Acute Kidney Failure

Pathophysiology

: AKI/ARF has sudden onset, usually reversible decrease in kidney function.

Acute renal failure commonly affects clients who are hospitalized and is contributing factor to decision to admit for other medical conditions.

The most common comorbidities for ARF

are DM types 1, 2, HTN, HyperLipidemia (DHH)

Depression is most common psychological complication.

People who have renal failure can struggle with anxiety finances, treatment, adjusting to a new normal way of life.

Acute kidney failure has an impact on

many other organs .

As adults age, changes in kidney function decrease and presence of comorbidities increase the incidence of acute renal failure among clients 75 years +.

Pre-renal:

Decreased blood flow/PERFUSION to Kidneys: 

Approximately 60% of ARF cases are due to _______

Cause: HypOTension, HypOVolemia, Heart/Liver failure

Pre-renal Medications

can also lead to pre-renal ARF, such as (NSAIDS), angiotensin receptor blockers (ARB), angiotensin-converting enzyme inhibitors (ACEI), Cyclosporine.

Intra-renal: 

damage has occurred to the functional part of kidney, parenchyma (renal cortex, renal medulla) 

Approximately 35% of ARF cases are due to _____ causes

Intra-renal causes

Nephrotoxic agents/medications, contrast dyes, extended prerenal failure, aminoglycosides.

Other causes: Acute interstitial nephritis, CT disorders- Lupus, Fat emboli, Rhabdomyolysis

Acute Tubular Necrosis

most common type of INTRARENAL causation with High rates of morbidity and mortality.

Cells of renal tubules become damaged and proceeds to cell death and (GFR) decreases.

Preceded by Sepsis, Acute ischemic event, toxic event due to Nephrotoxic mechanism.

Nurse should be aware of risk of development of ATN (acute tubular necrosis) in Pt who

have hypOtension, Sepsis, taking nephrotoxic meds/agents, like Vancomycin, Contrast dye.

Post-Renal

involves urinary system below kidney, preventing urine from draining, like obstruction in urinary tract . 

Post-renal ARF accounts for approximately 5% of cases.

Post-Renal Causes

Compression or obstruction of urinary tract from enlarged prostate, masses, clots/calculi, neurogenic bladder.

The most common INITIAL manifestation of AKI

is OLIGURIA, less than 400 mL/day.

Usually occurs within 1 - 7 days of injury

If cause is ischemia, then within 24 hours.

The oliguric phase lasts

•lasts about 10 - 14 days, can last Months in some cases.

The longer the phase , the poorer the prognosis for complete recovery of kidney function.

About 50% of Pt will NOT

be oliguric, making initial diagnosis more difficult.

Changes in urine output generally DON’T correspond to changes in GFR.

Changes in urine output helpful in differentiating Etiology of AKI. For example,

Anuria usually seen with urinary tract obstruction

Oliguria commonly seen with PRErenal causes,

Nonoliguric seen with acute interstitial nephritis and ATN.

A Urinalysis may show

Casts, RBCs, WBC.

Casts are formed from mucoprotein impressions of necrotic renal tubular epithelial cells, which detach or slough into tubules.

Urinary specific gravity

gravity (measure of concentration of solutes in urine) is normally 1.003-1.030.

Urine osmolality is used

to measure number of DISSOLVED particles in urine.

Range is 300-1300 mOsm/kg.

As a measure of urine concentration, it is more accurate than specific gravity.

Hypovolemia (volume depletion) has the potential

to exacerbate all forms of AKI, especially PRErenal causes.

When urinary output decreases, fluid retention occurs.

Severity of manifestations depends on extent of fluid overload.

In case of reduced urine output (anuria and oliguria),

the neck veins may become distended with a bounding pulse. Edema, HTN may develop.

•Fluid overload can eventually lead to heart failure, pulmonary edema, and pericardial and pleural effusions.

In Metabolic acidosis- The

Impaired kidneys cannot excrete hydrogen ions or acid products of metabolism.

Serum bicarbonate (HCO3−) production decreases

from defective reabsorption and regeneration of HCO3− ions.

Serum HCO3− is depleted through buffering of acidic hydrogen ions and metabolic end products.

The patient with severe acidosis may

develop Kussmaul respirations (rapid, deep respirations) to try to compensate by increasing CO2 exhalation.

Damaged tubules cannot

conserve sodium.

Urinary sodium excretion may increase, resulting in normal or below-normal levels of serum sodium.

Excess sodium intake is avoided because it can lead to volume expansion, HTN, HF.

The kidneys normally excrete

80% to 90% of body’s potassium.

In AKI, serum potassium level increases because kidney’s normal ability to excrete potassium is impaired.

Hospital-acquired AKI often occurs

in patients who have multiorgan failure. Leukocytosis is often present.

MOST COMMON CAUSE OF DEATH IN AKI IS INFECTION

The kidneys are the

primary excretory organs for Urea (end product of protein metabolism) and Creatinine (end product of endogenous muscle metabolism).

BUN and serum creatinine levels increased in kidney disease.

Neurologic Disorders

Neurologic changes can occur as nitrogenous waste products accumulate in brain and other nervous tissue.

Diuretic phase

•Daily urine output is 1 - 3 L

•May reach 5 L or more

•Monitor for hypONatremia, hypOKalemia, Dehydration (HHD)

Recovery phase begins when

the GFR Increases, allowing BUN and serum creatinine Decrease.

Major improvements occur in first 1 to 2 weeks of this phase, but kidney function may take up to 12 months to stabilize.

Some Pt don’t recover and progress to end-stage renal disease.

Older adult less likely to have complete recovery of kidney function.

Serum creatinine M: 0.7-1.3 mg/dL, F: 0.6-1.1 mg/dL

Analyzes kidney function

Creatinine is byproduct and levels of creatinine rise if unable to be excreted from body through kidneys.

Blood urea nitrogen (BUN) 6-24 mg/dL

Provides information on how kidneys are processing UREA nitrogen which is a byproduct of Protein metabolism.

BUN levels RISE as the kidney function decreases

Glomerular filtration rate (GFR)

The purpose of this test determines how well kidneys are filtering excess fluids and waste products from blood

GFR less than 15 mL/min/1.73 m² indicates need for intervention, like dialysis

Dialysis is a procedure in

which waste products and excess fluid are removed from blood through machine that has special filter when kidneys unable to function

Fluid and Electrolytes

•Inadequate blood flow

•Decreased perfusion and urine output

•Retention of fluid and sodium

•Accumulation of waste

•Electrolyte disturbances

AKI Causes

UAEION

Uremic toxins

Acid/base imbalance

Electrolyte

Inflammation

Oxidative stresses

Neuro-hormonal dysfunction

Brain

Uremic encephalopathy

Dementia (long-term)

Stroke (long-term)

Heart

CHF

Arrythmia

Ischemic heart disease

Lung & Liver

Acute lung injury

Pulmonary edema

Liver- Altered hepatic metabolism/synthesis

Intestine & Immune system

Altered gut macrobiotia

Uremic toxin accumulation

Immune- systemic inflammation

Studies have shown chemicals in

pesticides and long-term exposure to farm workers and families may raise incidence of kidney failure (clothing)

Relationship between hard physical labor and excessive sweating in elevated temperatures causing damage to kidney tubules due to dehydration. 

The nurse should provide education ensuring

maintaining hydration with a clean water source while working in high temperatures.

Safe handling of potentially contaminated work clothing, wash thoroughly and launder contaminated clothing separately.

Nurses can advocate for

Safe work practices and protection for workers, like hydration stations providing clean water and adequate time for the workers to hydrate and for protective garments to shield from contaminants.​​​​​​​