Week 12: GU and Kidney Disease

Normal urine output (mL/kg/hr)

0.5 mL/kg/hr (0.5 cc)

• 30 cc/hr

Oliguria urine output volume

< 0.5 cc’s per hour

< 400 mL/day

Anuria urine output volume

< 50-100 mL per day

Kidney function 

• maintenance of fluid balance, electrolyte balance, and acid-base balance

• BP regulation 

• Excretion of waste product

• Regulate RBC production, vitamin D activation, and secretion of prostaglandins

How do the kidneys regulate BP?

renin

Acute Kidney Injury (AKI)

rapid decrease in renal function d/t damage to the kidneys that can result in potentially life-treatening metabolic complications and fluid and electrolyte imbalances

Acute kidney injury (AKI) 

• Onset?

• Reversible?

• Length?

• % of nephrons involved?

• Rapid onset

• Often reversible 

• Lasts 2-4 weeks 

• 50% nephron involvement 

End-stage kidney disease (ESKD)

• Onset?

• Reversible?

• % nephron involvment

• Prognosis?

• Gradual onset 

• Permanent 

• 90-95% nephron involvement

• Poor prognosis — chronic condition that requires a lot of medical treatment 

Stage 1 AKI

• Creatinine

• Urine output

• Creatinine: 1.5-1.9 x baseline or an increase > 0.3 mg/dL

• Urine output: : < 0.5 mL/kg/hr for 6–12 hr

Stage 2 AKI

• Creatinine

• Urine output

• Creatinine: 2.0-2.9 x baseline 

• Urine output: < 0.5 mL/kg/hr for ≥ 12 hr

Stage 3 AKI

• Creatinine

• Urine output

• Creatinine: 3 × baseline or ≥ 4.0 mg/dL OR Initiation of renal replacement therapy

• Urine Output: < 0.3 mL/kg/hr for ≥ 24 hr OR anuria ≥ 12 hr

Intrarenal AKI

damage to the structure within the kidney

Prerenal AKI

reduced blood flow to the kidneys

Postrenal AKI

obstruction of urine outflow for the kidney

Prerenal AKI causes

• Volume depletion (ie hypovolemia)

• Impaired cardiac output: Shock, HF, MI

• Renal artery stenosis or occlusions (thrombi)

• Systemic vasodilation: Sepsis, anaphylaxis, certain meds

• NSAIDs a reduce renal blood flow; dilate the afferent arteriole

• ◦ACE inhibitors/ARBs impair auto-regulation; dilate the efferent arteriole

How is prerenal AKI corrected?

by correcting hypovolemia, increasing BP and cardiac output, and improving renal blood flow

• restore BF ASAP, or else AKI will become intrarenal AKI!!!

Intrarenal (AKI) causes (3)

• Glomerular obstruction and inflammation

• Immune mediated microvascular diseases

• Nephrotoxic agents: Contrast dye, Aminoglycosides, Penicillins, NSAIDS

What kidney tissues may be damaged that are r/t intrarenal AKI?

• Glomeruli

• Tubules

• Interstitium 

Acute Tubular Necrosis

damage to renal tubules = the major pathologic mechanism

• Injured cells slough off into the tubular lumen and forms occlusions, leaving to increased intertubular pressure and reduced GFR

Ischemic Acute Tubular Necrosis (ATN)

• Prolonged prerenal states

• tubular cells die from lack of O2 – which is how prerenal turns into intrarenal

Causes of Ischemic ATN

• Shock

• sepsis

• prolonged hypotension

• hypovolemia

How can NSAIDs cause prerenal AKI?

• Inhibit prostaglandins, which normally dilate the afferent arteriole

• Without prostaglandins → the afferent arteriole constricts → ↓ renal blood flow

Acute Interstitial Nephritis (AIN)

NSAIDs are a classic cause of drug-induced allergic interstitial nephritis, which is another form of intrarenal AKI

How can NSAIDs cause intrarenal AKI?

If prerenal hypoperfusion is prolonged because of NSAID-induced vasoconstriction, the kidney becomes ischemic → ischemic ATN

Postrenal AKI obstruction causes

• Urinary calculi

• Tumors

• Benign prostatic hyperplasia (BPH)

• Strictures

• Blood clots

Stage 1 of AKI: Onset or initiating phase

• Begins hours to days after triggering event

• May begin to see increase in BUN and creatinine

Stage 2 of AKI: Olliguric (anuric) phase 

• Urine output < 400 ml/day

• Increase in BUN and creatinine levels

• Electrolyte disturbances: K⁺, PO₄^-, Mg⁺,Ca⁺

• Metabolic acidosis: HCO₃^-

• Fluid overload

• Uremic symptoms

• Duration usually 1-2 weeks but may be longer

  • longer oliguria = worse prognosis 

Stage 3 AKI: Diuretic phase

Gradual increase in urine output to > 400 ml/day; increased diuresis (up to 10 L/day)

• Start to see electrolyte losses/changes bc of how much they are urinating

Stage 3 AKI characteristics

• BUN and creatinine stabilize

• Renal function remains impaired

• Uremic symptoms persist

• Potential dehydration

• Potential hypokalemia

• Duration usually 1-2 weeks

Stage 4 AKI: Recovery Phase

• GFR

return of GFR to 70-80% of normal

Stage 4 AKI characteristics

• Decreased edema

• Normalization of fluid and electrolyte balance

• Decreased energy level and stamina, but is significantly improved

AKI diagnostic studies

• X-rays

• Renal ultrasound

• Nuclear imaging

• CT scan

• MRI

• Cystoscopy and retrograde pyelography

• Renal biopsy

What should be held when doing AKI diagnostic studies?

Contrast dye because the kidneys can’t filter it out well

What drug should be held when a patient is getting an AKI diagnostic study?

Metformin and other nephrotoxic drugs

AKI management

• Identify and correct the underlying cause

• Fluid therapy — maintain fluid balance and avoid fluid excess

• Nutritional therapy

• Renal replacement therapy

Assessment for fluid therapy

• Strict I&O

• Vital signs

• Daily weights — must be measured same way each time

Fluid therapy for prerenal AKI

fluid bolus for hypovolemia and hypotension

Fluid therapy for oliguric phase

fluid restriction

Fluid therapy for diuretic phase

• patient may loose up to 10 L/day

• may need to increase fluids to prevent dehydration d/t diuresis

Hyperkalemia management

• Monitor EKG

• Eliminate K+ intake

• Increase K+ output

• Reverse cardiac cell membrane effects of increased K+ by administering IV Ca2+ gluconate

• Dialysis in patients with persistent hyperkalemia

Nutrition and fluid therapy in AKI

• Calories, carbs, and protein

• Electrolytes

• Fluids

• High calorie and carb diet

• Protein varies with treatment

• Electrolyte restriction as indicated

• Fluid needs vary by phase

• Nutritional consult

Indications for renal replacement therapy in AKI (4)

• fluid volume overload

• persistent hyperkalemia

• metabolic acidosis

• uremia

Uremia

increased nitrogenous wastes in the blood d/t the kidneys being unable to excrete it because of AKI

Uremia symptoms

• Metallic taste in mouth

• Anorexia

• N/V

• Muscle cramps

• Itching

• Dry, flakey skin

• Fatigue/lethargy

• Hiccups

• Edema

• Parenthesias (sensation of pins and needles)

Continuous renal replacement therapy (CRRT) indication

meant for patients who are hemodynamically unstable and cannot tolerate quick fluid shifts and intermittent dialysis

Continuous Venovenous Hemofiltration (CVVH)

uses ultrafiltration to drag solutes across a membrane - no dialysate, requires replacement fluid

CVVH indications

• fluid overload

• septic shock

• multisystem organ failure

Continuous Venovenous Hemodialysis (CVVHD)

uses diffusion to clear toxins via concentration gradient, less aggressive than CVVH

CVVHD indications

• metabolic derangements like acidosis or hyperkalemia

• rising BUN/Cr

Continuous Venovenous Hemodiafiltration (CVVHDF)

combines diffusion and convection, provides broadest solute clearance

CVVHDF indications

• severe metabolic instability

• septic shock

• multisystem ICU patients

Slow Continuous Ultrafiltration (SCUF) and use

pure fluid removal only, minimal solute clearance

• used for volume overload

Temporary dialysis access location

• Subclavian vein

• Internal jugular vein

• Femoral vein (last choice)

Most important AKI nursing considerations

• Strict I&O, daily weights (most accurate fluid indicator)

• Monitor urine output hourly (oliguria < 0.5 mL/kg/hr)

• Avoid nephrotoxic agents (NSAIDs, contrast, aminoglycosides)

• Manage hemodynamics (optimize perfusion, MAP > 65)

  • AVOID HYPOTENSION***** — especially prolonged hypotension

Chronic Kidney Disease (CKD)

A progressive and irreversible loss of kidney function where they can't effectively remove waste and extra fluid from the body

• Present for >3 months

Most common risk factors for CKD

• Diabetes — most common

• Hypertension — 2nd most common

• CAD

• Obesity

• Recurrent AKI episodes

• Nephrotoxicity medications

What 2 ways can CKD be diagnosed? (via labs)

Decreased GFR

• < 60 mL/min/1.73 m²

OR

Evidence of kidney damage, regardless of GFR:

• Albuminuria ≥ 30 mg/day

• Structural abnormalities

• History of kidney transplant

• Electrolyte abnormalities d/t tubular disorders

What disease is at high risk for developing d/t CKD?

Cardiovascular disease

Complications associated with CKD (3)

• Anemia

• Bone/mineral disorders

• Fluid/electrolyte imbalances

Early stages of CKD are often _____

asymptomatic

Normal GFR (mL/min)

> 90 mL/min

CKD stage 1

• GFR

• Kidney damage?

• Symptoms

• Albuminuria

• Normal GFR

• Evidence of kidney damage with normal function

• Usually asymptomatic

• Albuminuria may be present

CKD stage 2

• GFR

• Kidney damage?

• Albuminuria

• Urine changes

• Mild decrease in GFR = 60-89 mL/min

• Evidence of kidney damage — nephron damage with normal labs

• Albuminuria

• Subtle urine changes — increase urine output with dilute urine

CKD stage 2: Why is there an increase in urine output and dilute urine?

Kidneys lose ability to concentrate urine and get the excess electrolytes out

• which is why people will get hyperkalemia

CKD stage 3A

Mild-moderate decrease in GFR = 45-59 mL/min

• **Turning point in diagnosis — progression accelerates

CKD stage 3B

• GFR

• Nephron function

• Kidney filtration

• Fluids, proteins, and electrolytes?

• Moderate-severe decrease in GFR = 30-44 mL/min

• Remaining nephrons do not function properly

• Kidney cannot manage metabolic wastes, fluid balance, or electrolyte balance

• Restriction of fluids, proteins, and electrolytes instituted

CKD stage 4

• GFR

• Restrictions

• Complications of CKD

• Severe decrease in GFR = 15-29 mL/min

• Unable to manage metabolic wastes, fluid balance, or electrolyte balance

• Restrictions of fluids, proteins, and electrolytes required

• Complications of CDK (CV issues, anemia, HTN, bone disease) likely

CKD stage 5: End Stage Kidney Disease (ESKD)/Chronic RF

• GFR

• What builds up in the blood?

• What is particularly imbalanced?

• GFR < 15 mL/min Remaining

• Severe uremia: excessive amounts of urea and creatinine buildup in blood

• Uncontrolled fluid and electrolyte imbalances

CKD stage 5 requirements for survival

dialysis and/kidney transplant

Albuminuria and relationship to CKD

a measurement of how much protein is leaking into the urine

• More albumin = more kidney damage and faster CKD progression

Body systems affected by End Stage Kidney Disease (ESKD)

Systemic disease!

• Metabolic

• CV

• Respiratory

• Hematologic

• GI

• GU

• Neurologic

• Musculoskeletal

• Integumentary

CKD complications: Cardiovascular

• HTN — bc patient’s kidneys can’t excrete Na+ and H2O very well

• HF/hypervolemia

• Accelerated alerosclerosis

• Pericarditis

CKD complications: Hemotalogic

• Anemia — d/t decrease EPO

• Bleeding risk — d/t platelet dysfunction

CKD complications: Electrolyte and Acid-Base

• Hyperkalemia

• Metabolic acidosis

• Hyperphosphatemia

• Hypocalcemia — contributes to bone disease

CKD complications: Endocrine/Bone d/t hypocalcemia

• Secondary hyperparathyroidism

• CKD-Mineral Bone Disorder

• Renal osterodystrophy

CKD complications: Neurologic

• Peripheral neuropathy

• Cognitive changes

• Restless leg syndrome

• Uremic encephalopathy

CKD complications: GI

• N/V

• Anorexia/weight loss

• Uremic factor — ammonia breath

CKD complications: Dermatologic

• Pruritus (itchy skin)

• Uremic frost — crystallized urea on the skin bc there is so much urea in the body (“overflow”)

CKD complications: Immune System

impaired immunity = increased infection risk

CKD complications: Fluid balance

• Edema

• Pulmonary congestion

• Difficulty diluting or concentrating urine

Nutritional therapy for ESKD

• Calories and carbs

• Protein recommendations

• Na+, K+ and P

• High calorie and high carb diet

• Protein recommendations — before dialysis = restrict protein, on dialysis = replace protein

• Restrict Na+, K+ and P

Fluid therapy in ESKD: Diuretics purpose

symptom control and fluid management

Loop diuretics ESKD contraindications

• Anuria!

  • because they work by blocking sodium reabsorption in the kidneys

• Severe dehydration

• Hypovolemia

• Severe electrolyte abnormalities

Hemodialysis

Life-sustaining treatment that uses an artificial kidney (dialyzer) to filter waste, extra fluid, and chemicals from the blood when kidneys fail, essentially acting as an external kidney to clean the blood and manage blood pressure

Small solutes that hemodialysis removes via diffusion (3) (hint — they are the most concerning ones for body function!)

• Urea

• Creatinine

• K+

*Hemodialysis indications (AEIOU)

• Acid-base imbalance

• Electrolyte abnormalities (esp K+)

• Intoxication (certain toxins)

• Overload (fluid)

• Uremia

Dialyzer

2 compartments separated by a semipermeable membrane in which blood and dialysate flow in opposite directions, allowing for waste products and excess fluid to be removed from the blood

AV fistula vs AV graft

• AV fistula connects an artery directly to a vein — 1st choice bc less invasive

• AV graft connects an artery to a vein using a synthetic tube — external

AV fistula precautions

• Do not take BP in extremity

• No venipunctures or IV access allowed

• Assessment includes palpating for thrill and auscultating bruit — turbulent BF bc the connection of an artery and vein

• Assess distal pulses

• Assess for infection and bleeding

• Patient instruction

  • No heavy lifting or activity that would compress access

  • Do not sleep on access arm

Hemodialysis complications

• ***Hypotension

• Hypovolemia

• Dialysis disequilibrium

• Muscle cramps

• Hemmorage

• Air embolus

• Hemodynamic changes

• Cardiac dysrhythmias (d/t fluid and electrolyte shifts)

• Infectious disease

Hemodialysis: Assessment at vascular access

• Bruit and thrill — we WANT this because the hemodialysis is making the vessels abnormal

• No BP/IV/lab draws on fistula arm

Intradialytic hypotension

hypotension that occurs during dialysis

• most common complication of dialysis

Peritoneum

the serous membrane lining the cavity of the abdomen and covering the abdominal organs

Peritoneal Dialysis

exchange of wastes, fluids, and electrolytes via peritoneum by placing a catheter into the peritoneal cavity

Additives to peritoneal dialysis

• Heparin — prevent clots blocking catheter

• K+ — prevent hypokalemia

• Antibiotics

Continuous Ambulatory Peritoneal Dialysis (CAPD)

infused 4-5 exchanges in 24 hours, dwells for 4-6 hours

Continuous Cyclic Peritoneal Dialysis

over 8-10 hours at night, allows patient to be dialysis free during the day

Peritonitis

Peritoneum becomes inflamed d/t connection site contamination

• **must use sterile technique for prevention

Peritonitis symptoms

• Fever

• Abdominal tenderness + pain

• Malaise

• N/V

• **Cloudy effluent

Peritoneal Dialysis nursing care

• Use aseptic technique for dressing changes

• Maintain accurate I & O and obtain dry weight when empty

• Check BG and be aware of sneaky calorie load of dialysate — high glucose content in dialysate = increased “indirect” caloric intake

• Warm dialysate to body temp (reduce discomfort and improve solute transfer)