Acute and Chronic Kidney Injury

what do the kidneys do besides filter blood and reabsorb electrolytes

secretes renin - RAAS blood pressure, erythropoietin for RBC production, calcitriol for vitamin D

acute kidney injury (AKI) pathophysiology

most common caused by tubular necrosis due to hypotension, hypovolemia, or a nephrotoxic agent. results in azotemia and uremia. causes can be prerenal, intrarenal, or post renal.

azotemia

nitrogen waste product build up in the blood

prerenal AKI causes

cardiogenic shock, HF, MI, oliguria, low GFR. usually reverses quickly

intrarenal AKI causes

nephron damage - ischemia, nephrotoxins, aminoglycosides, contrast dye, increased HgB, myoglobin, shock. 55% mortality rate, must treat underlying cause.

postrenal AKI causes

mechanical obstruction of urinary outflow - cancer, stones, trauma.

AKI phases

oliguric, diuretic, recovery

oliguric phase AKI

low urine output/no waste filtered through to urine. <400 mL/day, volume overload. UA - casts, RBCs, WBCs, protein. metabolic acidosis. hemodilution - low Na+ and Ca+, high K+. high BUN + Cr

diuretic phase AKI

kidney excretes high volume 1-3L urine daily but with low osmolality. hyponatremia, hypokalemia, dehydration.

recovery phase AKI

GFR norm, BUN and Cr go down to normal range

osmolality levels in AKI

urine osmolality elevates more, urine becomes more concentrated if less blood runs through kidneys. fluid retention decreases blood osmolality by diluting it.

AKI diagnostic tests

BUN, Cr, electrolytes. Renal US, renal scan - blood flow + tubular function, CT, biopsy, U/A, C + S, CrCl, osmolality

AKI collab care

eliminate cause, fluid restriction, INCREASED protein, low K+ P+ Na+ diet, telemetry for hyperK+, BUN + Cr, Ca+/P+ ratio, loop diuretics, dialysis, CRRT

hyperkalemia collab care

dextrose + IV insulin, NaHCO3, calcium gluconate, Kayexalate, hemodialysis, K+ restriction 40 mEq/day

AKI nutrition

high protein, calcium encouraged, low Na+, K+, P+

chronic kidney disease (CKD) pathophysiology

irreversible nephron destruction, defined as GFR <60mL/min for 3+ mo.

normal GFR

90+

CKD stages GFRs

1) >=90, 2) 60-89, 3) 30-59 w/ polyuria and anemia, 4) 15-29 induces renal failure, prep for dialysis, 5) <15 end stage, requires dialysis

CKD clinical manifestations

uremia - frost + prioritis, polyuria → oliguria → anuria, chronic metabolic acidosis, edema, HTN, HF, anemia, bleeding tendencies, CVD, dysrhythmias - hyperK+, hypoCa+, CNS depression,

metabolic acidosis symptoms and collab care

confusion, lethargy, seizures, kussmaul, n+v+d, arrhythmia and muscle weakness due to Na+ K+ changes. I/O, LOC, NaHCO3, tx underlying problem

priority for patient with high BUN (>200 mg/dL)

check for safety, patient in acidosis

metabolic alkalosis symptoms and collab care

loss of stomach acid/steroids/K+ depletion → decreased calcium → dizzy/tingly/tetany/tremors. decreased resp rate, lethargy, arrhythmia, cramps. I/O, LOC, resp + VS, electrolytes *Ca+, IV fluids, tx underlying problem

CKD diagnostic tests

CrCl most accurate, BUN/Cr, electrolytes, lipid profile due to CVD risk, renal US, scan, CT, biopsy, UA

CKD collab care

cardiac monitor for electrolytes. control HTN, dyslipidemia, electrolyte imbalances. Restrict P+ and give Ca+ for bone problems. RESTRICT protein, Na+, K+. fluid restriction to <300 w/ meals and at bedtime, no fluids running 100mL/hr or more, daily weights. Parathyroidectomy for low Ca+. dialysis, CRRT.

CKD pharm tx

phosphate binders, Ca+ supplements, anti-HTN, ACEis, ARBS, erythropoietin, statins. *adjust to renal function, esp older adults.

peritoneal dialysis contraindications

thoracic/abdominal surg, COPD, Crohns (checks. lol)

peritoneal dialysis complications

site infection, peritonitis, abd pain, lower back pain, bleeding, blockage, PE, atelectasis, pneumonia (fluid build up), CHO and lipid abnormalities

what to do when peritoneal dialysis blockage

turn side to side, reposition self, have a BM

hemodialysis nursing priorities

monitor VS closely - HTN during and hTN after, BP usually held during.

AV fistula assessment + nursing interventions

Bruit, thrill, limb alert, monitor for complications, no heavy lifting, clean w/ mild soap

hemodialysis complications

hypotension, muscle cramps, blood loss - I+O, hep B + C, sepsis, infection, irritation, clotting, disequilibrium (solute change) → cerebral edema

CRRT mechanism

hemodialysis for a hemodynamically unstable patient, slow continuous removal of fluids with a low risk of hypotension. operated by a trained ICU RN.

dialysis collab care

high quality protein, strict Na+/K+/P+/fluid limit, I+O and weights, neuro status, site assessment.

CKD kidney transplant criteria

candidates meet physical and psychological requirements, withstand surgery and be complaint with regimen for life

kidney transplant time limit

kidney should be used before 24 to avid acute tubular necrosis, but may go up to 74 hr

new kidney transplant recipient collab care

12-24 hr ICU, large urine expected, low urine is concerning. I+O balanced. CVP for fluid status. May require dialysis due to acute tubular neurosis of transplanted kidney. electrolytes, urinary catheter blockage, check patency.

long term kidney transplant recipient collab care

infection, hand washing. CVD - higher incidents of vascular disease. monitor weight gain, blood glucose, manage HTN

kidney transplant recipient pharm regimen

immunosuppressant - high risk of infection and malignancy

transplant recipient rejection symptoms

increased BUN/Cr, fever, HTN, weight gain, edema, oliguria, tenderness over graft, apprehension, frequently reversible by increasing immunosuppressants and corticosteroids

live donor collab care

observe for retro bleed, usual post op care.