Acute Kidney Injury (AKI) - PART I

Functions of the Kidney

Waste elimination

Release of erythropoietin

Secretion and reabsorption

Vitamin D conservation

Regulation of pH

Kidney elimination

metabolic waste - urea, uric acid, creatinine

- drugs/ foreign toxic - penicillin

- degrades polypeptide hormones - insulin/ glucagon/ PTH

Erythropoietin (EPO)

hormone secreted by the kidney to stimulate the production of red blood cells by bone marrow

Ca+ absorption

Activated vitamin D helps with ___ _________

RAAS

renin-angiotensin-aldosterone system

135-145 mEq/L

normal sodium levels

98-108

Chloride

3.5-5

Potassium

22-26

HCO3-

8.5-10.5

normal calcium levels

10-20

normal BUN

0.7-1.4

normal creatinine

7.35-7.45

pH of blood

2.5-4.5

normal phosphorus levels

Kidney Biopsy

Evaluates cellular function.

Post procedure care: pressure to site, bedrest following test, no heavy lifting

Renal Ultrasound

Evaluates size and anatomy of kidney

Pyelogram

x-ray of the renal pelvis

Cystourethrogram

Contrast via cystoscopy to view ureters and bladder

Renal arteriogram

Contrast via the femoral artery to view renal patency of renal vessels

Risks for AKI

Sepsis

Cardiac surgery

Cardiac failure

Respiratory failure

Mechanical ventilation or PEEP

Trauma

Rhabdomyolysis

Chronic Kidney Disease

Contrast Dye

Rhabdomyolysis

dissolution of striated muscle

Causes buildup of MYOGLOBIN

Tumor Lysis Syndrome (TLS)

an oncologic emergency with rapid lysis of malignant cells

Causes buildup of URIC ACID

decreased blood flow

A lot of kidney damage occurs due to a _______ ______ ______

Pre-renal AKI

Low perfusion states

Hypertension

Shock states

Cardiac failure

Intra-renal AKI

Progression of pre-renal type d/t ischemia

Toxins such as myoglobin, NSAIDs, chemotherapy, contrast dye

progress

Pre-renal can _____ to intra-renal, if ischemia results from low perfusion

Prerenal to intrarenal

Decreased blood flow

Decreased GFR

Renal tubular damage - urine may be heme +

Cell death and shedding - seen as casts in urine analysis

Manifestations of AKI

Uremia

Decreased UOP

Increased creatinine

Increased K+

Signs of hypervolemia

Metabolic acidosis

Decreased Ca+

Increased Phos+

Decreased Na+

Kussmaul breathing

gasping, labored breathing, also called air hunger

Sign of metabolic acidosis

Hypervolemia S/S

HTN, edema, crackles, elevated CVP

3-5 mmHg

Normal CVP

Chvostek's and Trousseau's signs.

hypocalcemia

Pruritis

itching

Sign of increased phos+

Signs of decreased Na+

nausea, tachycardia, decreased LOC, seizures

Hyperkalemia treatment

IV Ca gluconate

IV glucose, followed by IV insulin

IV sodium bicarbonate

Dialysis

Sodium polystyrene (kayexalate) or Patiromer (Veltassa)

IV Calcium gluconate

Stabilizes heart and antagonizes K+

IV glucose, IV insulin

Moves K+ intracellular

IV sodium bicarb

Pushes K+ into the cells and fixes acidosis

Prerenal AKI treatment

volume repletion, typically just NS

Intrarenal AKI treatment

Fluid restriction and diuretics

Low-dose dopamine

supports cardiac output and kidney perfusion by dilating the renal artery

Anemia treatment

Epoetin alfa, darbepoetin alfa, RBC infusion

Phosphorus binding drugs

-Calcium carb

-Aluminum carbonate

-Sevelamer HCL/Lanthamum carbonate

Na, K, Ph

With AKI, we want a dietary restriction of __, _, and __

NSAIDs

To protect the kidneys, avoid ______

1 hour

For patients with AKI, we want to measure I+O q______

15 minutes

AKI: Check vital signs Q__ _______

daily weight

best indicator of fluid balance