kidney/dialysis slides

kidney function

• filter blood

• excrete waste products, excess fluid

• produce urine

• help regulate BP

• electrolyte regulation

acute kidney injury

a sudden loss of kidney function that occurs over hours or days

• can occur WITHOUT permanent kidney damage

• potentially reversible

chronic kidney disease

slow and progressive destruction of nephrons and glomeruli that occurs over years

• results in kidney failure

• IRREVERSIBLE

risk factors for AKI

ICU patients most at risk (30% will need dialysis)

also…

• anyone w/diabetes

• CKD

• long standing HTN

• heart failure

• 60+

• recent hx of sustained low BP

• receiving more than 1 nephrotic drug

prerenal clinical manifestations AKI

caused by conditions that impair blood flow to the kidneys

• hypovolemia, decreased cardiac output, decreased peripheral vascular resistance, renal artery obstruction

sudden oliguria

• urine output LESS THAN 0.5 ML/KG/HR OVER 6-12 HRS

often providers will write these orders for adults: “notify provider if urine output is <30 mL/hr for 2 hrs”

azotemia (buildup of nitrogenous waste products in blood)

• BUN (10-20 mg/dL)

• Cr (male 0.6-1.2 mg/dL; female 0.5-1.1 mg/dL)

fall in GFR

fall in amt of sodium in urine (fractional excretion of sodium less than 1%)

intrarenal AKI causes

caused by conditions that cause ACTUAL DAMAGE to the glomeruli and the tubules

nephrotoxic injury

• drug or chemical exposure

interstitial nephritis

• allergic reaction

• infections (acute pyelonephritis)

other causes

• prolonged prerenal ischemia

• prolonged postrenal hydronephrosis

• acute glomerulonephritis

postrenal clinical manifestations AKI

caused by conditions that cause mechanical obstruction to the outflow of urine

s&s depend on cause

• urinary urgency

• flank or groin pain

• hematuria

bilateral obstruction can result in

• sudden oliguria and anuria

• azotemia if obstruction is not relieved in 48 hours

stage 1 AKI

creatinine: Cr 1.5-1.9 times baseline OR Cr increase > 0.3 mg/dL over 48 hours

urine output: < 0.5 mL/kg/hr for 6-12 hours

stage 3 AKI

creatinine: Cr > 3 times baseline, OR Cr > 4 mg/dL OR initiation of dialysis

urine output: < 0.5 mL/kg/hr for > 24 hours OR anuria > 12 hrs

prerenal collaborative care

• closely monitor I/Os (report urine output of less than 30 mL/hr for 2 hrs

• quickly restore circulating volume (pt drink, IV fluids, blood products

• increase cardiac output (admin meds that optimize HR, preload, afterload, contractility

• maintain MAP >60 mmHg

postrenal collaborative care

prevent hydronephrosis (inflammation of kidneys due to fluid buildup) with timely relief of obstructions

what kind of conditions lead to ischemia and intrarenal damage

prolonged prerenal and postrenal

common nephrotoxic medications

analgesics: NSAIDs

antihypertensives: ACE inhibitors and ARBs (usually kidney protective but CAN cause problems if dehydrated)

antimicrobials: aminoglycosides (gentamycin, tobramycin, amikacin), amphotericin B, vancomycin

chemotherapy agents: cisplatin, ifosfamide, methotrexate

heavy metals: lead, mercury

immunosuppressants: cyclosporine

IV radiographic contrast dye

nursing considerations for nephrotoxic meds

• for IV rad con dye screen all pt for pre existing impairment of kidney function (alternatives for at risk pt)

• follow agency protocols for patients at risk for contrast induced AKI (IV admin of isotonic saline before and after dye)

• hold metformin and for 48 hours after admin of contrast dye

• check Cr and BUN levels and urine output

• maintain hydration

• identify at risk pt

intrarenal AKI clinical manifestations

oliguria

• onset of oliguria is 24 hours to 7 days after insult

• patient can be non-oliguric

azotemia

sodium wasting

• fractional excretion of sodium (FE_Na ) is high (above 2-3%)

intrarenal AKI collaborative management

prevention

• prevent prolonged kidney hypoperfusion

• prevent prolonged hydronephrosis

• admin nephrotoxic drugs w/caution

• identify and treat group A beta streptococcus throat cultures w/penicillin or amoxicillin

fluid volume excess

clinical manifestations: distended neck veins and hand veins, bounding pulses, hypertension, dyspnea, crackles, pulmonary edema, weight gain, peripheral edema

collab interventions: low sod diet, loop diuretics, fluid restriction, dialysis or CRRT

monitor: I/Os, daily weights, vitals, lung sounds, skin (peripheral edema), electrolytes (sodium)

metabolic acidosis

cause: impaired kidney cannot excrete hydrogen ions, reabsorb bicarbonate, or gen new bicarb which is needed to buffer acids

manifestations: kussmaul breathing, restlessness, confusion, promotes hyperkalemia

collab interventions: oral sodium bicarb supplements, dialysis

when hospitalized monitor RR and rhythm, monitor serum bicarb lvls (goal 20-22 mEq/L, monitor ABGs or venous pH

hypermagnesemia (Mg2+ > 2.6 mEq/L)

cause: impaired kidney cannot excrete magnesium

clinical manifestations: neuromuscular (muscle weakness, lethargy, depressed deep tendon reflexes), GI (N/V), cardiovascular (hypotension, bradycardia, cardiac arrest

collab interventions: eliminate mag containing meds (antacids, laxatives), admin fluids and loop diuretics, dialysis

hyperkalemia (K+ > 5.0 mEq/L)

cause: impaired kidney cannot excrete potassium due to reductions in GFR

manifestations: neuromuscular (muscle weakness), GI (N/V, abdominal cramps and diarrhea), cardiovascular ( when K+ >= cardiac dysrhythmias, if >7 cardiac arrest )

collab interventions: restrict K+, hold K+ sparing diuretics (ACEi, ARB’s), admin loop diuretics (not effective for severe kidney impairment), admin GI cation exchange agents (sodium polystyrene sulfonate Kayexalate, patiromer Veltassa, sodium zirconium cyclosilicate Lokelma)

hyperphosphatemia (PO₄^3- greater than 4.5 mg/dL)

cause: impaired kidney cannot excrete phosphorus due to restrictions in GFR

manifestations: acute: s/s of hypocalcemia (muscle spams or cramps), prolonged: calcium phosphate deposits (can cause calcium to deposit in blood vessels, making them stiff)

collab interventions: dietary phosphorus restrictions, non calcium containing phosphate binders (ex: sevelamar (renagel or renvala), admin with every meal

• calcium containing binders like acetate should be avoided (they promote vascular and soft tissue calcification)

hypocalcemia (total calcium < 9 mg/dL; ionized calcium < 4.5 mg/dL)

cause: damaged kidney can’t produce calcitriol, serum phosphorus lvls increase with kidney failure

manifestations: acute hypocalcemia (tetany muscular spasms or muscle cramps, cardiac dysrhythmias), hypocalcemia assoc. w/renal failure is usually asymptomatic due to metabolic acidosis, prolonged hypocalcemia (osteomalacia and osteoporosis, vascular and soft tissue calcifications)

collab interventions: obtain 800-1000 mg of calcium daily from diet or supp., limit dietary phosphorus, admin phosphate binders, admin calcitriol

anemia

cause: damaged kidney not able to produce erythropoietin, poor appetite or dietary restrictions leads to iron, folate, vit B12 deficiency, uremia can cause hemolysis of RBC, blood loss w/hemodialysis

collab interventions: iron or folic acid supplements to support RBC synthesis, treated w/recombinant DNA erythropoietin agent (epoetin alfa Epogen subQ or IV 2-3x a week), target Hgb no greater than 12g/dL

9 clinical manifestations of oliguric phase of AKI

1. normal or decreased urine output

2. fluid overload if UO decreased

3. metabolic acidosis

4. hypermagnesemia

5. hyperkalemia

6. azotemia

7. hyperphosphatemia

8. hypocalcemia

9. anemia

usually lasts from 10 days to several months

azotemia

cause: impaired kidneys cannot excrete urea or creatinine

manifestations: none w/elevated creatinine, pt can experience uremic encephalopathy w/very high blood urea nitrogen (s&s: lethargy, mood swings, diminished ability to concentrate, disorientation and confusion)

collab interventions: low protein diet helps lower BUN, dialysis

foods high in phosphorus

• dairy foods (milk, cheese, ice cream)

• nuts and seeds

• dried beans and lentils

• meats

• bran cereal

• beer and cola

• chocolate

• honeydew melon

diuretic phase of AKI

clinical manifestations: high urine output (may result in hypovolemia, hypokalemia, hypomagenesemia), gradual resolution of azotemia, improved mental alertness

collab care: monitor I/O daily, monitor serum electrolytes (replace potassium and magnesium as needed)

this phase lasts 2-3 weeks

recovery phase AKI

• recovery continues for one year

• kidneys are particularly vulnerable to further insults

• some residual renal impairment is common

chronic kidney disease markers

evidenced by 1 or more of the following for greater than 3 months:

• albumin to creatinine ratio >30

• urine sediment abnormalities (ex: hematuria)

• abnormalities detected by histology or imaging

OR

GFR less than 60 mL for greater than 3 months

stages of CKD

stage 1

• evidence of kidney damage with normal GFR (> 90)

• clinical action is diagnosis and treatment, CVD risk reduction, slow progression

stage 2

• evidence of kidney damage w/mild low GFR (60-89)

stage 3a

• mod low GFFR w/or without other evidence of kidney damage (45-59)

• clinical action is slow progression, eval and treat complications, GFR <60 + KIDNEY FAILURE

stage 3b

• mod low GFR w/or without other evidence of kidney damage (GFR 30-44)

• clinical action is more aggressive treatment of complications

stage 4

• severe low GFR w/or without other evidence of kidney damage, GFR 15-29

• clinical action is preparation for RRT (dialysis or transplant)

stage 5

• kidney failure, end stage kidney disease, GFR less than 15 or dialysis

• clinical action is RRT started if pt desires, necessary to maintain life

collab interventions to slow progression of CKD

• healthy diet, physical activity, no smoking, weight management

• manage BG (keep HbA1c < 6.5)

• aim for SBP < 120 mmHg

• avoid meds that can worsen kidney functions (NSAIDS, some antibiotics, iodinated contrast dye…)

meds to slow CKD

SGLT2 inhibitors

• decrease BP and reduce workload on kidneys

ACEi or ARB

• add diuretics and dihydropyridine CCB if needed to achieve BP target

Mineralocorticoid receptor antagonists

Mod or high intensity statins (dose adjusted as CKD progresses)

nutritional therapy for kidney disease

• individualize diet based on stage of kidney failure

• pt should work w/dietician

• control protein intake (mod CKD stages 3-4 limit protein intake 0.6-0.8 g/kg/day

• eliminate red and processed meat (plant based sources best)

• severe CKD (stage 5) limit protein to 0.4 g/kg/day

• pt on dialysis may have more protein (esp peritoneal dialysis)

limit sodium (2k mg or less per day)

limit potassium (stages 3-5, while on dialysis, prevent hyperkalemia)

limit phosphorus (stages 3-5, while on dialysis, prevent hyperkalemia)

vit and mineral supplements

monitor caloric intake (anoxia common stages 4-5)

clinical manifestations CKD

often no symptoms until later stages

• oliguria → anuria

• fluid balance disturbances

• azotemia

• electrolyte acid imbalances

• uremic syndrome (N/V, fatigue, anorexia, weight loss, muscle cramps, pruritus, changes mental status

• cardio renal metabolic syndrome (CKD → insulin resistance → diabetes and elevated triglycerides → CVD

• depression

indications for dialysis

when diet and meds can no longer control the life threatening complications of renal failure

• AKI: fluid volume excess (subseq pulmonary edema or HF), hyperkalemia, uncompensated metabolic acidosis, uremic complications

• chronic renal failure: indicated when GFR less than 15 (end stage)

dialysis

process in which waste products (solutes) and excess water move from the blood through a semipermeable membrane into dialysis solution (dialysate)

general principles of dialysis

excess water is removed by OSMOSIS

excess solutes are removed by DIFFUSION

excess water and solute are also removed by ULTRAFILTRATION (solution moves by pressure gradient)

in center hemodialysis

pros

• trained staff perform treatment

• other ppl dialyzing, friendship and camaraderie may develop

cons

• treatment day and times scheduled by center

• must travel 3x week

• less privacy

• no loved ones allowed during

• rules against eating and drinking

home dialysis

pros

• studies that at home 5-7x week has better outcomes in every way (longer life, more survival)

• comfort

• flexibility of scheduling

• greater sense of control

cons

• dialysis partner must be present

• you and partner must take time off work or reg routine to attend training

• space in home needs to be dedicated to the machine

• no med professionals to answer questions or monitor treatment

peritoneal dialysis

pros

• studies show PD pt live longer

• more mobility and flexibility

• no machine needed

• may have fewer fluid and diet restrictions

• no needles needed

• can be good bridge to kidney transplant

• although PD is everyday, it takes less time than going to a center

cons

• done everyday

• catheter may affect body image

• BG can be more difficult to control in diabetes

• potential for weight gain due to glucose in dialysis fluid

• storage space req at home

• potential for infection in catheter

hemodialysis vascular accesses

internal access

• arteriovenous fistula (AV fistula)

• arteriovenous graft (AV graft)

external access

• central lines: short term is nontunneled double lumen, can be used immediately after insertion and removed 1-2 weeks after insertion. long term inserted into subclavian vein, can be used immediately after insertion and used long term

AV fistula or AV graft nursing considerations

assess for patency

• palpate or thrill

• auscultate for bruit

monitor for signs of infection

never take BP, draw blood, or use a wrist restraint on an extremity w/a graft or a fistula!

a lifeline for a lifetime…

complications of hemodialysis

• hypotension

• muscle cramps

• bleeding/loss of blood

• blood borne infectious diseases (Hep B and C)

• disequilibrium syndrome

complications of peritoneal dialysis

• exit site infection

• peritonitis (cloudy dialysis drainage, WBC present, temp > 101.5, abdominal pain, malaise, N/V (use sterile technique!)

• respiratory distress

• obstruction to inflow/outflow

• protein loss