Acute Kidney Injury and Chronic Kidney Disease

Acute kidney injury

Abrupt decline in GFR à loss of kidney function

• Inability to excrete wastes and water, maintain f/e balance, hormone production, RBC production

  • Azotemia – nitrogenous wastes in the blood

  • Uremia – urea in the blood

• Most common causes are ischemia and exposure to nephrotoxins

  • Major surgery, sepsis and severe pneumonia

• AKA:

  • Renal dysfunction

  • Renal insufficiency

  • Acute renal failure

• Associated with a significant increase in morbidity and mortality, LOS, complications and cost

  • Affects nearly 20% of patients admitted to the hospital

Azotemia

• nitrogenous wastes in the blood

Uremia

• urea in the blood

Causes of AKI

• Prerenal - 55% of cases

• Intrarenal - 40% of cases

• Postrenal - 5% of cases

Causes of AKI - prerenal

• 55% of cases

• hypoperfusion

Causes of AKI - Intrarenal

• 40% of cases

• Direct damage to the kidney

Causes of AKI - postrenal

• 5% of cases

• Obstruction

Prerenal image - patho note

• about 60%

• Decreased renal function

• ex. renal stenosis, hypotension

Intrarenal image - patho note

• about 35%

• direct kidney damage - tubular, glomerular, vascular, interstitial

• ex. acute tubular necrosis, glomerulonephritis, hemolytic uremic syndrome, tubulointerstitial nephritis

Postrenal image - patho note

• about 5%

• obstruction to urinary flow

• ex. stone, tumor

Causes of AKI - Prerenal

Anything that decreases vascular volume, cardiac output, systemic vascular resistance

• Decreases renal blood flow & perfusion

• Dehydration, hemorrhage, hypovolemia, renal artery stenosis/occlusion, hypotension, sepsis

• Decreased perfusion (Cardiac Output) leads to decreased GFR

  • Kidney needs 20-25% of cardiac output to maintain GFR

Prerenal AKI can reverse rapidly if blood flow is restored quickly

• Unresolved ischemia leads to nephron damage

Causes of AKI - Intrarenal

Direct damage to the kidneys

• Nephrotoxins:  due to medications injuring kidney tissue

  • Aminoglycoside Antibiotics:  gentamycin, vancomycin, neomycin, tobramycin

  • Contrast dye*

  • Acute, high dose exposure to NSAIDS:  acetylsalicylic acid (aspirin), ibuprofen, naproxen (causes decreased perfusion)

• Acute Glomerulonephritis:  due to severe inflammation reducing renal blood flow or prolonged ischemia

• Rhabdomyolysis - rapid muscle breakdown - athletes, statins, working out hard, seizures, crushing injuries

• Acute pyelonephritis

• Acute tubular necrosis (ATN)

  • severe consequence of prolonged exposure to any of the above

How to know its rhabdomyolysis:

• dark urine

• creatinine kinase high

• myoglobin high (damages the kidneys)

Causes of AKI - intrarenal - nephrotoxins

• due to medications injuring kidney tissue

  • Aminoglycoside Antibiotics:  gentamycin, vancomycin, neomycin, tobramycin

  • Contrast dye* - (nephrotoxic, monitor kidney function - give fluids to flush kidneys, give meds such as steroids to protect the kidneys)

  • Acute, high dose exposure to NSAIDS: acetylsalicylic acid (aspirin), ibuprofen, naproxen (causes decreased perfusion)

Causes of AKI - intrarenal - nephrotoxins - when to draw a trough

• (the low point)

• 30-60 minutes before

Causes of AKI - intrarenal - nephrotoxins - when to draw a peak

• (highest point)

• 30-60 minutes after COMPLETED administration, get it at its peak in the body (IV)

Causes of AKI - intrarenal - how to protect pts

• peak and trough!!

Causes of AKI - postrenal

Obstruction in the urinary tract – Postrenal

• Ureteral obstructions – renal calculi, tumors, fibrosis

• Bladder neck obstructions – BPH, CA prostate

• Urethral obstruction – strictures, tumor

• Spinal cord injury – inability to empty bladder

Acute kidney injury - urine volumes

• Anuria - less than 100 ml/24 hrs

• Oliguria - 100-400 ml/24 hrs

• Polyuria - excessive amount of urine in 24 hrs

Phases of acute kidney injury

1. Initiation phase - from insult to vein

2. Maintenance phase - Unstable period, severe drop in GFR, metabolic acidosis, neurological: confusion, agitation, lethargy, seizures/coma

3. Recovery phase - Process of tubular cell repair and regeneration and return of GFR to normal - renal function improves quickly in the first several weeks of this phase and continues up to 1 year

Phases of acute kidney injury - Initiation phase

• From insult to injury (hours to days)

  • Begins with initiating event and ends with tubular injury

  • If intervene now, can reverse

    • Often asymptomatic

Phases of acute kidney injury - Maintenance phase

• Unstable period, severe drop in GFR

• Urine output – usually less than normal

  • Oliguria – ischemic damage – 66% mortality

  • Non-oliguria– 25% mortality

• Salt/water retention cause

  • Edema

  • Hyperkalemia: Impaired potassium secretion (cardiac, neuromuscular function, nausea, diarrhea)

• Metabolic acidosis

• Anemia

  • Decreased production of erythropoietin

• Neuro: confusion, agitation, lethargy, seizures/coma

Phases of acute kidney injury - Recovery phase

• Process of tubular cell repair and regeneration and return of GFR to normal

• Diuresis:

  • Initially, abnormally large amounts of urine excreted as nephrons recover

  • Tubular function begins to recover

    • Increased urea and creatinine in the tubules, but not able to concentrate urine yet

• This increased diuresis may cause low BP, low fluid volume:  Closely monitor!

• Renal function improves quickly in the first several weeks of this phase and continues up to 1 year

Detecting AKI

• YOU may be the first to recognize the development of AKI!

  • Recognize risk factors and subtle changes

• Healthcare provider will determine type of AKI (pre, intra, post)

  • heart failure, dehydration, calculi, tumor, use of antibiotics?

Acute Kidney Injury - AKI

• Prevention is the goal!

• Assess history and risk factors

  • exposure to toxins, ischemia, meds, surgery, trauma

    • UTI

• Assessment

  • serum creatinine, BUN, urinary output, BP, pulse strength, edema, crackles, daily weight

Acute Kidney Injury - collaborative care

• Maintain adequate hydration and electrolyte balance

• Monitor aminoglycoside drug levels

• Identify clients at risk and initiate prompt treatment!

  • Elevated BUN with normal Cr = dehydration

    • Relieve post-renal obstructions

    • Correct pre-renal hypovolemia

    • Increase CO when inadequate

    • Restore renal perfusion

      • Renal dose dopamine

AKI treatment:

• Fluid/electrolyte balance

  • Fluid Restrictions?

  • Treat elevated electrolyte levels!

• Careful diuresis (furosemide or other loop diuretic)

  • Newest recommendation is to limit use

• Fluid challenge?

Hyperkalemia Treatment

• K-cocktail (D50 and insulin-R IV), sodium polystyrene sulfonate, sodium bicarbonate

  • Decreases potassium levels in blood

  • Binds to extra potassium in GI tract so it cannot be absorbed into the blood

• Calcium gluconate

  • Stabilizes cardiac cell membranes

Hyperkalemia Treatment - early symptoms

• Peaked T waves

Hyperkalemia Treatment - late symptoms

• Prolonged PR, loss of PR, wide QRS, bradycardia, vfib or asystole

AKI treatment cont.

• Maintain glycemic control

  • Elevated BG increases risk for infection, Multisystem Organ Dysfunction (MODS)

  • Hyperglycemic nephropathy

• Dialysis or CRRT? (Continuous Renal Replacement Therapy)

• Ongoing monitoring

  • Nephrologist

  • Skin care

  • Daily weight

  • Dietary restrictions

Chronic kidney disease (CKD)

• Progressive reduction of functioning nephrons

• A chronic problem!

  • Irreversible

  • Destroyed nephrons replaced by scar tissue

  • Results in uremia and azotemia

CKD causes:

• Diabetes: leading cause of ESRD

• Hypertension: closely follows diabetes

• Chronic glomerulonephritis

• Chronic pyelonephritis

• Polycystic kidney disease

• Systemic lupus erythematosus

CKD patho

• deterioration of nephrons

• GFR falls

• BUN/ creatinine rises

• Urine creatinine clearance decreases

• Increased glomerular capillary pressure damages capillaries which leads to sclerosis

CKD stages - stage 1

• GFR normal

• GFR - > 90 mL/min

  • BUN and Cr still normal

  • Asymptomatic

  • Normal kidney function as long as no stressors

CKD stages - stage 2

• GFR mildly decreased

• GFR – 60-89 mL/min

  • Mild hypertension

CKD stages - stage 3 (when its noticed usually)

• GFR 30-59 mL/min

  • Moderate decrease in GFR

  • HTN, anemia & fatigue, mild edema

  • BUN and serum creatinine elevated

CKD stages - stage 4

• GFR 15-29 mL/min

  • Severely decreased GFR

  • Kidneys can no longer maintain homeostasis

  • HTN, anemia & fatigue, malnutrition, edema, metabolic acidosis

  • BUN and serum creatinine continue to elevate

CKD stages - stage 5

• GFR <15 mL/min

• ESRD

  • Altered fluid/electrolyte balance

  • Accumulated metabolic waste affects every system of body

  • If left untreated, will die

    • Fluid/electrolyte problems

    • Cardiac arrhythmias, pulmonary edema, cerebral edema, death

  • Need dialysis or transplant

CKD S&S:

Affects all body systems!

• Fluid/Electrolyte/Acid-Base Balance

• Cardiovascular Effects

• Hematologic Effects

• Immune System Effects

• Gastrointestinal Effects

• Neurologic Effects

• Musculoskeletal Effects

• Endocrine and Metabolic Effects

• Dermatologic Effects

CKD - collaborative care

***Preserve renal function, delay need for dialysis and decrease risk of cardiovascular death!

• Control underlying disease

CKD - collaborative care - BP control

• Utilization of ACE and/or ARB

• ACE has kidney protective qualities and decreases proteinuria

CKD - collaborative care - Diabetic clients

• Keep HbA1C < 7

CKD - collaborative care - SGLT2 inhibitors

• empagliflozin, dapagliflozin

Blocks reabsorption of glucose and sodium to increase glucose excretion and reduce preload and afterload

Reduces risk of heart attack and stroke in CKD

Slows CKD progression

CKD - collaborative care - Mineralocorticoid receptor (MR) antagonist:

• finerenone

Slows CKD progression with DM II, decreases risk of cardiac death

Potent like spironolactone without risk of hyperkalemia

CKD - collaborative care - GLP1 receptor agonists:

• semaglutide, tirzepatide

Improve blood sugar control, reduce renal inflammation, slow disease, reduce risk for MI and stroke

CKD - collaborative care - symptom control

• Accumulation of nitrogenous waste/Fluid Excess

  • Monitor cardiac & respiratory systems

• Diet – low protein, low sodium, low potassium, low phosphorous

• Avoid nephrotoxins

• Fluid restriction?

  • Strict I&O

  • Daily weight

• Continue active lifestyle as long as possible

  • Walking, swimming, stretching

CKD additional meds:

• Diuretics

• Phosphate binders: sevelamer

• Supplemental vit D

• Vitamins and minerals

• Sodium bicarb

• Erythropoietin (epoetin alpha)

CKD additional meds - diuretics:

• Fluid volume excess prior to dialysis dependence

• *Selection and safety based on electrolyte levels

CKD additional meds - Phosphate binders:

• sevelamer

• Bind to and excrete phosphate

CKD additional meds - Supplemental Vitamin D

• Prevent osteodystrophy

CKD additional meds - vitamins and minerals

• nephrocaps-water soluble vitamins for renal disease

CKD additional meds - sodium bicarbonate

• tablets or infusions

• correct metabolic acidosis

CKD additional meds - erythropoietin

• (epoetin alpha)

• Decreased production by kidneys

• Stimulate bone marrow production of RBC

CKD - Hemodialysis

• An artificial kidney designed to provide controllable transfer of solutes and water across a semi permeable membrane - (dialysis of the blood) (3-4 hrs, 3 days a week)

Uses principles of

• Diffusion – movement of solutes from greater to lesser concentration

• Osmosis – movement of fluid from lesser to greater concentration of solutes

• Ultrafiltration – water and fluid removal across a pressure gradient

CKD - Hemodialysis - what solution is used and why

• Dialysate

• Varying amounts of sodium, calcium, magnesium, bicarb, chloride

• Based on patient’s labs

• To promote fluid and solute transfer

CKD - Hemodialysis - acute indications

•AKI refractory to treatment - (refractory = not responding)

•Hyperkalemia with AKI

•Fluid overload not responding to diuretics

•Metabolic acidosis

•Drug overdoses (lithium, ethylene glycol)

CKD - Hemodialysis - chronic indications

•CKD Stage 5- End-Stage Renal Disease

CKD - dialysis catheter - vascular access

• temporary!!!

• Subclavian, IJ or femoral vein

• Typically, short-term

• AKI - CKD if waiting for fistula/graft to mature!!

• Dual lumen

• Waiting for fistula or graft to mature

• Ineligible for AV fistula/graft

CKD - arteriovenous fistula - vascular access

• Artificial connection between the vein and the artery

• Takes about 4 weeks to mature

CKD - arteriovenous graft - vascular access

• surgical procedure

• Access created by putting a tube in to connect the artery and the vein

• Higher risk for infection

• Can use in about 2 weeks

CKD - vascular access complications

• Loss of vascular access

• Infection

• Inadequate blood flow

• Bleeding

CKD - venous access nursing care - grafts and fistulas

• Assess for thrill and bruit

• No BP or venipuncture in limb with device

CKD - grafts and fistulas - what is a thrill

• is a palpable, vibratory sensation felt with the hands

• feel the thrill!!!

CKD - grafts and fistulas - what is a bruit

• is an audible, whooshing sound heard through the bell of a stethoscope

• do you hear the brat!!

CKD - venous access nursing care - Early identification of thrombus

• Embolectomy

• Angioplasty

• Thrombolysis

CKD - venous access nursing care - education

• No constrictive clothing

• Do not sleep on arm

CKD - peritoneal dialysis

• utilizes the peritoneum rather than the pts blood

• not as efficient

• Uses peritoneal membrane as the dialyzer

• Catheter is placed into peritoneal cavity

• Dialysate instilled via catheter

• Dialysate is then drained by gravity in to “collection” bag

CKD - peritoneal dialysis - dwell time

• waste and electrolytes move into dialysate from highly vascular peritoneum

CKD - peritoneal dialysis - what often happens?

• Hypotension!! - removal of fluids! - always have more fluid going out rather than going in!!

• air embolism - air through peritoneal catheter possible

CKD - peritoneal dialysis - problems

• Not as efficient

• Inability to correct fluid or electrolyte problems quickly

• Respiratory difficulty

• Infection

• Peritonitis

• Occlusion of catheter from fibrin deposits

• Hypotension

• Air embolism

• Hemorrhage

CKD - peritoneal dialysis - care and assessment

• Catheter site

• Drained dialysate (COCA)

CKD - peritoneal dialysis - advantages

• Can be done at home

• More "normalcy"

CKD - dialysis complications

• hypotension!!! - number one!!

• bleeding

• infection

• dysrhythmias - shifting fluid and electrolytes in a short time span

CKD - what to think about for a pt getting dialysis that day

• Hold BP meds - beta blockers, ACE - worried about hypotension as is - don’t want it to be dialyzed out

• Hold antibiotics - will be dialyzed out

• Hold anti seizure meds - will also be dialyzed out

CKD - Continous renal replacement therapy - CRRT

• Similar to intermittent hemodialysis but done constantly

  • Useful in AKI and patients who are hemodynamically unstable

  • Continuously and slowly removes fluid and solutes

• Usually short term use (AKI)

• Process of ultrafiltration

  • very slow removal of blood, fluid and solutes

  • nurses manage machine and monitor effluent removal

CKD - renal transplant

• high success rates

• original kidney left in place

• lifelong immunosuppressants

• new kidney placed in iliac space

• donors - live or deceased

(donating is more dangerous than receiving) (wait time is over 5 yrs in OH)