CCRN (~6%)

 Acute kidney injury

 Acute renal failure

 Acute tubular necrosis

(ATN)

 Chronic kidney disease

 Incontinence

 Infections

 Life threatening electrolyte

imbalances

7 – 9 questions

CCRN Testable Nursing Actions

 Recognize normal & abnormal physical assessment findings

 Identify & monitor normal & abnormal diagnostic test results

 Manage patients receiving renal medications & monitor

response

 Recognize indications for & manage patients requiring renal

therapeutic intervention (e.g., CRRT, peritoneal dialysis)

 Monitor patients & follow protocols for:

•  renal surgery
•  pre-, intra-, and post-procedure (e.g., renal biopsy,
• ultrasound)

 Recognize signs & symptoms of renal emergencies, initiate

interventions, & seek assistance as needed

Review of the renal system

Approximately

20%

of cardiac output

goes to the kidneys

Renal arteries

branch

directly off aorta

The kidney functions

to cleanse & detoxify

blood

The Kidneys

Main functions:

Filtration

Reabsorption

Secretion

Acid/base balance

BP regulation

Erythropoietin

The Nephron

 Glomerulus

 Network of capillaries

 Filters blood

 Proximal Convoluted Tubule

 Reabsorbs H2O, sodium, amino

acids & glucose

 Loop of Henle

 Reabsorbs Na, water &

concentrates urine

 Distal Convoluted Tubule

 Regulates pH, K+, Na+ & Ca

 Collecting Duct

 Collects urine from the nephrons

Fluid balance is regulated by:

 Thirst

 ADH

 Aldosterone**

•  Elevated K+ triggers release of aldosterone

 ANP

•  Overstretch of the atria

 Renin Angiotensin

Aldosterone System

(RAAS)

Urine

 Normal UOP

 1500 mL/day or 0.5 mL/kg/hr

 Anuria

 0 – 100 mL/day

 Oliguria

 100 – 400 mL/day

 Polyuria

 > 2500 mL/day

Are we measuring the same?

Typical order – Call < 30 cc/hr

0.5 ml/kg/hr

Acute Kidney Injury (AKI)

< 400 mL/day

 a.k.a. Acute renal failure (ARF)

 Incidence: ~18% in hospitalized patients

 Abrupt decline in glomerular filtration rate (GFR)

 Results in retention of metabolic waste

•  Protein catabolism (azotemia)
•  Electrolyte & acid-base imbalance
•  Volume imbalance

Causes:

 Low perfusion, medications, parenchymal disease

 Reversible if prompt treatment is received

Risk factors for developing AKI

 Elderly

 Female > male

 Heart failure

 Baseline renal function

 Elevated BMI (>32)

 COPD

 Liver disease

 Sepsis

 GI Bleeding

 Burns

 Multi-System Organ

Failure

 Hypotension

 Trauma injury

 Rhabdomyolysis

 Contrast

RIFLE Criteria/Classification

 BUN & creatinine

•  Up to 12 hr lag time

 Normal BUN/Creat

ratio – 10:1

 GFR*

 Proteinuria

 Casts

•  Tubular cell death

 Urine lytes

 Urine glucose

 What does the future

hold?

 Biomarkers?

 Insulin-like growth

factor-binding protein

 TIMP-2

•  Tissue inhibitor of metalloproteinases-2

Glomerular Filtration Rate

 Estimated by creatinine clearance

 The measurement of how much filtrate is made by the

kidney (ml/min)

 ~ 80 – 120 ml/min

 Males slightly higher

 Isolated plasma creatinine is not a sensitive marker for

GFR in early stages of kidney injury

Estimating Equations

A. Cockcroft-Gault

GFR = (140 - age) x (weight) / (sCr x 72) (x 0.85 for ♀)

B. MDRD

GFR = 186 x (serum creatinine in mg/dL)-1.154 x (Age in years)-0.203

(x0.742 if female) (x1.210 if African-American)

3 Categories of AKI (location of cause)

 Postrenal

•  Injury caused by disruption
• of urine flow
•  Think obstruction!
•  Examples: urethral obstruction, prostatic disease, infection,
• neurogenic problems
•  BUN/creat 10:1

3 Categories of AKI (location of cause)

 Prerenal

 Injury occurs before

blood reaches the kidney

 Results in hypoperfusion

 Kidney structure & function is

preserved

 Examples: Sepsis, heart

failure, trauma, severe

hypovolemia

 BUN/Creat 25:1

 Urine Na < 10 mEq/L

3 Categories of AKI (location of cause)

 Acute Tubular Necrosis

(ATN)

 May also be referred to as

“intrinsic”, “infra-renal”

kidney injury

 Injury occurs at the nephrons

 Renal failure requiring renal

replacement therapy

 Examples: Hypotension,

glomerulonephritis, DM,

rhabdomyolysis, nephrotoxic

meds, shock

 BUN/Creat 10:1

 Urine Na > 40 meq/L

 Ischemic ATN

 Irregular damage along tubular membranes

 Tubular cell damage & cast formation

 Poor – no perfusion to kidneys

 Recovery long (> 8 days)

 Toxic ATN

 Caused by drugs or bacteria

•  Aminoglycosides, antivirals

 Uniform, wide spread damage

 Recovery more rapid (< 8 days)

 ***Reversible!

Phases of ATN

 Initiation/Onset Phase

 Insult to injury

 Lasts hours to days

 GFR is decreased d/t

decreased flow

 50% are oliguric, 50% are

non-oliguric with UOP > 600

mL/8 hrs

 Oliguric Phase

 Lasts 7 – 16 days

 Inability to excrete fluids &

metabolic wastes

 Often requires total renal

support

 Mortality: 25% with nonoliguria,

66% with oliguria

 Diuretic Phase

 Lasts 7 – 14 days

 Increase in GFR & polyuria

 2 – 4 L/day

 HD may cover polyuria

 Kidneys can often clear volume,

but not solute

 Recovery Phase

 GFR returns to < 80% of within

1 – 2 years

Contrast induced nephropathy

 At risk:

•  Diabetics, HTN
•  Pre-existing renal insufficiency
•  Dehydrated
•  10% of all hospital acquired renal insufficiency

 ***HYDRATION!!!***

 Sodium bicarbonate – IV 1 hour before & 6 hours after

 N-Acetylcysteine for prevention

•  600 mg PO day before & day of (4 doses)
•  Prevents toxicity to renal tubules

Overall Recovery of ATN

 Of those who survive,

 ~ 62% will recover renal function

 33% will have renal insufficiency

 5% will require long term dialysis

Indications for Dialysis

 A: Acid/base imbalance

 E: Electrolyte imbalance (hyperkalemia)

 I: Intoxications (ODs/toxins)

 O: Overload (fluid)

 U: Uremic symptoms

Laboratory Findings

 BUN > 100

 Creatinine > 10

 Cr climbing ≥ 1

point/day

 Metabolic acidosis

 Anemia

 Electrolyte imbalances

 Increased K+/Phos

 Decreased Ca, HCO3

 Abnormal urine lytes

Uremic Syndrome

 Neurologic

 Lethargy, fatigue, seizures,

coma

 Cardiovascular

 ECG changes

(d/t hyperkalemia)

 Signs of fluid overload;

tachycardia, S3

 Hematologic

 Anemia

 Pulmonary

 Crackles, pulmonary

edema

 Edema/SOB/effusions

 Pleuritis from uremia

 GI

 Decreased appetite

 N/V

 Ascites – fluid overload

General Treatment Goals for AKI

 Hemodynamic stability

 Improve renal perfusion

 Correct chemistry

(Lytes/BUN/Creat)

abnormalities

 Electrolyte imbalances

•  During therapy
•  After therapy

 Adequate

hydration/careful use of

diuretics

•  Accurate, meticulous daily weights

 Aggressive dialysis

 Monitor drug levels

 Monitor coags

 *Alter medication

schedules if needed

 Minimize exposure to

nephrotoxins

 Prevent infection

 Maintain nutritional state

Chronic Renal Failure

 CRF is a slow, progressive deterioration of renal

function

 Diminished renal reserve puts patients at a higher

risk for development

Lab findings:

 Anemia*

 ↑BUN/creat/PO4

 ↓Ca, HCO3, Protein

Risk Factors for CRF

 Diabetes*

 Hypertension*

 Autoimmune diseases

 Systemic infection

 Urinary stones or

lower urinary tract

obstructions

 Prolong exposure to

nephrotoxic drugs

*Responsible for 70% of CRF cases

 Increasing in age

 Race or ethnic

background

 Exposure to chemicals

or environmental toxins

 Family history

Classification of Function

 Diminished renal reserve

•  50% nephron loss
•  Creatinine levels elevated
•  Otherwise symptom free

 Renal insufficiency

•  75% nephron loss
•  Clinical evidence of impairment
•  Requires medication

 ESRD – 90% nephron loss

 Stage 1: Damage w/increased GFR

 (> 90 ml/min/1.73 m2)

 Stage 2: Mild reduction GFR

 (60 – 89 ml/min/1.73 m2)

 Stage 3: Moderate reduction in GFR

 (30 – 59 ml/min/1.73 m2)

 Stage 4: Severe reduction in GFR

 (15 – 29 ml/min/1.73 m2)

 Stage 5: Kidney Failure

 (< 15 ml/min/1.73 m2)

Dialysis Modes

 Hemodialysis

•  Intermittent
•  Slow Low Efficiency

Dialysis (SLED)

 Continuous Renal

Replacement Therapy

 Slow, continuous

 Used in patients with

hemodynamic instability

 CRRT

•  Slow Continuous Ultrafiltration (SCUF)
•  Continuous Venovenous hemofiltration (CVVH)
•  with hemodialysis (CVVHD)
•  with hemodiafiltration (CVVHDF)
•  Continuous arteriovenous (CAVH/CAVHD/F)

Principles of Dialysis

 Two compartments (blood & filtrate) separated by

a semi-permeable membrane

 Pressure gradients are created

 Water, toxins, electrolytes & drugs can cross the

membrane

 Goal is to reach equilibrium on each side of the

membrane

Peritoneal Dialysis

 Soft catheter inserted percutaneously into

abdominal cavity

 Abdominal mesenteric capillary bed is utilized as

the SPM

 Glucose based dialysate is used

 (1.5%, 2.5%, 4.25%)

 Usually 2 Liter exchanges q 3 - 4 hrs.

 glucose conc =  fluid removal (via diffusion

gradient)

 Advantages: patient can do, cost effective, no need for

anticoagulation or vascular access

 Soft catheter inserted percutaneously into

abdominal cavity

 Abdominal mesenteric capillary bed is utilized as

the SPM

 Glucose based dialysate is used

 (1.5%, 2.5%, 4.25%)

 Usually 2 Liter exchanges q 3 - 4 hrs.

 glucose conc =  fluid removal (via diffusion

gradient)

 Advantages: patient can do, cost effective, no need for

anticoagulation or vascular access

Complications of PD

 Peritonitis

 Hyperglycemia

 Diaphragmatic pressure/resp. compromise

 Pleural effusion

 Visceral herniation or perforation

 Contraindications: Recent abdominal surgery,

abdominal adhesions, need for emergent dialysis

Hemodialysis

 Artificial kidney (hemofilter) with a synthetic

membrane

 Dialysate is bicarbonate & sodium based with

electrolytes

 Short term access

•  Double lumen catheter

 Long term access

•  AV fistula/shunt

Hemodialysis Complications

 Hypotension

 Angina

 Dysrhythmias

 Fever / pyrogenic reaction

 Coagulopathy/Thrombocytopenia

 Disequilibrium Syndrome (post-treatment cerebral

edema)

 Exsanguination

 Air embolus

Air Embolus

Venous signs:

 Shortness of breath

 Chest pain

 Acute right heart failure

(if obstructs flow from right

heart to the lungs)

Treatment:

 Lay on left side,

Trendelenburg position

 Hyperbaric with 100% FiO2

(accelerates the removal of

nitrogen)

Arterial signs:

 Change in LOC

 Decreased arterial

flow/perfusion

 2 ml fatal in artery

 0.5 ml fatal in coronary

artery

CRRT

 Must have sufficient MAP or AV gradient

 AV Gradient: MAP – CVP (> 60 mmHg)

 Indications: fluid removal refractory to diuretics

 Complications:

•  Hypotension

•  Bleeding (anticoagulation)

•  Hypothermia

•  Filter/circuit clotting

•  Membrane rupture

Renal Terms

 Azotemia

•  Acute rise in blood urea nitrogen (BUN)

 Anuria

•  Complete suppression of urine output

 Oliguria

•  Urine output < 400 mL/day

 Glomerular filtration rate (GFR)

•  The amount of glomerular filtrate formed in the kidneys each minute

•  It is used to evaluate the kidneys’ ability to remove waste products from

the body

 Urine casts

•  Cylindrical structures formed by the kidneys in certain disease states

•  Released from the distal tubule & collecting ducts

•  Detected on urinalysis

Laboratory norms

Laboratory norms

Laboratory norms

Renal Laboratory norms

Name that renal injury…

Name that renal injury…

(ie. Prerenal, ATN (infranrenal), or postrenal:

 Creatinine of 5.6 caused from a UTI in a patient with an

enlarged prostate

•  Postrenal

 BUN 80/Creatinine10, Urine Na 56, one week after a

prolonged cardiac arrest

•  ATN - Infrarenal (intrinsic)

 BUN 50/Creatinine 2.2, Urine Na 9, 12 hours after a 4 hour

period of hypotension

•  Prerenal

Name that renal injury…

 3 weeks after hypotension post surgery, urine output of 1

L/day with casts present, urine specific gravity of 1.010 &

urine Na of 60

•  ATN - Infrarenal (intrinsic) renal failure

 58 yo with prostate enlargement and unable to urinate for 2

days. Blood is present, urine Na is 25, BUN 30, creat 3.0.

Urinary catheter inserted for a return of 2 liters of urine.

•  Postrenal

 46 yo with cardiogenic shock after an acute anterior wall MI.

On Dopamine & Dobutamine infusions with low cardiac output.

Urine output averages 5 – 10 ml/hr, urine specific gravity is

1.025, Urine Na is 6. Bun 125/creatinine 5

•  Prerenal

Hypernatremia Na+ > 145 mEQ/L

Dehydration

 Increased Hct

 Increased Cl

•  > 106 mEQ/L

 Urine specific gravity

•  > 1.025

 Decreased urine Na

 Increased osmo

Treat Cause

•  Excess administration of NaCl or NaHCO3

•  Hypertonic enteral feedings

•  Comatose patient

•  DKA

•  Burn injury

 Treatment:

•  Free H2O

•  Diuretics

Hyponatremia – Na+ <130, Cl < 98

Excess H2O or Na+ depletion

Water retention

•  Neuro changes,

• headache, confusion,

• coma, death

Dehydration

•  Anxiety, weakness,

• abdominal cramping,

• seizures, hypotension,

• tachycardia, shock

Causes:

•  NG tube suction

•  SIADH

•  Diarrhea

•  Intestinal surgery

Treatment:

•  Slow correction!!!

•  Na+ Phos:

  •  1 – 2 mmol/hr for 1st 3 –

  • 4 hrs

•  Hypertonic saline

•  Na tabs

Potassium 3.5 - 5.0 mEq/L

 90% intracellular, 10% in serum

•  Na/K+ pump = maintains normal cell volume and
• electro-neutrality of the cell membrane

Functions:

 Transmission of nerve impulses

 Intracellular osmolality

 Enzymatic reactions

 Acid-base balance

 Myocardial, skeletal & smooth

muscle contractility

Potassium Regulation

 Kidneys - Primary excretory source

 Intestines (excretion)

 So efficient rarely have hyper states in normal RF

 In the presence of aldosterone, K+ is excreted by

the renal tubules

 K+ and Na+ constantly in

competition

Hypokalemia: < 3.5 mEq/L

 Increased loss

•  GI: Vomiting, NGT suctioning (aggravated by Met Alkalosis)

•  Diarrhea, fistula, ileostomy ( LGI K+ 30 mEq/L)

 Excessive urinary loss

•  Hyperaldosterone states, Thiazide Diuretics, Ampho, Gent,

• cisplatin

 Inadequate intake

•  Anorexia, ETOH, IV (K free)

•  Magnesium depletion

 Intracellular shift

•  Alka-LO-sis 0.1 unit  in pH  K  0.4 mEq/L

•  Insulin

Hypokalemia

Clinical presentation – symptoms < 3.0

 Cardiovascular

• •  Ventricular irritability (PVCs) < 2.8

  •  Ventricular fibrillation

  •  Depressed ST segment

  •  U-wave

  •  Prolonged QT interval

  •  Potentates Digoxin activity

Hypokalemia: Treatment

1. Replace K+

•  Oral supplements or increased dietary intake when

• possible

•  IV

  •  Standard dose 10-20 mEq over 1 hours

  •  Central line administration is best

  •  Monitor IV site – irritant

2. Eliminate or treat conditions that promote K+

shifts (ie. alkalosis)

•  Ensure adequate renal function

Hyperkalemia K+ >5.5 mEq

Causes of hyperkalemia:

 Renal failure (~75% of all cases)

•  Inability of renal tubules to excrete K+

 Acidosis

 Decreased cardiac output

 Elderly taking K+ sparing diuretics

 Severe trauma

 Severe burns

 Infection

 Addison’s Disease

 ↑ Consumption of table salt or antacids

Hyperkalemia Symptoms

 N/V

 Diarrhea

 Tingling skin

 Numbness in hands & feet

 Flaccid paralysis

 Cardiac signs

 Apathy

 Confusion

Cardiovascular

 Tall tented symmetrical T

waves

(K+ >6.5)

 Widened QRS, prolonged

PR, widened P wave (K+

>8.0)

 Decreased

automaticity

(K+ 10-11.0)

 P waves disappear

QRS merges with T to

form sine wave

 Asystole or ventricular

fibrillation

 Decreased strength of

contraction

Hyperkalemia Treatment

Emergency: (Move potassium)

 Regular Insulin

•  Dextrose if normal or low glucose

•  Calcium Chloride (cardio protectant; no effect on K+ levels)

•  NaHCO3

 Nebulized albuterol

•  onset ~15 min., duration ~ 15 - 90 min.

 Dialysis* (Remove potassium)

 Loop diuretics

 Sodium polystyrene sulfonate (Kayexalate)

•  Dose 15 Grams 1- 4 doses/day, 24 hrs to correct

Magnesium 1.5 – 2.5 mEq/L

Functions:

 Neuromuscular transmission

 Cardiac contraction

 Activation of enzymes for cellular metabolism

 Active transport at the cellular level

 Transmission of hereditary info.

Hypomagnesemia <1.3 mEq/L

 Increased excretion

•  NG suctioning, diarrhea, fistulas

•  Diuretic: blocks Na reabsorption

•  Osmotic diuresis

•  Antibiotics & antineoplastics

•  Hypercalcemia

 Decreased intake

 Chronic alcoholism

 Malabsorption

 Acute pancreatitis

Hypomagnesemia symptoms:

CV: Tachycardia, depressed ST segment, prolonged QT

 PACs & PVCs

•  Increased risk for digoxin toxicity

•  Hypotension

•  Coronary artery spasm

 Neuromuscular

•  twitching, paresthesias, cramps, muscle tremors

 CNS: mentation changes, seizures

 Hypokalemia

Hypomagnesemia

 Management:

•  Assess renal function

•  Increase intake

  •  Dietary: diet or PO supplementation

  •  IV 1-2 G MgSO4 over 60 minutes, emergency 1 – 2 minutes

  •  Add to IV or TPN

 Monitor BP & airway

 Monitor neurological status

 Monitor K+ and Ca+

 Serial Magnesium levels

Hypermagnesemia >2.5 mEq/L

 Extremely rare!

 Etiology

•  Decreased excretion – renal failure - most common

•  Acidosis, DKA

 Clinical presentation

•  3-5 mEq/L Peripheral dilation, facial flushing, hypotension

•  4-7 mEq/L Drowsiness, lethargy

•  Treat

  •  Increase excretion

  •  Fluids & diuretics

Hypocalcemia – Ca++ <8.5

Hypercalcemia: rare (Treatment: IV fluids)

 Hypocalcemia: more common

•  Follow ionized (active) Ca++

•  Normal: 1.1 - 1.35 mmol/L

•  Symptoms:

  •  Diarrhea

  •  Diuretics

  •  Malabsorption

  •  Chronic renal failure

  •  Alkalosis – Ca++ bound to albumin & is inactive

•  Increased PO4 = Decreased Ca++

•  Alkalosis – Decreased iCa

•  Acidosis – Increased iCa

Hypocalcemia signs

Hypocalcemia

 Clinical presentation

•  Cardiovascular

  •  prolonged QTc, ↓BP, ↓CO, ventricular ectopy, ventricular fibrillation

•  Neuromuscular

  •  Tingling, spasms, tetany, seizures

•  Respiratory

  •  bronchospasm; labored shallow breathing

•  Gastrointestinal – smooth muscle hyperactivity

•  Bleeding – Ca++ needed to clot

 Safety – confusion & seizures

 Muscle cramps can precede tetany

 Monitor airway – bronchospasm

Hypophosphatemia < 2.5 mg/dL

Etiology

•  Decreased intake

  •  ETOH, Small bowel disease

•  Increased elimination

  •  Vomiting and diarrhea

  •  Use of phosphate binding antacids

  •  Increased urinary losses: osmotic diuresis, thiazide diuretics

•  Increased utilization

  •  Necessary for cellular energy

  •  Tissue catabolism: increase use in tissue repair

•  Intracellular shifts

  •  Alkalosis (respiratory)

  •  Refeeding syndrome

Etiology

•  Decreased intake

  •  ETOH, Small bowel disease

•  Increased elimination

  •  Vomiting and diarrhea

  •  Use of phosphate binding antacids

  •  Increased urinary losses: osmotic diuresis, thiazide diuretics

•  Increased utilization

  •  Necessary for cellular energy

  •  Tissue catabolism: increase use in tissue repair

•  Intracellular shifts

  •  Alkalosis (respiratory)

  •  Refeeding syndrome

 Clinical Manifestation: symptoms are secondary to

decreases in ATP and 2,3 DPG

•  Acute: Confusion, seizures, coma, chest pain due to poor oxygenation of the myocardium, numbness and tingling of the fingers, circumoral region, and incoordination, speech difficulty, weakness of respiratory muscle,

•  Chronic: Memory loss, lethargy, bone pain, hypomagnesemia

Hypophosphatemia < 2.5 mg/dL

 Management

•  Identification and elimination of the cause

•  Increase dietary intake of phosphate

•  Oral phosphate supplements – K+ Phos. tabs, neutraphos. capsules

•  IV : potassium phosphate

  • sodium phosphate

 Etiology

•  Increased intake

  •  phosphate containing antacids

•  Decreased excretion

  •  Renal failure

•  Transcellular shifts

  •  Respiratory acidosis

  •  Intracellular release

  •  Cell lysis of RBC, skeletal muscle or tumor cells

Hyperphosphatemia > 4.5 mg/dL

 Clinical Manifestation

•  Rebound hypocalcemia – phosphate binds with free

• calcium and ionized serum calcium falls

•  Ectopic disposition of Ca-PO4

•  Anorexia, nausea, vomiting

•  Muscle weakness, hyperreflexia, tetany,

•  Tachycardia

•  Increased PO4 = Decreased Ca++

 Management

•  Identification and elimination of cause

•  Use of aluminum, magnesium or calcium gels or

• antacids: binds phosphorus in the gut

•  Diet low in phosphorus

  •  avoid meats, fish, poultry, milk, whole grains, seeds, nuts, eggs, dried beans

•  Dialysis therapy

•  Acetazolamide stimulated urinary PO4 excretion

 Metabolic alkalosis

•  Always associated with hypochloremia

  •  Excess serum HCO3 displaces Cl in ECF resulting in

  • hypochloremia

  •  Decreased Cl delivery to nephron

  •  Volume sensing cells in distal tubules are chloride dependent

  •  Interpret hypochloremia as volume depleted

  •  RAA system activated = Na and HCO3 reabsorbed

  •  Acidosis – Cl excreted

  •  Alkalosis – Cl reabsorbed

Venous measure CO2

 Most acid/base disturbances can be detected by

evaluating venous CO2 i.e. HCO3

•  Laboratories typically measure HCO3 indirectly using

• CO2

•  This measured CO2 approximates HCO3 in the serum