatment of underlying causes

Controlling cardio risk factors and blood glucose lvls, monitoring lab values, managing anemia, weight loss, exercise, reducing salt/alcohol intake

Nephroscelrosis

Definition: Hardening of the renal arteries, often secondary to hypertension or diabetes.

Clinical Signs: Elevated BUN/Creatinine and mild proteinuria

Forms of Nephroscelrosis

acute hypertensive and benign

Acute Hypertensive- Nephroscelrosis

Associated with severe hypertension; involves patchy necrosis.

Benign- Nephroscelrosis

Typically found in older adults with atherosclerosis.

Management of Nephroscelrosis

Typically found in older adults with atherosclerosis.

Primary Glomerular Disease

Antigen-antibody complexes become trapped in glomerular capillaries, inducing inflammation

Acute Nephritic Syndorme

type of glomerulonephritis characterized by hematuria (cola-colored urine), edema, azotemia, and proteinuria.

also known as Acute glomerulonephritis

Manifestations of Primary Glomerular Disease

Hematuria, edema, azotemia (concentration of nitrogenous wastes in blood), uremia, and proteinuria (excess protein)

Diagnosis of Primary Glomerular Disease

Kidney biopsy is the standard for definitive classification. Immunoflouriscent analysis helps identify nature of lesion 

Urine output will increase and proteinuria and sediment will diminish if pt improves

Others may develop severe uremia and require dialysis

Complications of Primary Glomerular Disease

Hypertensive encephalopathy, heart failure, and pulmonary edema

w/o treatment, ESKD develops within weeks or months

Medical management of Primary Glomerular Disease

Hypertensive encephalopathy, heart failure, and pulmonary edema

w/o treatment, ESKD develops within weeks or months

Chronic Glomerulonephritis

Chronic Glomerulonephritis- Pathophysiology

Kidneys reduced in size, glomeruli and tubules are scarred and branches of renal artery is thickened 

Can progress to stage 5 CKD

Manifestations of Chronic Glomerulonephritis

Some may have no symptoms 

May be discovered w/hypertension or elevated BUN and serum creatinine lvls or proteinuria 

Yellow-gray pigmentation of skin and peripheral edema may appear

Assessment/Diagnostic Findings of Chronic Glomerulonephritis

Urinary casts form 

Anemia secondary to decrease erythropoises 

Decreased serum calcium 

Hyperkalemia, metabolic acidosis, impaired nerve conduction, mental status changes

CXR may show cardiac enlargement

Management of Chronic Glomerulonephritis

Reduce BP, sodium/fluid restriction, ACE inhibitors or angiotensin receptor blockers (ARBs)

Monitor weight, I&Os

Nephrotic Syndrome

Increased glomerular permeability leading to massive proteinuria (over 3.5 g/d)

The liver increases albumin production but cannot compensate for the massive daily loss

Key Findings of Nephrotic Syndrome

Hypoalbuminemia, diffuse edema, high serum cholesterol, and hyperlipidemia

Complications of Nephrotic Syndrome

A hypercoagulable state increases the risk of deep venous thrombosis (DVT) and pulmonary embolism

Polycystic Kidney Disease

genetic disorder where fluid-filled cysts destroy nephrons and enlarge the kidneys

Symptoms of Polycystic Kidney Disease

Hematuria, hypertension, renal calculi, and abdominal fullness or flank pain

Management of Polycystic Kidney Disease

There is no definitive cure.

Tolvaptan: Slows the decline of kidney function.

Supportive: BP control, pain management, and eventually KRT. polyuria is common SE and liver damage may be rare SE

Kidney Cancer Renal Cell Carcinoma

Accounts for 90% of kidney cancers

Clear cell is the most common type

Silent Tumor of Kidney Cancer

Many tumors produced no symptoms and are found incidentally

Staging of Kidney Cancer

Stage is based on tumor, node, metastasis including tumor size lymph node involvement, and distant metastasis

The Triad of Kidney Cancer

Only 10% of pts

Painless hematuria, pain in flank, a palpable mass

Risk Factors of Kidney Cancer

Tobacco use is significant

Higher incidence in men

High BMI

64 yrs +, Native American, Black, Alaska Native

Management of Kidney Cancer- Surgical Options

includes radical nephrectomy and partial nephrectomy

Radical Nephrectomy

Removal of kidney, adrenal gland, fat, and lymph nodes.

Used if tumor has spread to inferior vena cava

Partial Nephrectomy

Preferred for smaller tumors to preserve renal function

Preferred surgery for local disease and those w/CKD risk factors

Management of Kidney Cancer- Pharmacologic Therapy

Standard chemotherapy is generally not effective.

Immunotherapy: Checkpoint inhibitors and antiangiogenic agents are standard for clear cell carcinoma

Management of Kidney Cancer- Renal Artery Embolization

Used for large tumors to impede blood supply before surgery

Management of Kidney Cancer- Minimally Invasive Technologies

Radiofrequency, ablation, cryoablation, or microwave ablation performed by urologists or interventional radiologists

Used for small localized renal tumors, poor surgical candidates, or to preserve renal function

Acute Kidney Injury (AKI) Overview

Definition: Rapid, often reversible loss of kidney function

Can be on top of chronic problems

Diagnostic Criteria for AKI

Serum creatinine increases 0.3 mg/dL within 48 hours.

Urine output of less than 0.5 mL/kg/h for more than 6 hours

AKI Pathophysiology- Causes: Blood Flow and Obstruction

Hypovolemia

Hypotension

Septic shock and heart failure

Urinary Tract obstructions: tumor, blood clots, stones

AKI Pathophysiology- Systemic Disturbances

Fluid, electrolyte, and acid-base imbalances(High urea, creatinine, excess fluid, acid ions)

Metabolic acidosis

Early ID of AKI

Potential reversal, reduced BUN/creatinine, improved urine output (oliguria resolved)

Delayed Treatment of AKI

permanent kidney damage

Recovery Factors and CKD Risk

Pts w/preexisting CKD risk factors → decreased chance of full recovery

AKI as potential risk factor → future development of CKD

AKI Prerenal Injury-

includes: hypoperfusion

decreased intravascular volume

decreased cardiac output

vasodilation

obstruction

potentially reversible if identified and treated before permanent kidney damage occurs

If it persists, it can lead to intrarenal damage

AKI Prerenal Injury-Decreased Intravascular Volume

Common causes/risk factors

GI losses (vomiting, diarrhea, nasogastric suction), hemorrhage, and kidney losses from diuretics or osmotic diuresis

AKI Prerenal Injury- Decreased Cardiac Output

Common causes/risk factors

Arrhythmias, cardiogenic shock, HF and MI

AKI Prerenal Injury- Vasodilation

Common causes/risk factors

Sepsis, anaphylaxis, and antihypertensive or other meds causing vasodilation

AKI Prerenal Injury- Obstruction

Common causes/risk factors

Renal artery or vein thrombosis, stenosis, emboli, or trauma

AKI Intrarenal Injury

includes:

prolonged renal ischemia

nephrotoxic agents

infectious processes

AKI Intrarenal Injury- Prolonged Renal Ischemia

Common causes/risk factors

Hemoglobinuria (transfusion reaction), pigment nephropathy (blood cell breakdown), and rhambomyolysis/myoglobinuria (muscle trauma, burns)

AKI Intrarenal Injury- Nephrotoxic Agents

Common causes/risk factors

Aminoglycoside antibiotics, chemo agents, NSAIDs, contrast agents, heavy metals (lead, mercury), illicit drugs, and solvents

AKI Intrarenal Injury- Infectious Processes

Common causes/risk factors 

Acute glomerulonephritis and acute pyelonephritis

AKI Postrenal Injury

includes:

obstruction

Urinary Tract Obstruction

potentially reversible if identified and treated before permanent kidney damage occurs

If it persists, it can lead to intrarenal damage

AKI Postrenal Injury- Urinary Tract Obstruction

Common causes/risk factors

Benign prostatic hyperplasia (BPH), blood clots, calculi (stones), strictures, and tumors

Management of AKI- Fluid Status and Monitoring

Nurses must perform accurate daily weights and meticulous I&O records. Physical indicators like edema, jugular venous distention (JVD), and alterations in heart/breath sounds must be assessed

Management of AKI- Electrolyte Balance

Hyperkalemia is the most immediate life-threatening imbalance; all sources of potassium (dietary and medication) must be screened

Management of AKI- Reducing Metabolic Rate

Fever and infection increase the metabolic rate and catabolism; nurses must provide prompt treatment for these conditions to protect kidney function

Management of AKI-Pulmonary and Infection Prevention

Assistance with turning, coughing, and deep breathing prevents atelectasis. Asepsis is essential with invasive lines, and indwelling catheters are avoided when possible to reduce UTI risk

Management of AKI- Skin Care

Because the skin may be dry or susceptible to breakdown from edema and toxins, nurses provide cool water baths, frequent turning, and fragrance-free moisturizing

Management of AKI- Psychosocial Support

Continued assessment of the psychological needs and concerns of the patient and family is essential during the recovery period

End Stage Kidney Disease (ESKD)

5th and final stage of Chronic Kidney Disease (CKD) characterized by kidney damage requiring permanent Kidney Replacement Therapy (KRT)

ESKD Treatment- Hemodialysis (HD)

Most common start: 83.3% beginning with in center HD

Filters blood outside the body using a dialyzer and machine

ESKD Treatment- Peritoneal Dialysis (PD)

Utilized 12.7% of new pts

Cleans the blood using the lining of the abd (peritoneum)

Often done at home

ESKD Treatment- Transplantation

3.1% receive preemptive transplant (transplant from living donor before dialysis is ever initiated)

Placing healthy donor kidney into pt’s body

American Kidney Health Initiative

A 2019 Executive Order aims to move more patients toward home dialysis (PD and home HD) and increase transplant rates

Gero Considerations

Older adults are the fastest-growing group with CKD. In this population, symptoms of kidney failure may be masked by other comorbidities like heart failure or dementia

ESKD Pathophysiology- Uremia

Accumulation of protein metabolism waste products (normally excreted)

Confusion, fatigue, pruritus, dyspnea

ESKD Diagnostic Markers

GFR: decreased due to nonfunctioning glomeruli

Creatinine and BUN: serum lvls increase; creatinine is more sensitive indicator of renal function than BUN

ESKD Pathophysiology- Fluid and Electrolyte Shift

Renin-Angiotensin Aldosterone Axis Activation→ sodium/water retention → edema → HF → hypertension

ESKD Clinical Manifestations

CVD: predominant cause of death in ESKD pts

Peripheral neuropathy: Common in diabetic pts, Restless leg syndrome and burning feet

Maintaining Fluid Status in ESKD

Nurses must monitor daily weights and meticulous I&O records.

Identify potential sources of imbalance (e.g., IV medications should be given in the smallest volume possible)

Complications of ESKD

includes:

anemia, hyperkalemia, pericarditis, acidosis, calcium and phosphorus imbalance

Complications of ESKD- Anemia

Decreased production → Erythropoietin hormone (EPO) → low production in bone marrow → low RBC count

Complications of ESKD- Hyperkalemia

Decreased excretion → potassium accumulation leads to life threatening imbalance due to decreased excretion and catabolism → cardiac arrhythmias, life threatening