Massive proteinuria (hyperalbuminuria) ^ urine albumin

(protein is leaking out of the kidneys into the urine from the glomerulus - any serious damage to glom. cause cause this)

Hypoalbuminemia - decreased blood albumin

Hyperlipidemia(cholesterolemia)

Edema - decr osmotic pressure, incr hydrostatic pressure = edema

Primary disease(idiopathic) 20% adult 80% children

occurs 2x >in boys than girls/2-7yrs age/can grow out of it

Secondary d/o r/t known glom. damage - more common in adults r/t lupus, glomerularnephritis, CK disease, DM

Congenital (autosomal recessive trait) - rare, does not respond to tx, end up needing dialysis

RAAS

Renin-angiotensin aldosterone secretion

Renin>angiotensinI>ACE convert to angiotensinII=vasoconstriction, ^BP l/t ^ perfusion

Aldosterone release=reabsorption of Na & H2O(where salt goes water follows)

Pathology of Nephrosis

1 of 2

Increased permeability of glomeruli to protein, especially albumin

Cause and mechanism not completely understood

Involves a threat to the immune system

(immunoglobulins lost throught the urine l/t greater risk for infection)

Pathology of Nephrosis

2 of 2

damage to epithelial cells of bowman's capsule l/t

^ permeability of glomeruli to proteins l/t

dec serum oncotic pressure l/t

tissue edema, third spacing fluid l/t

stimulation of RAAS & SNS l/t

Na & H2o retention l/t

edema

generalized edema(anasarca),periorbital scrotal,abdomen,intestinal mucosa (interferes w/ absorption)

anorexia, diarrhea

irritability, fatigue, lethargy, dec activity

pallor

normal BP or Hypotension

dec urine output, urine dark, frothy(lipuria)

^ susceptibility to infec

^ weight

Intravascular volume depletion=decreased UOP (urine output)

urinalysis - massive proteinuria

dec sp gr, dec volme, dark, frothy, hyaline casts

spot u/a or 24 hr urine collection

blood and serum studies

dec protein,^ lipids, ^ Cr(dec Cr if renal damage is present), nl or ^ H&H (b/c hemoconcentration)

renal bx

to determine cause

Therapeutic Medical Interventions for Nephrosis

Decreased excretion of Protein

(Corticosteroids(solumedrol/prednisone) & Cytoxan or Neoral)

Dec fluid retention - low Na diet, nl prot diet, fluid restr. use diuretic cautiously(monitor K level) plasma expander(25%salt poor albumin & diuretic)

Prevent Infection - antibiotics, observe closely/aseptic tech

Treat hyperlipidemia- statin Zocor

Susceptible to renal vein thrombosis(clots)resulting in PE/may use anticoagulants more often in children

Meds, monitor response, fluid balance (wt daily, I&O, assess for edema, abd girth, sp gr, ck for dec BP d/c of VD), bedrest

maintain skin integrity (turn/assess), NAS diet, nl prot, fluid restr, incr cal intake, s/s infection(cellulitis, fever, monitor visitors

Flare-ups can occur 2-4xyr x several yrs, watch for periorbital edema, chk for Hypovolemia, thromboembolism

Educate test urine for protein & f/u care

Excretory

-conserve/dicard H2O

-keep lytes WNL

-preserve acid-base balance

-eliminate nitrogenous wastes (result of prot brkdwn (urea, nitrogen, creatinine)

-rid body of bacterial toxins & water soluble drugs

Non-Excretory

-produce erythropoetin (make RBCs) (pts with Kid Dis are anemic - not producing enough erythropoetin)

regulate renin production = angiotensin II can l/t HTN

activate vit D ( for calcium absorption)

Glomerular Filtration (125L/d - kidneys filter fluid)

(+kid dis=dec GFR)

Tubular reabsorption(Loop of Henle+distal convoluted tubule)

Tubular secretion (kidneys excrete about 1.5L/d urine)

Age - elderly lose nephrons as they age, preexisting diseases more likely to Kid Dis (HTN, DM)

Children - more likely to regain normal function

Gender - Men prostate gland >obstruction

Women - shorter urethra, prone to UTI

Race - AA - 3-4x more common, live longer w/ ren dis & do better on dialysis

AA, Nat Amer, Mex Amer all have ^ incidence of ren dis

Family HX - predisposed  ex. polycystic kid dis

Renal Failure is:

*a severe impairment or total lack of renal function

*results in an inability to excrete metabolic wastes

*disturbs function of all body systems

Kidneys can maintain UOP even up to 75% of non functioning nephrons and only 25% functioning nephrons

ARF

*acute onset

*decline in glomerular filtration

*accumulation of waste products

(azotemia)

Azotemia

is the accumulation of nitrogenous waste products in the blood

3 Causes

Pre-renal

Intr-renal

Post-renal

List Pre-renal causes of ARF

*note -pre-renal causes are the most common

*hypovolemia - resonsible for 2/3 of ARF ex. hemorrage

*Decreased cardiac output -(low MAP) ex. MI

*intravascular pooling of blood - not enough pumped forward =dec venous return to the heart , ex. shock

*renal vascular obstruction - ex. clot in renal artery

see page III-B-20

MAP is the average pressure to vessels

normal MAP is 60-70

MAP= systolic + diastolic x2

________________

3

What are the intra-renal causes of ARF?

Intra-renal causes account for 25-40% of ARF

Pro-longed pre-renal disease

Nephrotoxins(IVcontrast dye,aminoglycosides(mycins)nasaids)

Intra-tubular Obstruction = acute tubular necrosis

Infection - pyleonephritis, glomerulonephrosis

trauma

malignant HTN

PIH

systemic disease - DM, autoimmune disease (lupus)

Intra-tubular obstruction is caused by acute tubular necrosis. 

The kidneys are hypoperfused over a long period of time causing the kidneys to suffer from ischemia. 

Ischemia occuring in the tubules shed (lining) causing obstructed urine flow

Mechanical (Obstructions)

-calculi, tumors, strictures & BPH

Functional

- neurogenic bladder (d/t spinal cord injury), diabetic nephropathy (d/t DM)

* if the bladder does not empty, damage will occur to the kidneys

Onset aka initiating phase

Oliguric phase

Diuretic phase

Recovery phase

The onset aka initiating phase is the initial insult or injury to the kidneys. 

Immediate intervention may cause reversal.

S/S may not appear x1week

8-14days duration

UOP<400cc/d, or anuric

dec spec grav & fixed

^Cr, ^BUN, ^K, metabolic acidosis

Na nl or dec r/t renal wasting & hemodilution

fluid retention, ^edema

dec H&H, dec Ca, ^Phos

uremic syndrome

The diuretic phase = recovery & treatment

lasts 1-3 wks

glomerular filtration recovers, azotemia levels off

osmotic diuresis

fluid & electrolyte fluctuations

can l/t dehydration, tachycardia, & hypotension

may still require dialysis

excretion of 4-5L of non concentrated urine

osmotic diuresis excretes waste indicriminately

watch electrolytes

correct imbalances

lasts up to 12m

improvement of renal function

BUN & Cr begin to stabilize and dec

labs begin to normalize

may be residual impairment

Lab studies

Radiologic

KUB, IVP, u/s, renal scan, ct scan

Other

renal arteriogram

renal biopsy

limited use w/ARF***injectable dye damaging to kidneys

contrast induced nephropathy=damage to kidneys

can see stones, tumor, cysts & urinary system

check for allergies (shellfish & iodine)

bowel prep, NPO after midnight

after proc ^fluids to flush dye

marginal ren function=mucomyst(renal vasodilator)

no metformin 24 prior & 48h after study

***good choice for a renal patient

non invasive

painless

no dye

Renal Scan

&

Ct Scan

Renal Scan =

nuclear medicine

radioactive dye

gamma camera

Cat Scan =

can show more subleties than u/s

similar to cardiac catherization

access through femoral artery to the aorta

inject dye to show renal artery stenosis

Open or Percutaneously (most common)

prone position, sand bag under kidney (to raise up)

local, needle bx

consent, may have bowel prep prior

coag studies prior

***lie very still during procedure

**apply pressure x10min after & lie still for a period of time

Bedrest x24h

ck vs q15mx4 > q30x2

ck site for bleeding

flank pain = possible internal bleeding

ck urine for gross blood

ck H&H

^fluids

determine cause & correct

manage complications

provide support

Prevention

****recognize early

close assessment to prevent dehydration, sepsis & shock

identify at risk pts (elderly, nephrotoxic drugs, hemodynamically unstable)

Early intervention

restore circulating blood volume

Management of Oliguric Phase in ARF

1 of 3

Manage Fluids

replace insensible loss

strict I&O

daily wgt

s/s VE=JVD, edema, ^CVP

Manage Electrolytes

replace lost electrolytes

phosphate binders (for ^phos levels)

treat hyperkalemia

^ K levels are toxic to the heart

^ K levels can cause dysrhythmias, heart standstill, ekg chgs

>5.5 TREAT w/ diet & meds(same as CRF)

may use dialysis

Management of Oliguric phase in ARF

2 of 3 

Control Acid Base D/O

metabolic acidosis may occur

monitor ABG's give NaHCO3 (sod bicarb-poss infusion)

dialysis (if sod bicarb does not work)

Decrease Metabolic wastes and Manage Nutrition

dec prot, ^CHO, ^ fat & calories

prot must have high biologic value=amino acids

meat, fisk, poultry, eggs/ enteral feed/Nepro

monitor & treat other effects of uremia

Management of Oliguric phase in ARF

3 of 3

Prevent infection & injury

judicious antibiotic use - monitor closely

Dialysis as indicated

^K, FVE, BUN>80, Cr>8-10

acidotic & uremic symptoms

avoid foley=source of infection

psychologic support

Manage fluid and electrolytes****be vigilant**mortality can occur b/c of shifts of fluid and lytes

careful fluid & lyte replacement (q2h)

dialysis may still be needed

Medical follow up***very important

**not totally 'out of the woods'

may take up to 1 year to return to normal

Chronic Renal failure

=

Chronic Kidney Disease(CKD)

CKD is a slow decline of kidney function

the slow onset is the progressive, irreversible destruction of both kidneys

Nephrons and glomeruli are destroyed and replaced by scar tissue

CKD results in uremia (^CR & ^BUN)

CKD is a systemic disease effecting every body system

congenital malformations (congenital nephrotic syndrome)

systemic diseases (DM, HTN**leading causes of CKD)

infection

toxins (including drugs)

obstructive nephropathy (prolonged BPH)

ARF progressing to CKD

Decreased renal reserve -GR 50%of nl, nl BUN & Cr, no s/s

Renal Insufficiency -GFR 20-50% of nl, polyuria, Dec fixed spec gr, azotemia, anemia, HTN

Renal Failure <20%of nl, ^azotemia, edema, met acid., hypercalicemia, poss uremia

EndStage Renal Dis. -<5% of nl, kidney atrophy & fibrosis, overt uremia

Fluid restriction based on individual circumstance

Limited PROT - must have high biologic value, need essential amino acids, brkdwn of PROT produces nitrogenous wastes

K & Na restrictions

avoid salt substitutes

*dietary restrictions most severe in non-dialysed pt

*diet more liberal for CAPD pt

*movement of fluid & molecules across a semi-permeable membrane from one compartment to another

*fluid & molecules move from blood through a semi-permeable membrane into the dialysate

Diffusion - movement of SOLUTES from an area of GREATER concentration to LESSER contration

Osmosis - movement of FLUID from an area of LESSER concentration of solutes to an area of GREATER concentration of solutes

Ultrafiltration - movement of FLUID across a semipermeable membrane as a result of an artificially induced pressure gradient **(not for peritoneal dialysis)

Peritoneal: uses the peritoneal membrane as the semipermeable membrane

Hemodialysis: uses an artificial membrance as the semipermeable membrane

*Peritoneal membrane is the dialyzing surface

*use a Tenckhoff cath thr abd wall - x18m

*dialysis solution 1-2L bags conc.gluc. warmed to body temp

*concentration is 1.5% or 4.25% glucose

*3 phases - inflow, dwell time, drain

*May add hep., K, or antibiotics to bag

*^ fluid to drain - turn side to side, gentle abd massage

**major problem ^^risk infec, strict aseptic techn.

Automated -occurs while pt is asleep

cath is opened 2x/d

a cycler (automated device is used to control phases of each cycle (inflow, dwell, & drain)

CAPD- 4-5 exchanges/d with 4-8h dwell time

Peritonitis s/s infec,cloudy dialysate, straw/clear color nl

Infection at exit site

abdominal pain

bleeding

resp difficulties

low back pain

catheter obstruction - fibrin clots

hernias (recurrent of abd wall)

protein loss

CHO & lipid abnormalities (gluc in dialysate absorbed)

Daily cath care - mask, sterile gloves

warm dialysate to body temp

strict aspetic technique

weigh pt before & daily

I&O

turn&massage to promote drainage

pt education

emotional support

Assess: thrill(feel) bruit(hear w/ bell) no venip & bp on shunt side, no heavy lifting, s/s infec& hand steel syndrome, no tight clothing on arm

Complications: can clot off, infection can occur, aneurysm may develop, may develop hand steel syndrome (affected perfusion to hand -colder in comparison to oppos extrem)

Dialyzer: primed w/NSS, blood in at top>fills fibers>dialysate enters & bathes outside of fibers>flushed w/NSS last

Procedure:access AVG/AVF w/2needles(14-16g), blood leaves pt>heperinized>through dialyzer>bubble detector(no air to pt)>blood back to pt

Performed 3xwk for 3-5h/d

Disequilibrium syndrome(dialysis diequilibrium)(generally do not feel well on dialysis days

Cardiovascular-arrhythmias, hypotension, blood loss, air embolus, hemmorrhage (have clamps ready), "steal synd"

muscle cramps(rapid lyte shifts)

infectious disease b/c anemia & ^incidence of Hep B&C

Sepsis

CSF not cleared well, drawing in more fluid=N,V

slowing rate can help with N,V

No treatment

Hemodialysis

Peritoneal Dialysis

Transplant

The surgical implantation of a human kidney from one person to another. (allograft)

Renal transplants are highly recommended for children w/ renal failure (may require 2nd&3rd as they age)

Typically an 18m-4y wait

Sources are 25-35% living donor &

65-75% cadaver donor(brain dead)

Good renal function

no evidence of infection (Hep, HIV, CMV)

no long-standing diabetes

no h/o cancer

no major systemic health problems

informed consent w/ psychologic eval

family consent for cadaver kidney

cost covered by recipient insurance

Kidney ok for 72h

Best to transplant w/in 24h of retrieval

medical evaluation

psychosocial evaluation

high risk*** patients***

diabetes

h/o cancer >5y w/o mets

very young, very old (2-70ys)

Hep B or Hep C

No Alcohol

active/chronic infection

chronic (severe) respiratory disease

disseminated malignancies

refractory heart disease

extensive vascular disease

unresolved psychosocial issures, (noncompliance, chem dependency)

ABO blood grouping

HLA (human leukocyte antigens) tissue typing (there are 6 antigens that ideally must be matched)

****does not have to be matched perfectly...can manage w/ immunosuppresants

Management of Renal Transplant Patient

Pre-Op

Pre-Op

blood & tissue typing, labs, EKG, blood trans (PRN)

pre-op teaching

 dialysis day prior to sx

 immunosuppresive tx pre-op or intra-op

Management of Renal Transplant Patient

Intra-Op

Intra-Op

donor kidney

kidney is transplanted w/ vessels and ureter

kidney is transplanted into iliac fossa

bilateral nephrectomies usually not done

diuretics

Management of Renal Transplant Patient

Post-Op

Post Op

SICUx24h, monitor fluid bal, chec lytes, BUN, &Cr., foley I&O,

titrate IV to UOP,check dressing (no bloody or clear drainage) urine may be blood tinged first, possible oliguria, poss dialysis

VS (adequate BP, no fever)

cough, Turn & DB, OOB, mouth cae

psychologic care, education

Hyperacute - rare, occurs intra-op or w.in a few hrs

remove kid, not reversible, dialysis

Acute - w/in24-72h-weeks, s/s ^temp, ^BP,^Cr, s/s uremia enlarged tender kidney

managed w/ immunosuppresants

Chronic - occurs months to years later

graft is destroyed by ischemia s/s, ^wt, ^BP, ^Cr, s/s uremia

back on transplant list when kidney completely fails

Infection

Cardiovascular disease-^atherosclerosis from immunosuppresants

malignancies-^risk for ca 100xgreater

reoccurrence of renal disease

corticosteroid related complications(gi bleed osteo,hypergly..)

Damage to joints-avascular necrosis, cataracts, DM, PVD

Goal: adequately suppress the immune system to prevent rejection of the transplanted kidney

Triple Drug Approach

1. Corticosteroid (prednisone)

2. Cellcept (chemotherapeutic agent)

3. Neoral (cyclosporine)

or

ProGraf (tacrolimus)

prevents rejection

complications; infection, malignancies, recurrent renal dx

meds to prevent infection/ulcers (Bactrim for UTI prev, Nystatin for fungal prev, Pepcid for ulcer prev(b/c steroids)

Private room to decrease exposure

meticulous care of invasive lines

patient education- s/s organ rejection, compliance w/ med, monitor for infec, f/u w/dr

Chronic Grief in CKD (renal failure)

&

Mnagement of Chronic Grief

accumulated, prolonged

decreased functioning

powerlessness

new waves occur w/ exacerbation

manage: help pt understand disease

link pt w/ needed services

encourage communication of concerns, feeling w/ family & caregivers

help pt use coping stategies

support family

Advantages:

Fewer dietary restrictions

less cardivascular stress

preferred for children(^independence, older kids can perform)

mimics normal kidney function

Disadvantages:

peritonitis

exit-site & tunnel infections

hyperglycemia

contraindicated in pt w/ mult sx or trauma

Advantages:

Rapid fluid removal

rapid removal of urea and creatinine

effective potassium removal

Disadvantages:

Vascular access problems

dietary and fluid restrictions

disequilibrium

NSS (0.9%)

Lactated Ringer's

0.45% NS

D5W

(push out)

3% & 5% NS

pull in

Fluid Volume Deficit(FVD)

Assessment Findings

dec Daily Bdy Wt

dec UOP ^ spec gr & concentrated urine

dec fontanel, salivaton, tears, turgor, dry skin +tenting

3rd spacing, ascites, dev intravascular volume

^ rapid thready weak pulse, dec BP

^ or nl breath sound/resp rate

dec CVP, no JVD

^hematocrit,^BUN, altered sensorium

Fluid Volume Excess(FVE)

Assessment Findings

^daily bdy wt

^uop if nl perfusion, dec UOP if heart disease

dec spec grav, light colored urine

edema, tears, swollen legs pitting, pleural eff, anasarca

^BP, if heart disease may go down

^ pulse (bounding)

^SOB, orthopnea, wheezes, crackles, pulm edema

dec hematocrit, dec BUN

altered sensorium

Taken lying, sitting, & standing

one minute inbetween

if systolic 15 less and pulse ^20 = +test

MAP is an indication of overall perfusion

normal 60-70 mmHg

systolic + 2x diastolic

_______________

3

central venous pressure

2-6 normal

assess @ 45 degree angle-semi-fowlers

ALG (antilymphocytic globulin)

ATG (antithymocytic globulin(ATGAM)IV, PO

OKT (Orthoclone) IV or (Muromonab-CD3), IV

Basiliximab (Simulect) IV

Daclizumab (Zenapax) IV

Cyclosporine (Sandimmune)PO, IV (Neoral, Gengraf) PO

Tacrolimus (Progaf) PO

Corticosteroids (Prednisone)PO, (Methylprednisolone(soluMedrol))IV

Myciohenolate mofetie (CellCept)PO, 

Sirolimus (rapamune)

TBW=60% of the adult body

ICF=fluid located in the cells containing dissolved solutes

ECF=fluid located outside the cell composed of plasma & ISF

Plasma=water, straw colored fluid component of lymph and blood in which WBC,PBC, and platelets are suspended

ISF=fluid that fills the spaces between the cells in the body

Cells=ICF=fluid in the cells

Cells=ECF=fluid outside the cells

Blood Vessels=IVF=inside the blood vessels

Blood Vessels=EVF=ouside the blood vessels

Tissues=ISF=in spaces between the cells but not the plasma or in the cells

TBW 60%

↓

                                        ECF                   &                 ICF (most stable is the ICF)

↓

Plasma (least stable) & ISF (reserve fluid)                                                          

Chronic Kidney Disease

Kidney Function Disturbance Causes the following:

↓ Erythropoietin Production

↓in activation of VitD and ↓excretion of phosphate

↓ Potassium excretion

↓ hydrogen ion excretion

↑ uric acid (nitrogenous waste)

altered sodium balance

↓ excretion of fluids

↑ renin production

Erythropoietin is produced in the kidneys and is markedly decreased in CKD.

Erythropoietin stimulated bone marrow to create RBC's

Body needs adequate iron levels for erythropoietin to work

EPOGEN=artifical erythropoietin, SQ or IV@ end of dialysis

PROCRIT=too much can cause ♥ problems

Hem & HCT levels ↓

pale

↓O2 capacity 

activity intolerance

♥ works harder

tachycardia

Uremia refers to ↑ BUN & Creatinine in the blood (nitrogenous waste product/urine in the blood)

*accelerated artherosclerosis

*impaired insulin production and insulin resistance

*impaired platelet function due to metabolic toxins

*irritation to gastrointestinal system

*irritation to neurological system

*irritation to integumentary system(rare)

*impairment of reproduction system

*Physcosocial impact

ESRD

End Stage Renal Disease

ARF

Acute Renal Failure